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How to treat type 1 herpes: Dealing With Knowing You Have Genital Herpes

Содержание

Herpes Simplex Type 1 – StatPearls

Continuing Education Activity

Herpes simplex virus type 1 (HSV-1) is a linear dsDNA virus that is a member of the Alphaherpesviridae subfamily. HSV-1 is responsible for establishing primary and recurrent vesicular eruptions, primarily in the orolabial and genital mucosa. HSV-1 infection has a wide variety of presentations, including orolabial herpes, herpetic sycosis (HSV folliculitis), herpes gladiatorum, herpetic whitlow, ocular HSV infection, herpes encephalitis, Kaposi varicelliform eruption (eczema herpeticum), and severe or chronic HSV infection. Antiviral therapy limits the course of HSV infection. This activity describes the evaluation, and treatment herpes simplex virus type 1 and reviews the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

  • Describe the pathophysiology of a herpes type 1 infection.

  • Review the risk factors for herpes type 1 infection.

  • Explain the presentation of a patient with herpes type 1 infection.

  • Outline the importance of improving care coordination amongst interprofessional team members to improve outcomes for patients affected by the herpes type 1 virus infection.

Earn continuing education credits (CME/CE) on this topic.

Introduction

Herpes simplex virus type 1 (HSV-1) is a member of the Alphaherpesviridae subfamily. Its structure is composed of linear dsDNA, an icosahedral capsid that is 100 to 110 nm in diameter, with a spikey envelope. In general, the pathogenesis of HSV-1 infection follows a cycle of primary infection of epithelial cells, latency primarily in neurons, and reactivation. HSV-1 is responsible for establishing primary and recurrent vesicular eruptions, primarily in the orolabial and genital mucosa. HSV-1 infection has a wide variety of presentations, including orolabial herpes, herpetic sycosis (HSV folliculitis), herpes gladiatorum, herpetic whitlow, ocular HSV infection, herpes encephalitis, Kaposi varicelliform eruption (eczema herpeticum), and severe or chronic HSV infection. Antiviral therapy limits the course of HSV infection.[1][2][3]

Etiology

Risk factors for HSV-1 infection differ depending on the type of HSV-1 infection. In the case of orolabial herpes, risk factors include any activity that exposes one to an infected patient’s saliva, for example, shared drinkware or cosmetics, or mouth to mouth contact.

The major risk factor for herpetic sycosis is close shaving with a razor blade in the presence of an acute orolabial infection.

Risk factors for herpes gladiatorum include participation in high-contact sports such as rugby, wrestling, MMA, and boxing.

Risk factors for herpetic whitlow include thumb sucking and nail biting in the presence of orolabial HSV-1 infection in the child population, and medical/dental profession in the adult population (although HSV-2 most commonly causes herpetic whitlow in adults).

A major risk factor for herpes encephalitis is mutations in the toll-like receptor (TLR-3) or UNC-93B genes. It has been postulated that these mutations inhibit normal interferon-based responses.

The major risk factor for eczema herpeticum is skin barrier dysfunction. This can be seen in atopic dermatitis, Darier disease, Hailey-Hailey disease, mycosis fungoides, and all types of ichthyosis. The increased risk is also associated with mutations in the filaggrin gene, which is seen in atopic dermatitis and ichthyosis vulgaris. Pharmaceutical risk factors for eczema herpeticum include the use of topical calcineurin inhibitors such as pimecrolimus and tacrolimus.

Risk factors for severe or chronic HSV infection include immunocompromised states such as transplant recipients (solid organ or hematopoietic stem cells), HIV infection, or leukemia/lymphoma patients.[4][5]

Epidemiology

It has been hypothesized that approximately one-third of the world’s population has experienced symptomatic HSV-1 at some point throughout his or her lifetime. HSV-1 first establishes primary infection in patients with no existing antibodies to HSV-1 or HSV-2. Non-primary initial infection is defined as infection with one HSV subtype in patients who already have antibodies to the other HSV type (i.e., HSV-1 infection in a patient with HSV-2 antibodies, or vice versa). Reactivation results in recurrent infection and most commonly presents as asymptomatic viral shedding.

Approximately 1 in 1000 newborns in the United States experience a neonatal herpes simplex virus infection, resulting from HSV exposure during vaginal delivery. Women with recurrent genital herpes have a low risk of vertically transmitting HSV to their neonate. However, women who acquire a genital HSV infection during pregnancy have a higher risk.

Epidemiologically, it is important to note that herpes encephalitis is the leading cause of lethal encephalitis in the United States, and ocular HSV infection is a common cause of blindness in the United States.[6][7][8][9][10]

Pathophysiology

HSV-1 is typically spread through direct contact with contaminated saliva or other infected bodily secretions, as opposed to HSV-2, which is spread primarily by sexual contact. HSV-1 begins to replicate at the site of infection (mucocutaneous) and then proceeds to travel by retrograde flow down an axon to the dorsal root ganglia (DRG). It is in the DRG that latency is established. This latency period allows the virus to remain in a non-infectious state for a variable amount of time before reactivation.  HSV-1 is sly in its ability to evade the immune system via several mechanisms. One such mechanism is inducing an intercellular accumulation of CD1d molecules in antigen presenting cells. Normally, these CD1d molecules are transported to the cell surface, where the antigen is presented resulting in the stimulation of natural killer T-cells, thus promoting immune response. When CD1d molecules are sequestered intercellularly, the immune response is inhibited. HSV-1 has several other mechanisms by which it down-regulates various immunologic cells and cytokines.[11][12][13][14][15][16]

Histopathology

Classic, though not pathognomonic, histologic findings for HSV infection include ballooning degeneration of keratinocytes and multinucleated giant cells. Multinucleated keratinocytes may contain Cowdry A inclusions, which are eosinophilic nuclear inclusions that can also be seen in other herpesviruses such as varicella-zoster virus (VZV) and cytomegalovirus (CMV). There is no pathognomonic histologic finding for HSV-1 infection, and therefore, clinical correlation is crucial during histopathologic evaluation.[12]

History and Physical

It is important to note that HSV-1 infection is frequently asymptomatic. When symptoms do occur, there is a wide range of clinical presentations including orolabial herpes, herpetic sycosis (HSV folliculitis), herpes gladiatorum, herpetic whitlow, ocular HSV infection, herpes encephalitis, Kaposi varicelliform eruption (eczema herpeticum), and severe or chronic HSV-1 infection.

HSV-1 is the most common culprit of orolabial herpes (a small percent of cases are attributed to HSV-2). It is important to note that orolabial HSV-1 infection is most commonly asymptomatic. When there are symptoms, the most common manifestation is the “cold sore” or fever blister. In children, symptomatic orolabial HSV-1 infections often present as gingivostomatitis that leads to pain, halitosis, and dysphagia. In adults, it can present as pharyngitis and a mononucleosis-like syndrome.[17]

Symptoms of a primary orolabial infection occur between three days and one week after the exposure. Patients will often experience a viral prodrome consisting of malaise, anorexia, fevers, tender lymphadenopathy, localized pain, tenderness, burning, or tingling prior to the onset of mucocutaneous lesions. Primary HSV-1 lesions usually occur on the mouth and lips. Patients will then demonstrate painful grouped vesicles on an erythematous base. These vesicles exhibit a characteristic scalloped border. These vesicles may then progress to pustules, erosions, and ulcerations. Within 2 to 6 weeks, the lesions crust over and symptoms resolve.[18]

Symptoms of recurrent orolabial infection are typically milder than those of primary infection, with a 24-hour prodrome of tingling, burning, and itch. Recurrent orolabial HSV-1 infections classically affect the vermillion border of the lip (as opposed to the mouth and lips as seen in primary infection).[19]

Initial or recurrent HSV-1 infections may affect the hair follicle, and when this occurs, it is termed herpetic sycosis (HSV folliculitis). This will present on the beard area of a male with a history of close razor blade shaving. Lesions exist on a spectrum ranging from scattered follicular papules with erosion to large lesions involving the entire beard area. Herpetic sycosis is self-limited, with a resolution of eroded papules within 2 to 3 weeks.

Lesions of herpes gladiatorum will be seen on the lateral neck, side of the face, and forearms within 4 to 11 days after exposure. A high suspicion for this diagnosis is crucial in athletes, as this is commonly misdiagnosed as bacterial folliculitis.

HSV-1 infection can also occur on the digits or periungual, causing herpetic whitlow.  Herpetic whitlow presents as deep blisters that may secondarily erode. A common misdiagnosis is an acute paronychia or blistering dactylitis.  Herpetic whitlow can also lead to lymphadenopathy of the epitrochlear or axillary lymph nodes in association with lymphatic streaking, mimicking bacterial cellulitis.

HSV-1 infection of the eye leads to ocular HSV in children and adults. Primary ocular HSV presents with keratoconjunctivitis that can be unilateral or bilateral. There can be associated eyelid tearing, edema, photophobia, chemosis (swelling of the conjunctiva), and preauricular lymphadenopathy. It is common for patients to experience recurrence, and in these cases, it is usually unilateral. Ocular HSV is a common cause of blindness in the United States when it manifests as keratitis or a branching dendritic corneal ulcer (which is pathognomonic for ocular HSV).

Herpes encephalitis is a severe, typically fatal (mortality is greater than 70% if untreated) infection caused by HSV-1. It primarily affects the temporal lobe of the brain leading to bizarre behavior and focal neurological deficits localized to the temporal lobe. Patients may have a fever and altered mental status as well.

Kaposi varicelliform eruption, or eczema herpeticum, presents as an extensive spreading of HSV infection in the setting of a compromised skin barrier (e.g., atopic dermatitis, Darier disease, pemphigus foliaceous, pemphigus vulgaris, Hailey-Hailey disease, mycosis fungoides, ichthyosis). Patients will display 2 to 3 mm punched-out erosions with hemorrhagic crusts in widespread distribution. There may be secondary impetigo with Staphylococcus or Streptococcus species.

Neonatal herpes virus presents at day 5 to 14 of life and favors the scalp and the trunk. It may present with disseminated cutaneous lesions and involvement of oral and ocular mucosa. Central nervous system (CNS) involvement may occur and manifest as encephalitis with lethargy, poor feeding, bulging fontanelle, irritability, and seizures. 

In the immunocompromised patient population, HSV infection can result in severe and chronic infection. The most common presentation of severe and chronic HSV infection is quickly enlarging ulcerations or verrucous/pustular lesions. It is not uncommon for patients to have respiratory or gastrointestinal tract involvement and present with dyspnea or dysphagia.[20][21][22][23][24]

Evaluation

The gold standard for diagnosing HSV-1 infection is HSV-1 serology (antibody detection via western blot). The most sensitive and specific mechanism is viral polymerase chain reaction (PCR). However, serology remains the gold standard. Viral culture, direct fluorescent antibody  (DFA) assay, and Tzanck smear are alternative methods of diagnosing. It is important to note that the Tzanck smear identifies multinucleated giant cells, so it cannot distinguish between HSV and VZV. The DFA assay, however, can distinguish between the 2 entities.[14]

Treatment / Management

For the treatment of orolabial herpes, the current recommendation is oral valacyclovir (2 grams twice daily for one day). If the patient has frequent outbreaks, chronic suppression is warranted. For chronic suppression of immunocompetent patients, oral valacyclovir 500 mg daily (for patients with less than ten outbreaks per year) or oral valacyclovir 1 gram by mouth daily (for patients with greater than 10 outbreaks a year) is recommended.

For the treatment of eczema herpeticum, it is recommended to use 10 to 14 days of either acyclovir (15 mg/kg with a 400 mg maximum) 3 to 5 times daily or Valacyclovir 1 gram by mouth twice a day.

For immunocompromised patients with severe and chronic HSV, treatment is aimed at chronic suppression. For chronic suppression of immunocompromised patients, oral acyclovir 400 to 800 2 to 3 times daily, or oral valacyclovir 500 mg twice daily is recommended.[25][26][27][28]

Differential Diagnosis

The differential diagnosis of orolabial HSV-1 infection includes aphthous stomatitis, Stevens-Johnson syndrome, erythema multiforme (EM) major, and herpangina. These entities can be distinguished from orolabial herpes by history and physical exam findings. The differential diagnosis of herpetic whitlow includes blistering dactylitis and acute or chronic paronychia.

Prognosis

Overall, the vast majority of HSV-1 infections are asymptomatic, and if symptomatic present with mild recurrent mucocutaneous lesions. The prognosis of HSV-1 infection varies depending on the manifestation and location of the HSV-1 infection. The majority of the time, HSV-1 infection follows a chronic course of latency and reactivation. HSV encephalitis is associated with high mortality; approximately 70% of untreated cases are ultimately fatal. The prognosis of ocular HSV can also be grim if the patient develops globe rupture or corneal scarring, as these processes can ultimately lead to blindness.[29]

Enhancing Healthcare Team Outcomes

Herpes type 1 infections are best managed by an interprofessional team that includes the primary provider, pediatrician, nurse practitioner, infectious disease specialist and the internist. The key to treatment is starting the antiviral within 24 hours of symptoms. It is important to understand that most infections spontaneously subside on their own and delayed treatment has no impact on duration or severity of symptoms. During the infection, the patient should be educated on washing hands and avoiding close contact with others.

Continuing Education / Review Questions

Figure

Herpes Simplex. Contributed by DermNetNZ

Figure

A. Herpetic keratitis with neovascularization of the cornea
B. Herpes Simplex I of the lips and skin of the chin
C. Stage 1 Neurotrophic Keratitis: fluorescein epithelial staining together with Gaule spots. Gaule spots are scattered areas of dried epithelium, (more…)

Figure

This image depicts a close view of a patient’s penile shaft, highlighting the presence of a crop of erythematous vesiculopapular lesions, which were determined to have been caused by a herpes genitalis outbreak. Genital herpes is a sexually transmitted (more. ..)

Figure

Herpes Simplex on genitals. Contributed by Dr. Shyam Verma, MBBS, DVD, FRCP, FAAD, Vadodara, India

Figure

Herpes Simplex mouth. Contributed by Dr. Shyam Verma, MBBS, DVD, FRCP, FAAD, Vadodara, India

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Finger-Jardim F, Avila EC, da Hora VP, Gonçalves CV, de Martinez AMB, Soares MA. Prevalence of herpes simplex virus types 1 and 2 at maternal and fetal sides of the placenta in asymptomatic pregnant women. Am J Reprod Immunol. 2017 Jul;78(1) [PubMed: 28440579]
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Cruz AT, Freedman SB, Kulik DM, Okada PJ, Fleming AH, Mistry RD, Thomson JE, Schnadower D, Arms JL, Mahajan P, Garro AC, Pruitt CM, Balamuth F, Uspal NG, Aronson PL, Lyons TW, Thompson AD, Curtis SJ, Ishimine PT, Schmidt SM, Bradin SA, Grether-Jones KL, Miller AS, Louie J, Shah SS, Nigrovic LE. , HSV Study Group of the Pediatric Emergency Medicine Collaborative Research Committee. Herpes Simplex Virus Infection in Infants Undergoing Meningitis Evaluation. Pediatrics. 2018 Feb;141(2) [PMC free article: PMC5810597] [PubMed: 29298827]
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Giraldo D, Wilcox DR, Longnecker R. The Type I Interferon Response and Age-Dependent Susceptibility to Herpes Simplex Virus Infection. DNA Cell Biol. 2017 May;36(5):329-334. [PMC free article: PMC5421632] [PubMed: 28278385]
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Bin L, Li X, Richers B, Streib JE, Hu JW, Taylor P, Leung DYM. Ankyrin repeat domain 1 regulates innate immune responses against herpes simplex virus 1: A potential role in eczema herpeticum. J Allergy Clin Immunol. 2018 Jun;141(6):2085-2093.e1. [PMC free article: PMC5994174] [PubMed: 29371118]
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Herpes Simplex Virus (HSV) Mouth Infection

Not what you’re looking for?

What is a herpes simplex virus (HSV) mouth infection? 

Some people call it a cold sore, others a fever blister. Herpes
simplex virus is the cause of this annoying and often painful chronic condition.

The herpes sores (lesions) typically last a week to 10 days. They
most often occur on the lips, tongue, roof of the mouth, or the gums. The sores
occur first as fluid-filled blisters that burst (rupture) after a day or 2. The
sores will ooze fluid that has the virus. After a few days, the sores will form
crusts or scabs. The virus is highly contagious and can be spread by skin-to-skin
contact such as kissing.

What causes an HSV mouth infection?

The virus is spread by skin-to-skin contact with someone who
carries the virus. Most people with oral herpes were infected during childhood or
as
young adults from nonsexual contact with infected saliva. It can be passed by
kissing, touching the infected person’s skin, or sharing infected objects such as
lip balm, silverware, or razors.

The 2 most common forms of the virus are:

  • Herpes simplex virus type 1
    (HSV-1).
    HSV-1 is most often linked to infections of the mouth.
  • Herpes simplex virus type 2
    (HSV-2).
    This type is most often linked to genital herpes infections.

Both types of HSV can infect both the mouth and the genitals.

Once infected, a person will have the herpes simplex virus for the
rest of their life. When the virus is not active, it is dormant in a group of nerve
cells. Some people never have any symptoms from the virus while others have periodic
outbreaks of infections.

It is not clear what triggers the virus to return. But the risk
factors below may play a role:

  • Long or intense exposure to sunlight
  • A recent fever
  • Emotional stress
  • Menstruation
  • Surgery
  • Physical injury

Recurrent outbreaks are more common in the first year after the
initial episode. After that, the outbreaks diminish in frequency and severity as the
body builds antibodies to the virus.

What are the symptoms of an HSV mouth infection?

The initial (primary) infection of the oral herpes simplex virus
is often the worst. It may cause severe, flu-like symptoms, swollen lymph nodes, and
headache. But some people have no symptoms at all. In the initial infection, sores
can occur on and around the lips and all over the mouth.

Recurring infections tend to be much milder, and the sores often
erupt in the edges of the lips. Some people never have any more outbreaks beyond the
initial infection. These are the most common symptoms of a recurring oral HSV
infection:

  • Initial redness, swelling, heat, and pain, or itching in the
    area where the infection will erupt.
  • Painful, fluid-filled blisters may appear on the lips or
    under the nose. These blisters, and the fluid they contain, are highly
    contagious.
  • The blisters leak fluids and become sores.
  • After about 4 to 6 days, the sores start to crust over and
    heal.

The symptoms of an oral HSV outbreak may look like other
conditions or health problems. Always see your healthcare provider for a
diagnosis.

How is an HSV mouth infection diagnosed?

Herpes simplex virus may be difficult to diagnose because it may
be confused with many other infections, such as allergic reactions. HSV can be
confirmed only with a virus culture, blood test, or biopsy. A healthcare provider
can often diagnose it based on where the blisters are and how they look. 

How is an HSV mouth infection treated?

Treatment will depend on your symptoms, age, and general health.
It will also depend on how severe the condition is.

Treatment may include:

  • Keeping the infected area clean and dry
  • Antibiotic treatment for any secondary bacterial
    infections
  • Topical antiviral creams
  • Oral antiviral medicines

What can I do to prevent an HSV mouth infection?

These tips can help you prevent an oral HSV infection:

  • Don’t have direct contact with someone with herpes sores.
    According to the CDC, genital herpes (HSV-2) can be contagious without any
    symptoms.
  • Don’t share silverware, glasses, straws, or other items with
    someone who has oral herpes.
  • Wash bedding and towels in boiling hot water after each
    use.
  • Don’t have oral sex if you or your partner have oral herpes
    (HSV-1). HSV-1 can be spread to the genitals, especially if you have oral
    blisters.
  • To prevent a possible recurrence, use a sunblock that
    contains zinc oxide on your lips.

Key points about an HSV mouth infection

  • A cold sore or fever blister is caused by the herpes simplex
    virus.
  • The virus is highly contagious and can be spread by
    skin-to-skin contact such as kissing.
  • Once infected, a person will have the herpes simplex virus
    for the rest of their life.
  • Herpes sores typically last a week to 10 days. They most
    often occur on the lips, tongue, roof of the mouth, or the gums.

Next steps

Tips to help you get the most from a visit to your healthcare
provider:

  • Know the reason for your visit and what you want to
    happen.
  • Before your visit, write down questions you want
    answered.
  • Bring someone with you to help you ask questions and
    remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis and any
    new medicines, treatments, or tests. Also write down any new instructions your
    provider gives you.
  • Know why a new medicine or treatment is prescribed and how
    it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the
    results could mean.
  • Know what to expect if you do not take the medicine or have
    the test or procedure.
  • If you have a follow-up appointment, write down the date,
    time, and purpose for that visit.
  • Know how you can contact your provider if you have
    questions.

Medical Reviewer: Michael Kapner MD

Medical Reviewer: Rita Sather RN

Medical Reviewer: Stacey Wojcik MBA BSN RN

© 2000-2021 The StayWell Company, LLC. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional’s instructions.

Not what you’re looking for?

Effective Treatments for Herpes

Oral herpes, normally caused by HSV type 1, and genital herpes, normally caused by HSV type 2, are both treatable infections, but they are not curable. Home remedies, over-the-counter medications, and other options can help relieve pain and discomfort. Prescription medications and one over-the-counter antiviral medication can reduce the severity and duration of outbreaks.

Home Remedies and Lifestyle

There are some things that you can do at home to reduce the pain of a cold sore or genital herpes. Additionally, you can also take a few steps to prevent the lesions from getting worse and spreading or an infection from recurring. 

Illustration by Emily Roberts, Verywell

  • Apply cold compresses: Place a well-insulated ice pack on your lesions for as long as it makes you feel better. The cold will not worsen or improve the lesion, but it can lessen the pain. 
  • Don’t scratch: It is important to avoid touching and scratching lesions caused by herpes, because you can spread the infection to other areas of your own skin. 
  • Keep the sores clean: Cold sores and genital herpes infections can become infected with bacteria from your hands or, in the latter case, from urine or feces. It is important to keep the area of sores and blisters clean and dry to avoid an additional infection. 
  • Reduce stress: Stress can interfere with optimal immune system function. Reducing your stress may help prevent excessive herpes recurrences.

If you already know you have HSV-1 or HSV-2, take precautions to avoid infecting others.

Over-the-Counter Therapies

Over-the-counter antiviral therapy creams may help speed recovery from oral or genital herpes infections, and other options can help ease discomfort.

Some to consider include:

  • Abreva (docosanol): This is the only FDA-approved antiviral medication for herpes infection that you can get without a prescription. Antiviral medications inhibit the ability of a virus to multiply in the body, but they do not completely destroy or eliminate the virus. This medication comes as a cream that you apply directly to the affected area about every three to four hours. Take care to only apply it to the skin, not inside your mouth, eyes, or vagina. Wash your hands before and after use.
  • Pain-relieving lotions and creams: Medicated pain creams or lotions can ease discomfort associated with sores. There are a number of over-the-counter options available. Be sure to confirm with your doctor or pharmacist that the product you select is safe to use on herpes lesions, and wash your hands before and after you apply any product.
  • Oral pain relievers: Oral medications such as Tylenol (acetaminophen), Advil (ibuprofen), and Aleve (naproxen) can help relieve herpes-related pain for several hours. 

Prescriptions

There are several situations when prescription antiviral medication is recommended, and almost all apply to cases of genital herpes infection. The prescriptions used for herpes infection are all antiviral medications, and, like the over-the-counter antiviral cream Abreva, they inhibit the proliferation of the virus, but they do not rid the body of it.

If you have a first episode or a recurrence, a short course of one of the three options available is recommended. Those with frequent episodes may need to take one of these drugs daily on an ongoing basis, which is known as suppressive therapy.

Taking herpes medication when you do not have symptoms has been shown to reduce the risk of sexual transmission to a partner.

The following recommendations for adults with genital herpes are from the Centers for Disease Control (CDC) herpes treatment guidelines, but your doctor will decide which of these options is best for you. 

Drug First Outbreak Treatment Recurrent Outbreak Prevention Recurrent Outbreak Treatment
Zovirax, Sitavig (acyclovir) 400mg three times a day for seven to 10 days —OR— 200mg five times a day for the same duration* 400mg twice a day 400mg three times a day for five day —OR— 800mg twice a day for five days —OR— 800mg three times a day for two days
Famvir (famciclovir) 250mg three times a day for seven to 10 days* 250mg twice a day 125mg twice a day for five days —OR— 1g twice a day for one day —OR— 500mg once, followed by 250mg twice a day for two days
Valtrex (valacyclovir) 1g twice a day for seven to 10 days* 500mg or 1g daily 500mg twice a day for three days —OR— 1g once a day for five days

*If symptoms remain after 10 days, your doctor might choose to continue treatment.

Usually, treatment of cold sores is not needed unless the symptoms are severe and persistent, in which case acyclovir is generally used.

In general, prescription antivirals are not recommended for pregnant women or for infants under the age of one. They may be used for children under the age of 12 and the recommended dose is calculated by a physician based on weight.

Complementary Medicine (CAM)

Alternative therapies for herpes with some supporting research include:

  • Propolis: A sticky substance that bees produce from tree saps, propolis shows promise in the treatment of herpes.

Studies have found that people who are treated with propolis experience faster healing of herpes lesions and a higher likelihood of fully healed lesions by day 10 of treatment when compared to people who receive a placebo.

  • Algae extract: In a laboratory setting, algae extract has been shown to inhibit HSV-2 growth, so this may be considered a useful component in alternative treatments in the future. 
  • Acupuncture: Acupuncture has been used for the treatment of pain caused by herpes lesions with some beneficial results. This treatment method, while mildly helpful, has also rarely been associated with the transmission of HSV, so it is best to consider it with caution. 

Several other alternative options have been investigated for the treatment or suppression of genital herpes, including lysine, zinc, Echinacea, eleuthero, and bee products. There is no evidence to show that any of these options are beneficial for these purposes.

A recently marketed alternative therapy for herpes, Resolve Herpes is said to contain minerals and is marketed as a detox therapy. So far, there does not appear to be evidence that this product can cure or treat herpes infections.

There have been some promising trials of herpes vaccines. However, to date, no human trials have shown high enough efficacy to bring a herpes vaccine to market.

Frequently Asked Questions

What over-the-counter drugs are used to treat herpes?

Abreva (docosanol) 10% cream is the first over-the-counter antiviral drug approved for the treatment of herpes simplex type 1 (the type commonly associated with cold sores). If applied at the first sign of a cold sore (before a blister develops), it may reduce the duration of an outbreak to as few as 2.5 days.

What prescription drugs are used to treat herpes?

Herpes viruses are treated with antivirals. There are three commonly used to treat oral or genital herpes:

  • Zovirax (acyclovir)
  • Valtrex (valacyclovir)
  • Famvir (famciclovir)

Do all antivirals work equally well in treating oral or genital herpes?

All three antivirals are effective in reducing the severity and duration of a herpes outbreak. However, some authorities recommend Valtrex over Zovirax for the treatment of genital herpes.

How long does herpes last if treated with antivirals?

Studies have shown that, if started within 48 hours of the first appearance of lesions, antivirals can reduce the duration of oral herpes by one to two days and the duration of the first genital herpes outbreak by up to 50%.

Are there natural remedies that can help treat herpes?

Although evidence on the benefits of complementary and alternative medicines for treating herpes is scant, several natural compounds have shown promise, including:

  • African rue (Peganum harmala) extract
  • Green algae (Stypopodium zonale) extract
  • Red seaweed (Hypnea musciformis) extract
  • Verbena (Verbenaceae) essential oil
  • Yu Xing Cao (a traditional Chinese medicine)

Can herpes be cured?

There is no cure for herpes and there are no vaccines that can prevent either HSV-1 or HSV-2. Once you are infected, the virus remains in your body forever.

A Word From Verywell

The key to successfully treating any herpes outbreak is a timely response. The sooner you recognize the signs and access treatment, the shorter and less severe the outbreak is likely to be. Treatment should be started within 48 hours of the first appearance of symptoms.

If your primary care provider is unable to see you, do not hesitate to access treatment through a telehealth provider, the visit of which may be partially or fully covered by your health insurance.

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Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.

  1. Pereira DB, Antoni MH, Danielson A, et al. Stress as a predictor of symptomatic genital herpes virus recurrence in women with human immunodeficiency virus. J Psychosom Res. 2003;54(3):237-44.

  2. Modi S, Van L, Gewirtzman A, et al. Single-day treatment for orolabial and genital herpes: a brief review of pathogenesis and pharmacology. Ther Clin Risk Manag. 2008;4(2):409-17. doi:10.2147/tcrm.s1664

  3. Sauerbrei A. Optimal management of genital herpes: current perspectives. Infect Drug Resist. 2016;9:129-41. doi:10.2147/IDR.S96164

  4. Centers for Disease Control and Prevention. Genital HSV Infections. Updated June 4, 2015.

  5. Ursini T, Tontodonati M, Manzoli L, et al. Acupuncture for the treatment of severe acute pain in herpes zoster: results of a nested, open-label, randomized trial in the VZV Pain Study. BMC Complement Altern Med. 2011;11:46. doi:10.1186/1472-6882-11-46

  6. DailyMed. Label: Abreva – docosanol cream. Updated October 5, 2020.

  7. Pinder M, Wright A. Valaciclovir versus aciclovir for the treatment of primary genital herpes simplex: a cost analysis. Int J STD AIDS. 2015 Nov;26(13):971-3. doi:10.1177/0956462414563628

  8. Alvarez DM, Castillo E, Duarte LF, et al. Current antivirals and novel botanical molecules interfering with herpes simplex virus infection. Front Microbiol 2020;11:139. doi:10.3389/fmicb.2020.00139

  9. Hollier LM, Eppes C. Genital herpes: oral antiviral treatments. BMJ Clin Evid. 2015;2015:1603.

Additional Reading

  • Centers for Disease Control and Prevention, 2015 Sexually Transmitted Diseases Guidelines, Genital HSV Infections, accessed May 17. 2018
  • Deethae A, Peerapornpisal Y, Pekkoh J, Sangthong P, Tragoolpua Y. Inhibitory effect of Spirogyra spp. algal extracts against herpes simplex virus type 1 and 2 infection. J Appl Microbiol. 2018 Jun;124(6):1441-1453. doi: 10.1111/jam.13729. Epub 2018 Mar 13.
  • Sung SH, Choi GH, Lee NW, Shin BC. External Use of Propolis for Oral, Skin, and Genital Diseases: A Systematic Review and Meta-Analysis. Evid Based Complement Alternat Med. 2017;2017:8025752. doi: 10.1155/2017/8025752. Epub 2017 Feb 6.

Verywell Health is part of the Dotdash publishing family.

The Treatment of Herpes Simplex Infections: An Evidence-Based Review | Infectious Diseases | JAMA Internal Medicine

Genital and labial herpes simplex virus infections are frequently encountered by primary care physicians in the United States. Whereas the diagnosis of this condition is often straightforward, choosing an appropriate drug (eg, acyclovir, valacyclovir hydrochloride, or famciclovir) and dosing regimen can be confusing in view of (1) competing clinical approaches to therapy; (2) evolving dosing schedules based on new research; (3) approved regimens of the Food and Drug Administration that may not match recommendations of the Centers for Disease Control and Prevention or of other experts; and (4) dissimilar regimens for oral and genital infections. The physician must first choose an approach to treatment (ie, intermittent episodic therapy, intermittent suppressive therapy, or chronic suppressive therapy) based on defined clinical characteristics and patient preference. Then, an evidence-based dosing regimen must be selected. In this review, data from all sources are tabulated to provide a handy clinical reference.

Acyclovir, valacyclovir hydrochloride, and famciclovir are the 3 antiviral drugs routinely used to treat symptomatic herpes simplex virus (HSV) infections. Diagnosing HSV infections is usually straightforward in immunocompetent patients, and all the available drugs have an excellent margin of safety because they are converted by viral thymidine kinase to the active drug only inside virally infected cells. Unfortunately, confusion often arises because various dosing regimens are recommended for (1) each of the 3 available drugs; (2) HSV vs herpes zoster; (3) suppressive vs intermittent episodic indications; (4) primary vs secondary infections; (5) oral and genital infections; and (6) evolving treatment strategies approved by the Food and Drug Administration. Following a literature review to document important clinical information about HSV infections, we discuss the data regarding optimal treatment regimens. Three approaches to treatment are described: intermittent episodic therapy (IET), chronic suppressive therapy (CST), and intermittent suppressive therapy (IST).

An outbreak of genital or labial herpes is categorized as a primary HSV infection if the patient was seronegative for HSV types 1 and 2 before the episode and as a nonprimary HSV infection if previous infections had occurred. Without acquired immunity, initial primary infections are generally more severe than recurrences. Constitutional symptoms such as fever, chills, fatigue, and muscle aches accompany the disease and last 10 to 14 days. A first episode of genital or oral herpes in a patient already seropositive for HSV is termed a nonprimary initial infection, and these infections tend to be less severe. The disease course after initial infection is variable; some patients have recurrent infections, and others never experience a second episode.

Labial herpes typically results from infection with HSV type 1 and is commonly contracted during childhood or adolescence. In the US, 57% to 80% of adults are seropositive for the virus, with a larger proportion of these people being of lower socioeconomic status.1-4 Many people exposed to HSV demonstrate asymptomatic seroconversion. Initial primary episodes, however, can be severe, causing widespread 1- to 2-mm blisters associated with severe discomfort that interferes with eating and drinking to the point of dehydration, last 10 to 14 days, and occur 1 to 26 days after inoculation.4 Recurrent labial herpes affects roughly one third of the US population, and these patients typically experience 1 to 6 episodes per year.5-9 These infections appear at the vermillion border of the lip in about 90% of cases, the palate in 5% of cases, and elsewhere above the chin or on the oral mucosa more rarely (Figure). Papules on an erythematous base become vesicles within hours and subsequently progress through ulcerated, crusted, and healing stages within 72 to 96 hours.10,11 Before skin lesions appear, 60% of patients experience the prodromes tingling, itching, and burning.11

Genital herpes is most commonly contracted between the ages of 15 and 30 years, coinciding with increased sexual activity in this age group.12 It affects approximately 22% of the US population, with roughly 38% of symptomatic individuals experiencing 6 or more recurrences per year.13,14 Genital herpes can result from infection with either HSV type 2 or type 1, mainly HSV type 2 in this country, which typically causes more recurrent and severe manifestations of disease.2,15,16 Infection of the cervix, often subclinical, is the main site of involvement in women, yet the classic clinical picture is that of painful and disfiguring vaginal and vulvar lesions.12 Men typically develop lesions on the glans, prepuce, or shaft of the penis. The natural course of disease progression is decreased frequency and severity of recurrences over time. However, roughly a third of patients do not experience this time-dependent regression.17

Herpes zoster and other blistering diseases can mimic HSV infections. The diagnosis of herpes infections can be confirmed immediately by Tzanck preparation, within hours using immunofluorescence techniques, and within 48 hours using viral culture.

The clinical courses of genital herpes caused by HSV types 1 and 2 are indistinguishable. There is typically a 2- to 21-day incubation period following viral inoculation when randomly distributed vesicles clustered on a red base appear. Tiny papules develop into vesicles, which subsequently ulcerate and crust.18 Soreness, itching, dysuria, and inguinal or femoral lymphadenopathy may accompany constitutional symptoms, and dysuria is common in women.18,19 Untreated eruptions of genital herpes typically last longer than those of the oral variety, with a primary episode enduring for 2 to 4 weeks. Recurrent genital herpes produces localized vesicles on an erythematous base, which persist for 7 to 12 days without treatment.19,20


Intermittent episodic therapy

As is the case with most disease processes, HSV infections are commonly treated with the first clinical sign or symptoms. This form of intermittent treatment is termed episodic and focuses on management of isolated, acute episodes of a chronic, clinically silent disease. Although the treatment approaches used for oral and genital HSV infections are more similar than different, randomized controlled trials (RCT) have uniformly studied these infections separately. Therefore, dosage schedules derived from these trials are not identical.


IET in Labial Herpes Simplex


Initial Primary Infections

In moderate and severe cases, antiviral treatment is often recommended for uncomplicated episodes of primary oral herpes in healthy patients (Table 1).6 Oral acyclovir suspension, 15 mg/kg 5 times daily for 1 week, significantly decreased the disease duration and the period of infectivity in children in a small RCT. Median duration of oral lesions was 4 days vs 9 days for the placebo group, and median time to negative viral cultures was 1 day vs 5 days.21 Valacyclovir hydrochloride, 1 g twice a day for 7 days, and famciclovir, 500 mg twice a day or once a day for 7 days, are also logical regimens, although RCTs have not been performed.3,22 Treatment is most effective when initiated promptly. However, early treatment does not appear to diminish recurrences.

The intermittent use of an oral antiviral agent is effective in the treatment of recurrent labial herpes when initiated within 48 hours of an outbreak (Table 2). Randomized controlled trials have shown systemic acyclovir (400 mg 5 times daily for 5 days) decreases healing time and viral shedding and ameliorates symptoms when initiated early.11,23 Valacyclovir, the prodrug of acyclovir, provides a 3- to 5-fold increase in bioavailability of acyclovir.24 Two large RCTs demonstrated that single-day administration of valacyclovir (2 g given twice in 24 hours) significantly reduces episode duration, time to lesion healing, and time to cessation of pain and discomfort when compared with placebo. A 1-day reduction in lesion duration was documented.

Famciclovir, the oral prodrug of penciclovir, offers increased bioavailability as well as a substantially longer half-life compared with acyclovir. In an RCT, famciclovir, given as either a single 1500-mg dose or as two 750-mg doses during a 24-hour period, decreased healing time and provided symptomatic relief. Time to lesion healing and normal reepithelialization was 2 days shorter and symptom resolution was 1 day faster when compared with the control group.10,25

Intermittent episodic therapy with topical acyclovir and penciclovir creams have been shown to decrease lesion healing time and symptomseverity in recurrent labial herpes.11,26,27,29-32 Other studies, however, failed to prove acyclovir ointment and cream efficacious.33,34 Overall, topical treatments do not appear to be as effective as systemic medications. For instance, famciclovir decreases lesion healing time by 2 days, efficacy that has not been demonstrated with topical therapy.10,26,35-37


IET in Genital Herpes Simplex


Initial Primary Infections

Patients with primary episodes of genital herpes are effectively treated with antiviral drugs when taken within 72 hours of lesion appearance (Table 3). Oral and intravenous acyclovir have been used to shorten the course of primary genital herpes infections for decades. Unlike topical acyclovir, the oral form can prevent new lesion formation and modify accompanying constitutional symptoms, and does not cause local irritation on application.38 Oral acyclovir is more practical than the intravenous route for immunocompetent patients.38 Acyclovir (1 g to 1200 mg/d) produces results matching those of higher dosages (4 g/d). Neither regimen appears to affect the frequency or course of future genital herpes recurrences.39

Head-to-head trials comparing 10-day regimens of oral acyclovir (200 mg 5 times daily) and valacyclovir (1000 mg twice a day) found no statistically significant difference between the 2 in terms of disease outcome measures.40 However, valacyclovir, when taken once or twice daily, is likely to increase compliance compared with acyclovir, which is taken 5 times a day.40

Similarly, an RCT comparing the efficacy of 5- and 10-day regimens of several famciclovir dosages (250 mg, 500 mg, or 750 mg 3 times a day for 5 days and 125 mg, 250 mg, or 500 mg 3 times a day for 10 days) with acyclovir (200 mg 5 times a day for 5 or 10 days) in first-episode genital herpes cases found no significant differences between the two drugs. Duration of viral shedding, median time to lesion healing, and time to symptom resolution were comparable between both treatment groups.42,43 The 10-day treatment arm of the study demonstrated that higher doses of famciclovir (250 mg and 500 mg) were superior to the 125-mg regimen. The Centers for Disease Control and Prevention has chosen to recommend the 10-day dosing schedule, although the 5 and 10-day regimens of famciclovir (250 mg 3 times a day and all 500-mg groups) demonstrated comparable efficacy.42,43 Famciclovir 3 times a day should enhance compliance when compared with the 5 times daily dosage of acyclovir.

In the 1980s, oral acyclovir (200 mg 5 times daily for 5 days) was found to significantly decrease viral shedding, hasten lesion healing, and decrease the incidence of new lesion formation.41,44,45 It was also associated with a truncated course of pain and discomfort, but had no effect on recurrences.41,44 Abbreviated courses using higher dosages of acyclovir, 800 mg twice a day for 5 days and 3 times a day for 2 days, have proven to be as effective as earlier regimens.46,47 Moreover, the higher dosage was effective in healing established lesions in men, even when initiated after the prodromal period.46

Oral valacyclovir (500 mg twice a day for 5 days and 1 g once a day for 5 days) has been shown in placebo-controlled and head-to-head studies to match acyclovir in terms of decreasing episode length, viral shedding, and healing time.45,48 The 3-day valacyclovir regimen (500 mg twice a day) was shown to be as effective as 5 days of treatment.49 Multiple studies have also demonstrated that valacyclovir significantly decreases the duration and severity of pain and discomfort associated with genital herpes episodes.50 There is conflicting evidence regarding the ability of valacyclovir to abort outbreaks when taken at the onset of symptoms before any lesions are apparent. Data trends and our clinical experience suggest that at least some recurrences can be aborted through this approach.45,48,50

In addition, varying dosages of famciclovir (125 mg, 250 mg, or 500 mg twice a day for 5 days) significantly affect the characteristics mentioned previously. No dose-dependent advantages exist between regimens. Therefore, the lowest dosage of 125 mg twice a day is recommended. Viral shedding is decreased by 1½ days and roughly leads to complete lesion healing 1 day faster than placebo. There is a 50% absolute risk reduction of developing new lesions compared with placebo, and the treatment group enjoyed at least a half-day reduction in lesion-associated pain and discomfort.51,52 A single-day, 2-dose regimen demonstrated a 2-day reduction in median time to healing and overall efficacy equal to that of multiple day, lower-dose famciclovir regimens.14Table 4 summarizes these data.

The efficacy of topical acyclovir cream used as treatment in primary or recurrent episodes of genital herpes varies between RCTs and overall does not appear to be as reliable as oral acyclovir.56-58 Current Centers for Disease Control and Prevention guidelines discourage the use of the topical formulations, stating that they offer “minimal clinical benefit.”59


Chronic suppressive therapy

Although most patients with HSV infections do not require CST, those with frequent recurrences who experience severe pain or disfigurement, have difficulty swallowing, or experience a protracted disease course are appropriately treated with CST.8,9 Of all patients with labial herpes, 5% to 10% experience frequent recurrences (≥6 per year). Of patients infected with genital herpes, 20% to 50% have symptomatic, recurrent flares.60 Patients have a median of 4 recurrences the year after a first symptomatic episode and usually enjoy a decline in frequency of outbreaks over time.61,62 Recurrences of any frequency can negatively affect a patient’s quality of life. Thus, CST is appropriate for patients who are psychologically distressed by their disease.63 Long-term prophylactic therapy for genital herpes may also be used in an effort to decrease the risk of transmission to uninfected partners.64,65


CST in Recurrent Oral Herpes Simplex

Efficacy of acyclovir and valacyclovir as CST in patients with frequent recurrences of labial herpes has been demonstrated in RCTs. In the early 1990s, trials demonstrated that oral acyclovir (400 mg twice a day) was an effective mode of therapy. At the end of 4 months there was a 41% reduction in the number of patients experiencing labial herpes recurrences, and a 53% decrease in total number of outbreaks when compared with placebo-treated subjects.8 The efficacy of valacyclovir was first demonstrated in a 4-month trial: valacyclovir prophylaxis (500 mg once a day) resulted in 60% of treatment group patients remaining disease free, compared with 38% of subjects in the placebo group. Mean time to first recurrence was significantly longer in the treatment group (13.1 weeks) compared with the control group (9.6 weeks).9 In addition, a crossover study comparing valacyclovir given for 6 months as intermittent reactive therapy (two 2-g doses separated by 12 hours) and CST (1 g once daily) showed the chronic suppressive regimen to significantly decrease frequency of recurrences and pain severity scores.66

No RCTs have been conducted to specifically evaluate the ability of famciclovir to prevent recurrent labial herpes when given chronically (Table 5). The fact that short courses of prophylactic famciclovir (250 mg or 500 mg twice a day for 10 days started 1 day before the procedure) given in special circumstances (ie, facial laser resurfacing) have been shown to prevent recurrent episodes of labial herpes suggests long-term treatment may beefficacious.67


CST in Genital Herpes Simplex

Acyclovir was the first drug extensively studied and proven to markedly reduce genital herpes recurrences when taken daily for long periods in the immunocompetent population. A small trial in 1984 found that daily acyclovir (200 mg 3 times a day) taken for 125 days significantly decreased the number of genital herpes recurrences. All patients in the placebo group and 25% of subjects in the treatment group experienced at least 1 recurrence during a 4-month period.68

Studies have focused on efficacy in suppressing recurrences, safety profile, optimal dosage, and the effect on recurrence rates after treatment is discontinued. During the first year of a 6-year multicenter trial, acyclovir (400 mg twice a day) significantly increased the number of patients remaining recurrence free (44% vs 2%) and median time to first outbreak (246 days vs 18 days) compared with placebo.69 The following years of the trial demonstrated a “gradual and additional improvement” in response to therapy, with about 70% of patients remaining recurrence free during the fifth year of the trial.62,69-71(p586) Overall, studies suggest that acyclovir given as CST for 1 year allows 43% to 50% of patients to remain recurrence free, with a median time to first recurrence ranging from 246 to 274 days.69,72-74 When control was not achieved at lower doses, most initial nonresponders were controlled with increased doses ranging from 1000 to 1600 mg/d.62,75

Unfortunately, once suppressive therapy is discontinued, outbreaks often recur. When discontinued within a year, episodes recur at a frequency comparable to subjects’ baselines before chronic prophylactic therapy was initiated.76 Of note, a prolonged treatment schedule of 5 years was shown in one study to lower recurrence rates relative to previous baseline in about two-thirds of patients.70 To date, no RCTs have shown significant adverse effects related to prolonged treatment.62,68-74,76-78

The first RCT conducted on valacyclovir (500 mg once a day), a large 16-week study, demonstrated a significant reduction in recurrences (69% vs 9.5% recurrence free) and a significant increase in median time to first recurrence (>112 vs 20 days) in the treatment group compared with the placebo group.79,80 Another study evaluating daily single-dose regimens (250 mg, 500 mg, and 1 g), 250 mg twice a day, 400 mg twice a day, and placebo found 500 mg once a day, 1 g once a day, 250 mg twice a day, and 400 mg twice a day of similar efficacy with regard to the percentage of patients remaining recurrence free (40%, 48%, 50%, and 49%, respectively) after 1 year. All these regimens were superior to the 250 mg once a day dosage (22% recurrence free) and placebo (5%).80,81 More complete suppression was attained in patients with baseline disease activity of less than 10 recurrences per year, with the 500 mg once a day dosage typically sufficient for control. Patients with 10 or more recurrences per year often needed twice-daily dosing or 1 g once a day for adequate control.80,81

Famciclovir has also been proven effective as CST for genital herpes, demonstrating best efficacy when taken multiple times per days. A study conducted only in women evaluated multiple famciclovir dosages (125 mg once or twice daily, 250 mg once or twice daily, and 500 mg once a day) and found the famciclovir dosage of 250 mg twice a day to be the most effective regimen in significantly prolonging time to first clinically and virally confirmed recurrence. Once-daily dosing schedules were less effective or provided no significant benefit.65 A larger study evaluating 250 mg of famciclovir twice a day demonstrated that 70% of those receiving the drug were recurrence free for 1 year, compared with only 20% of patients in the placebo group.82 Various regimens of the drug (125 mg 3 times a day, 250 mg 3 times a day, and 250 mg twice a day) significantly increase time to first recurrence and percentage of patients remaining recurrence free for 1 year. Results attained with 250 mg of famciclovir twice a day or 3 times a day have been similar. Thus, the twice-daily dosing schedule has been suggested to provide a “convenient, effective, and well-toleratedregimen.”60(p892)

The length of CST has not been defined by the Food and Drug Administration and is patient- and disease-course dependent.70-72,78 Suppression for a year or longer is appropriate in many patients with frequent recurrences. Patients with herpes-associated erythema multiforme,83 eczema herpeticum (Kaposi varicelliform eruption),84 and herpetic keratitis,85 and immunocompromised populations, including human immunodeficiency virus–positive individuals, may require indefinite suppressive therapy.54,86-88 Acyclovir resistance occasionally occurs in immunocompromised patients.88 A recent meta-analysis was performed to elucidate the best CST regimens for genital herpes (Table 6).61


Intermittent Suppressive Therapy

When recurrences can be anticipated, IST can be initiated to prevent oral and genital herpes outbreaks. Oral antiviral drugs are used for short periods when known precipitating factors might otherwise trigger reactivation of disease. Anticipatory treatment is also recommended in situations where decreasing viral shedding decreases the likelihood of infecting seronegative individuals with the virus.

Common stressors that can initiate herpes recurrences include ultraviolet radiation,92-95 physical trauma or surgery,5,7,96 emotional stress, menstrual cycles,97-99 and hormonal factors. Clinical trials with topical (5% cream applied 5 times a day) and systemic (200 mg twice a day) acyclovir regimens have been proven effective in preventing sunlight-induced episodes of recurrent labial herpes.92,94,95 Oral acyclovir and placebo groups experienced similar frequencies of labial herpes recurrences during the first few days of sun exposure. Significant reduction in number of recurrences became evident on the fifth day of treatment in the oral acyclovir group and during the 4-day follow-up period in the topical acyclovir group.92,95 Prophylactic treatment has also been shown to significantly decreaserecurrence rates of labial herpes in patients undergoing dental procedures. A study of patients prophylactically treated with valacyclovir before dental procedures found that clinical lesions appeared in 11.3% of test group patients and 20.6% of patients receiving a placebo, illustrating a 46% reduction in the number of clinically evident lesions.7

Intermittent suppressive therapy is also useful in special populations to decrease the risk of virus transmission to noninfected individuals. Although only 5% to 10% of reproductive-age women have a history of genital herpes lesions, 25% to 30% are seropositive for HSV type 2. Roughly 5% to 10% of pregnant women experience a symptomatic herpes infection at some point during pregnancy. If such a recurrence occurs during the peripartum period, especially if the infection is primary, consequences to the fetus can be devastating. These cases are routinely managed with cesarean section, but anticipatory treatment offers a more practical solution. Decision making can be guided with vaginal herpes cultures at regular intervals during the third trimester. Acyclovir initiated at 36 weeks’ gestation has significantly reduced the rate of HSV recurrence in several small studies.100-102 Trials have also proven valacyclovir effective in significantly decreasing clinical recurrences and asymptomatic viral shedding.103,104

Intermittent suppressive therapy can also prevent viral transmission to uninfected athletes competing in wrestling (herpes gladiatorum) and rugby.105 A 2003 study of prophylactic valacyclovir was conducted at a month-long wrestling camp. Two diagnostically confirmed outbreaks were reported compared with 15 to 20 outbreaks in 2002 and 57 outbreaks in 2001, conferring 78% and 87% decreases in outbreaks,respectively.106

Dosing recommendations for IST of oral and genital herpes infections have not been published, but it has been our experience that using the same dosing during periods when outbreaks are anticipated as those used in long-term suppressive therapy is quite effective (Table 5 and Table 6).

Correspondence: Robert T. Brodell, MD, Brodell Medical Inc, 2660 E Market St, Warren, OH 44483 ([email protected]).

Accepted for Publication: December 18, 2007.

Author Contributions: Drs Cernik and Brodell had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Gallina and Brodell. Acquisition of data: Cernik. Analysis and interpretation of data: Cernik and Brodell. Drafting of the manuscript: Cernik and Brodell. Critical revision of the manuscript for important intellectual content: Gallina and Brodell. Study supervision:Gallina and Brodell.

Financial Disclosure: Dr Brodell has received honoraria for speaking engagements from Novartis (manufacturer of Famvir) and GlaxoSmithKline (manufacturer of Valtrex and Zovirax).

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  • Bacon TH, Levin MJ, Leary JJ, Sarisky RT, Sutton D. Herpes simplex virus resistance to acyclovir and penciclovir after two decades of antiviral therapy. Clin Microbiol Rev. 2003 Jan. 16 (1):114-28. [Medline].

  • Baker D, Eisen D. Valacyclovir for prevention of recurrent herpes labialis: 2 double-blind, placebo-controlled studies. Cutis. 2003 Mar. 71 (3):239-42. [Medline].

  • Rooney JF, Straus SE, Mannix ML, Wohlenberg CR, Alling DW, Dumois JA, et al. Oral acyclovir to suppress frequently recurrent herpes labialis. A double-blind, placebo-controlled trial. Ann Intern Med. 1993 Feb 15. 118 (4):268-72. [Medline].

  • Farr Zuend C, Nomellini JF, Smit J, Horwitz MS. Generation of a Dual-Target, Safe, Inexpensive Microbicide that Protects Against HIV-1 and HSV-2 Disease. Sci Rep. 2018 Feb 12. 8 (1):2786. [Medline].

  • Johnston C, et al. Standard-dose and high-dose daily antiviral therapy for short episodes of genital HSV-2 reactivation: three randomized, open-label, cross-over trials [published online ahead of print January 5, 2012]. Lancet. doi:10.1016/S0140-6736(11)61750-9.

  • Whitley R, Baines J. Clinical management of herpes simplex virus infections: past, present, and future. F1000Res. 2018. 7:[Medline].

  • Chen YC, Sheng J, Trang P, Liu F. Potential Application of the CRISPR/Cas9 System against Herpesvirus Infections. Viruses. 2018 May 29. 10 (6):[Medline].

  • Green LK, Pavan-Langston D. Herpes simplex ocular inflammatory disease. Int Ophthalmol Clin. 2006 Spring. 46(2):27-37. [Medline].

  • Bedoui S, Greyer M. The role of dendritic cells in immunity against primary herpes simplex virus infections. Front Microbiol. 2014. 5:533. [Medline]. [Full Text].

  • Byers RJ, Hasleton PS, Quigley A, Dennett C, Klapper PE, Cleator GM, et al. Pulmonary herpes simplex in burns patients. Eur Respir J. 1996 Nov. 9 (11):2313-7. [Medline].

  • Baras L, Farber CM, Van Vooren JP, Parent D. Herpes simplex virus tracheitis in a patient with the acquired immunodeficiency syndrome. Eur Respir J. 1994 Nov. 7 (11):2091-3. [Medline].

  • Taplitz RA, Jordan MC. Pneumonia caused by herpesviruses in recipients of hematopoietic cell transplants. Semin Respir Infect. 2002 Jun. 17 (2):121-9. [Medline].

  • Bouza E, Giannella M, Torres MV, Catalán P, Sánchez-Carrillo C, Hernandez RI, et al. Herpes simplex virus: a marker of severity in bacterial ventilator-associated pneumonia. J Crit Care. 2011 Aug. 26 (4):432.e1-6. [Medline].

  • Hutto C, Arvin A, Jacobs R, Steele R, Stagno S, Lyrene R, et al. Intrauterine herpes simplex virus infections. J Pediatr. 1987 Jan. 110 (1):97-101. [Medline].

  • Ratanajamit C, Vinther Skriver M, Jepsen P, Chongsuvivatwong V, Olsen J, Sørensen HT. Adverse pregnancy outcome in women exposed to acyclovir during pregnancy: a population-based observational study. Scand J Infect Dis. 2003. 35 (4):255-9. [Medline].

  • Management of Genital Herpes in Pregnancy: ACOG Practice Bulletinacog Practice Bulletin, Number 220. Obstet Gynecol. 2020 May. 135 (5):e193-e202. [Medline].

  • Scott LL, Hollier LM, McIntire D, Sanchez PJ, Jackson GL, Wendel GD Jr. Acyclovir suppression to prevent clinical recurrences at delivery after first episode genital herpes in pregnancy: an open-label trial. Infect Dis Obstet Gynecol. 2001. 9 (2):75-80. [Medline].

  • Stránská R, Schuurman R, Nienhuis E, Goedegebuure IW, Polman M, Weel JF, et al. Survey of acyclovir-resistant herpes simplex virus in the Netherlands: prevalence and characterization. J Clin Virol. 2005 Jan. 32 (1):7-18. [Medline].

  • Stone KM, Reiff-Eldridge R, White AD, Cordero JF, Brown Z, Alexander ER, et al. Pregnancy outcomes following systemic prenatal acyclovir exposure: Conclusions from the international acyclovir pregnancy registry, 1984-1999. Birth Defects Res A Clin Mol Teratol. 2004 Apr. 70 (4):201-7. [Medline].

  • James SH, Kimberlin DW. Neonatal herpes simplex virus infection: epidemiology and treatment. Clin Perinatol. 2015 Mar. 42 (1):47-59, viii. [Medline].

  • Harris JB, Holmes AP. Neonatal Herpes Simplex Viral Infections and Acyclovir: An Update. J Pediatr Pharmacol Ther. 2017 Mar-Apr. 22 (2):88-93. [Medline].

  • Looker KJ, Elmes JAR, Gottlieb SL, Schiffer JT, Vickerman P, Turner KME, et al. Effect of HSV-2 infection on subsequent HIV acquisition: an updated systematic review and meta-analysis. Lancet Infect Dis. 2017 Dec. 17 (12):1303-1316. [Medline].

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  • Corey L, Wald A, Celum CL, Quinn TC. The effects of herpes simplex virus-2 on HIV-1 acquisition and transmission: a review of two overlapping epidemics. J Acquir Immune Defic Syndr. 2004 Apr 15. 35(5):435-45. [Medline].

  • Nagot N, Ouedraogo A, Foulongne V, Konate I, Weiss HA, Vergne L. Reduction of HIV-1 RNA levels with therapy to suppress herpes simplex virus. N Engl J Med. 2007 Feb 22. 356(8):790-9. [Medline].

  • Baeten JM, Strick LB, Lucchetti A, Whittington WL, Sanchez J, Coombs RW, et al. Herpes simplex virus (HSV)-suppressive therapy decreases plasma and genital HIV-1 levels in HSV-2/HIV-1 coinfected women: a randomized, placebo-controlled, cross-over trial. J Infect Dis. 2008 Dec 15. 198(12):1804-8. [Medline]. [Full Text].

  • Posavad CM, Wald A, Kuntz S, Huang ML, Selke S, Krantz E, et al. Frequent reactivation of herpes simplex virus among HIV-1-infected patients treated with highly active antiretroviral therapy. J Infect Dis. 2004 Aug 15. 190 (4):693-6. [Medline].

  • Herpes Simplex Virus | NIH

    Epidemiology

    Infections with human herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are common. Among persons aged 14 to 49 years in the United States, the HSV-1 seroprevalence is 47.8%, and the HSV-2 seroprevalence is 11.9%.1 While most cases of recurrent genital herpes are due to HSV-2, over the past decade, HSV-1 has become an increasing cause of first-episode genital herpes, causing up to 70% of infections in some populations, such as young adult women and men who have sex with men.2 Approximately 70% of persons with HIV are HSV-2 seropositive, and 95% are seropositive for either HSV-1 or HSV-2.3 HSV-2 infection increases the risk of HIV acquisition two- to three-fold,4,5 and in coinfected patients, HSV-2 reactivation results in increases in HIV RNA levels in blood and genital secretions.6

    Clinical Manifestations

    Orolabial herpes (commonly known as cold sores or fever blisters) is the most common manifestation of HSV-1 infection. Classic manifestations of oral HSV-1 include a sensory prodrome in the affected area, rapidly followed by lesions on lips and oral mucosa that evolve in stages from papule to vesicle, ulcer, and crust. The course of illness in untreated patients is 5 days to 10 days. Lesions recur 1 to 12 times per year and can be triggered by sunlight or physiologic stress.

    Genital herpes is typically caused by HSV-2 and is the most common manifestation of HSV-2 infection. Increasingly, first-episode genital herpes is caused by HSV-1 and is indistinguishable from HSV-2 infection, although recurrences and viral shedding occur less often with genital HSV-1 infection. Typical genital mucosal or skin lesions evolve through stages of papule, vesicle, ulcer, and crust. Ulcerative lesions are usually the only stage observed on mucosal surfaces, but vesicles are commonly seen on skin on or around the genitals (e.g., the penile shaft, mon pubis, thighs). Local symptoms might include a sensory prodrome consisting of pain and pruritus. Mucosal disease is occasionally accompanied by dysuria or vaginal or urethral discharge. Inguinal lymphadenopathy is common with genital herpes, particularly in primary infection.7 These classic manifestations occur in some patients, but most individuals with genital herpes have mild and atypical lesions that are often unrecognized. Regardless of the clinical severity of infection, viral shedding on mucosal surfaces occurs frequently and can result in transmission. HSV shedding occurs more frequently in persons with CD4 T lymphocyte (CD4) cell counts <200 cells/mm3 than in those with higher CD4 counts.8,9 An episode of genital HSV-1 disease is indistinguishable from genital HSV-2 disease, but recurrences and viral shedding occur less often with genital HSV-1 infection.

    HSV is a significant cause of proctitis in men with HIV infection who have sex with men and may not be associated with external anal ulcers.10 In profoundly immunocompromised patients, extensive, deep, nonhealing ulcerations can occur. These lesions have been reported most often in those with CD4 counts <100 cells/mm3 and also may be associated with acyclovir-resistant HSV.11 In addition, atypical presentations such as hypertrophic genital HSV,12,13 which mimics neoplasia and requires biopsy for diagnosis, may be seen in persons with HIV infection.

    The manifestations of non-mucosal HSV infections (e.g., HSV keratitis, HSV encephalitis, HSV hepatitis, herpetic whitlow) are similar to those observed in HIV-seronegative individuals. Disseminated HSV infection is rare, even in profoundly immunosuppressed patients. HSV retinitis manifests as acute retinal necrosis, which can lead rapidly to loss of vision.

    Diagnosis

    Because mucosal HSV infections cannot be diagnosed accurately by clinical examination, a laboratory diagnosis of all suspected HSV mucosal infections should be pursued.14 HSV DNA polymerase chain reaction (PCR), and viral culture are preferred methods for diagnosis of mucocutaneous lesions potentially caused by HSV. PCR is the most sensitive method of diagnosis. HSV detected in genital lesions should be typed as HSV-1 or HSV-2. The frequency of recurrences is greater for HSV-2 than for HSV-1, and therefore knowledge of viral type is helpful for counseling purposes. 

    Type-specific serologic assays are commercially available and can be used for diagnosis of HSV-2 infection in asymptomatic individuals or those with atypical lesions. Type-specific serologic screening for HSV-2 for persons with HIV infection can be considered. However, providers should be aware that there are some important limitations of currently available serologic tests. In particular, false positive HSV-2 serologic test results occur with the enzyme immunoassay antibody tests, particularly at low index values (1.1–3.5).15-17 In such situations, confirmatory testing with a second serologic test is recommended in the 2015 Centers for Disease Control and Prevention (CDC) Sexually Transmitted Disease Treatment Guidelines.18 A diagnosis of HSV-2 should be accompanied by counseling that includes discussion of the risk of transmitting infection to sex partners. Guidelines for counseling are provided in the 2015 CDC Sexually Transmitted Disease Treatment Guidelines.18 Serologic screening for HSV-1 infection is not recommended.

    Preventing Exposure

    Although most people with HIV also have HSV-1 and HSV-2 infections, it is important to prevent HSV-2 acquisition in those who do not have HSV-2. Persons with HIV who are HSV-2 seronegative should consider asking their partners to be tested using HSV type-specific serology before initiating sexual activity because disclosure of HSV-2 in heterosexual HIV-negative, HSV-2-discordant couples was associated with reduced risk of transmission of HSV-2 (BII).19 Consistent use of latex condoms reduced HSV-2 acquisition among heterosexual couples, and their use should be encouraged to prevent transmission of HSV-2 and other sexually transmitted pathogens (AII).20,21 

    Sexual transmission of HSV most often occurs during episodes of asymptomatic viral shedding. However, persons with HIV should specifically avoid sexual contact with partners who have overt genital or orolabial herpetic lesions (AII).

    In HSV-2 seropositive persons who have symptomatic genital herpes but not HIV, suppressive antiviral therapy (e.g., valacyclovir 500 mg once daily) reduced HSV-2 transmission to susceptible heterosexual partners by 48%.22 However, in HIV-1/HSV-2-seropositive persons not on antiretroviral therapy (ART), suppressive acyclovir (400 mg twice daily) did not prevent HSV-2 transmission to HSV-2 seronegative partners.23 Suppressive anti-HSV therapy to prevent HSV-2 transmission to susceptible partners is not recommended for persons with HIV/HSV-2 coinfection who are not on ART (AI). There are no data available regarding use of suppressive therapy to prevent genital HSV-1 transmission.

    Preventing Disease

    Prophylaxis with antiviral drugs to prevent primary HSV infection is not recommended (AIII). In clinical trials, pre-exposure prophylaxis with vaginal tenofovir gel and oral tenofovir disoproxil fumarate (TDF) or with TDF/emtricitabine has been associated with reduced risk of HSV-2 acquisition in persons without HIV.24-26 However, HSV-2 seronegative persons with HIV on TDF-containing ART regimens are at similar risk of acquiring HSV-2 as those on non-TDF containing ART regimens, suggesting that TDF is not effective in preventing HSV-2 acquisition in persons with HIV infection.27 The dose, duration, timing, and efficacy of anti-HSV prophylaxis after known or suspected exposure to HSV has not been evaluated. No vaccine for prevention of HSV infection is available. Some studies have shown that medical male circumcision (MMC) decreased the risk of HSV-2 acquisition in African men without HIV,28,29 and may be associated with decreased risk of HSV-2 transmission to female partners.30 However, MMC to decrease risk of HSV-2 acquisition and transmission has not been studied among men with HIV and therefore is not recommended for the sole purpose of preventing HSV acquisition (AIII).

    Treating Disease

    Patients with HSV infections can be treated with episodic antiviral therapy when symptomatic lesions occur or with daily suppressive therapy to prevent recurrences. Acyclovir, valacyclovir, and famciclovir are effective for suppressive and episodic therapy. Valacyclovir is the prodrug of acyclovir, and has improved oral bioavailability, with decreased dosing frequency, compared to acyclovir. When deciding on suppressive therapy for genital HSV-2 infection in persons with HIV and HSV-2 coinfection, factors to consider include the frequency and severity of HSV recurrences and risk for genital ulcer disease (GUD) when initiating ART.31 Episodic treatment for individual recurrences of GUD does not influence the natural history of genital HSV-2 infection.

    Patients with orolabial HSV lesions can be treated with oral acyclovir, valacyclovir, or famciclovir for 5 days to 10 days (AIII). First episodes of genital HSV should be treated with oral acyclovir, valacyclovir, or famciclovir for 7 days to 10 days; recurrences can be treated for 5 to 10 days (AI). Severe mucocutaneous HSV lesions respond best to initial treatment with intravenous (IV) acyclovir (AIII).11,32 Once the lesions begin to regress, patients can be switched to oral antiviral therapy. Therapy should be continued until the lesions have completely healed. Although disseminated disease due to HSV is rare in persons with HIV, HSV necrotizing retinitis can occur, which may be difficult to distinguish clinically from retinitis caused by varicella-zoster virus.

    Special Considerations with Regard to Starting Antiretroviral Therapy

    Orolabial and genital HSV should not influence the decision on when to start ART in persons with HIV. Transient increases in HSV-2–associated genital ulcers have been observed during the first 6 months after initiation of ART in HIV/HSV-2 coinfected persons. In such cases, suppressive anti-HSV therapy can be considered. The frequency and severity of clinical episodes of genital herpes is often reduced in individuals after immune reconstitution on ART. However, immune reconstitution does not reduce the frequency of genital HSV shedding.33

    Monitoring of Response to Therapy and Adverse Events (Including IRIS)

    Acyclovir, valacyclovir, and famciclovir are occasionally associated with nausea or headache. No laboratory monitoring is needed for patients receiving episodic or suppressive HSV therapy unless they have advanced renal impairment. However, for patients receiving high-dose IV acyclovir, monitoring of renal function, and dose adjustment as necessary, are recommended at initiation of treatment and once or twice weekly for the duration of treatment.

    HSV-2 shedding and GUD can increase in the first 6 months after initiation of ART, particularly in those with low CD4 counts.34,35 Mucocutaneous lesions that are atypical and occasionally recalcitrant to therapy have been reported in individuals initiating ART and have been attributed to immune reconstitution inflammatory syndrome (IRIS).36

    Managing Treatment Failure

    Treatment failure due to acyclovir resistance should be suspected if herpes-related lesions do not begin to resolve within 7 days to 10 days after initiation of anti-HSV therapy. In persons with suspected acyclovir-resistant HSV, viral culture of the lesion should be performed, and if virus is isolated, susceptibility testing done to confirm drug resistance (AII).37 Phenotypic testing of viral isolates has been the gold standard method for assessing HSV resistance; genotypic testing is not yet available.

    The treatment of choice for acyclovir-resistant HSV is IV foscarnet (AI).38,39 IV cidofovir is a potential alternative (CIII). A novel agent, the helicase-primase inhibitor pritelivir, is currently being testing in clinical trials for treatment of acyclovir-resistant herpes in immunocompromised persons (ClinicalTrials.gov Identifier: NCT03073967). There is an Expanded Access Program available for oral pritelivir in these populations; for more information see AiCuris Pritelivir Early Access website. Topical trifluridine, foscarnet, cidofovir, and imiquimod also have been used successfully to treat external lesions, although prolonged application for 21 days to 28 days or longer may be required (CIII).40-44 

    Preventing Recurrence

    Suppressive therapy with oral acyclovir, valacyclovir, or famciclovir is effective in preventing recurrences of HSV lesions and is preferred for patients who have severe or frequent HSV recurrences or who want to minimize the frequency of recurrences (AI).14,45 Suppressive therapy for HSV may be continued indefinitely, without regard to improved CD4 count, although the need for continued therapy should be addressed on an annual basis, particularly if immune reconstitution has occurred (BIII). Persons starting ART with CD4 counts <250 cells/mm3 have an increased risk of HSV-2 shedding and GUD in the first 6 months on ART. Suppressive acyclovir decreases the risk of GUD nearly 60%, and may be recommended for persons with CD4 counts 250 cells/mm3 starting ART (BI).

    In persons with HIV not on ART, suppressive anti-HSV therapy also results in a decrease in HIV RNA levels in plasma, anal, and genital secretions, and in a lower risk of HIV progression.46 However, antiviral regimens for herpes do not decrease the risk of HIV transmission to sexual partners, and should not be used in place of ART to delay HIV progression.47 In persons who are taking ART, suppressive HSV antivirals do not delay HIV progression, improve CD4 recovery, or decrease markers of systemic inflammation48,49 and are not useful for these ends (AI).

    Although there is no data specific to persons with HIV, in hematopoietic stem cell recipients, the risk of developing acyclovir-resistant HSV was lower with daily suppressive acyclovir therapy than with episodic therapy.50

    Special Considerations During Pregnancy

    Laboratory testing to diagnose mucocutaneous HSV infections is the same for pregnant women as for non-pregnant women. Episodic therapy for first-episode HSV disease and for recurrences can be offered during pregnancy. Visceral disease following HSV acquisition is more likely to occur during pregnancy and can be fatal. Acyclovir is the antiviral drug with the most reported experience in pregnancy and appears to be safe, particularly during the second and third trimesters (AIII).51 One recent case–control study suggested a higher risk of gastroschisis associated with both genital herpes and acyclovir use during the first trimester of pregnancy.52 The use of valacyclovir and famciclovir during pregnancy has been described, and the antiviral drugs also appear to be safe and well tolerated during the third trimester.53 Given its simplified dosing schedule valacyclovir is an option for treatment and suppressive therapy during pregnancy (CIII).

    An additional concern with HSV during pregnancy is the potential for HSV transmission to the fetus or neonate. The rate of neonatal HSV transmission in HSV-2-seropositive pregnant women is low, except in those who acquire genital HSV infection late in pregnancy. However, when HSV transmission does occur, the adverse sequelae for the neonate can be very significant. The predominant risk for neonatal HSV transmission is maternal genital shedding of HSV at delivery. Cesarean delivery is recommended for women with a genital herpes prodrome or visible HSV genital lesions at the onset of labor (BII).14 Use of acyclovir or valacyclovir in late pregnancy suppresses genital herpes outbreaks and reduces the need for cesarean delivery for recurrent HSV in HIV-seronegative women54 and is likely to have similar efficacy in women with HIV infection. However, neonatal HSV disease has been reported in infants born to women treated with antenatal suppressive antiviral therapy.55 Suppressive therapy with either valacyclovir or acyclovir is recommended starting at 36 weeks’ gestation for pregnant women with recurrences of genital herpes during pregnancy (BII).56 Suppressive therapy for women who are seropositive for HSV-2 but no history of genital lesions is not recommended. Maternal genital herpes was a risk factor for perinatal HIV transmission in the era preceding availability of ART.57 Whether HSV facilitates HIV transmission in pregnant women on ART is unknown.

    Recommendations for Treating Herpes Simplex Virus Infections

    Note: Compared to acyclovir, valacyclovir has improved bioavailability and requires less frequent dosing.

    Treating Orolabial Lesions (Duration: 5–10 Days)

    • Valacyclovir 1 g PO twice a day (AIII), or
    • Famciclovir 500 mg PO twice a day (AIII), or
    • Acyclovir 400 mg PO three times a day (AIII)

    Treating Initial Genital Lesions (Duration: 7–10 Days) or Recurrent Genital Lesions (Duration: 5–10 Days)

    • Valacyclovir 1 g PO twice a day (AI), or
    • Famciclovir 500 mg PO twice a day (AI), or
    • Acyclovir 400 mg PO three times a day (AI)

    Treating Severe Mucocutaneous HSV Infections (AIII)

    • For initial therapy, acyclovir 5 mg/kg IV every 8 hours
    • After lesions begin to regress, change to oral therapy as above.
    • Continue treatment until lesions have completely healed.
    Chronic Suppressive Therapy
    Indications:

    • For patients with severe recurrences (AI), or
    • Patients who want to minimize the frequency of recurrences (AI), including pregnant women, or
    • To reduce the risk of genital ulcer disease in patients with CD4 counts <250 cells/mm3 who are starting ART (BI)

    Treatment:

    • Valacyclovir 500 mg PO twice a day (AI), or
    • Famciclovir 500 mg PO twice a day (AI), or
    • Acyclovir 400 mg PO twice a day (AI)
    • Evaluate ongoing need for suppressive therapy annually.

    For Acyclovir-Resistant Mucocutaneous HSV infections
    Preferred Therapy:

     IV Foscarnet 80–120 mg/kg/day in 2–3 divided doses until clinical response (AI)

    Alternative Therapy (Duration: ≥21–28 Days, Based on Clinical Response) (CIII):

    • IV cidofovir 5 mg/kg once weekly, or
    • Topical trifluridine 1% three times a day, or
    • Topical cidofovir 1% gel once daily, or
    • Topical imiquimod 5% cream three times a week, or
    • Topical foscarnet 1% five times a day

    Notes:

    • Topical formulations of trifluridine, cidofovir, and foscarnet are not commercially available.
    • Extemporaneous compounding of topical products can be prepared using trifluridine ophthalmic solution and the IV formulation of cidofovir and foscarnet.
    • An expanded access program of oral pritelivir is now available for immunocompromised patients with acyclovir-resistant HSV infection; for more information see AiCuris Pritelivir Early Access website. 

    References

    1. McQuillan G, Kruszon-Moran D, Flagg EW, Paulose-Ram R. Prevalence of herpes simplex virus type 1 and type 2 in persons Aged 14–49: United States, 2015-2016. NCHS Data Brief. 2018(304):1-8. Available at: https://www.ncbi.nlm.nih.gov/pubmed/29442994.
    2. Ryder N, Jin F, McNulty AM, Grulich AE, Donovan B. Increasing role of herpes simplex virus type 1 in first-episode anogenital herpes in heterosexual women and younger men who have sex with men, 1992-2006. Sex Transm Infect. 2009;85(6):416-419. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19273479.
    3. Xu F, Sternberg MR, Kottiri BJ, et al. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA. 2006;296(8):964-973. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16926356.
    4. Wald A, Link K. Risk of human immunodeficiency virus infection in herpes simplex virus type 2-seropositive persons: a meta-analysis. J Infect Dis. 2002;185(1):45-52. Available at: https://www.ncbi.nlm.nih.gov/pubmed/11756980.
    5. Looker KJ, Elmes JAR, Gottlieb SL, et al. Effect of HSV-2 infection on subsequent HIV acquisition: an updated systematic review and meta-analysis. Lancet Infect Dis. 2017;17(12):1303-1316. Available at: https://www.ncbi.nlm.nih.gov/pubmed/28843576.
    6. Nagot N, Ouedraogo A, Konate I, et al. Roles of clinical and subclinical reactivated herpes simplex virus type 2 infection and human immunodeficiency virus type 1 (HIV-1)-induced immunosuppression on genital and plasma HIV-1 levels. J Infect Dis. 2008;198(2):241-249. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18593294.
    7. Corey L, Adams HG, Brown ZA, Holmes KK. Genital herpes simplex virus infections: clinical manifestations, course, and complications. Ann Intern Med. 1983;98(6):958-972. Available at: https://www.ncbi.nlm.nih.gov/pubmed/6344712.
    8. Schiffer JT, Swan DA, Magaret A, Schacker TW, Wald A, Corey L. Mathematical modeling predicts that increased HSV-2 shedding in HIV-1 infected persons is due to poor immunologic control in ganglia and genital mucosa. PLoS One. 2016;11(6):e0155124. Available at: https://www.ncbi.nlm.nih.gov/pubmed/27285483.
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    10. Bissessor M, Fairley CK, Read T, Denham I, Bradshaw C, Chen M. The etiology of infectious proctitis in men who have sex with men differs according to HIV status. Sex Transm Dis. 2013;40(10):768-770. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24275725.
    11. Safrin S, Elbeik T, Phan L, et al. Correlation between response to acyclovir and foscarnet therapy and in vitro susceptibility result for isolates of herpes simplex virus from human immunodeficiency virus-infected patients. Antimicrob Agents Chemother. 1994;38(6):1246-1250. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8092821.
    12. Yudin MH, Kaul R. Progressive hypertrophic genital herpes in an HIV-infected woman despite immune recovery on antiretroviral therapy. Infect Dis Obstet Gynecol. 2008;2008:592532. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18784844.
    13. Sbidian E, Battistella M, Legoff J, et al. Recalcitrant pseudotumoral anogenital herpes simplex virus type 2 in HIV-infected patients: evidence for predominant B-lymphoplasmocytic infiltration and immunomodulators as effective therapeutic strategy. Clin Infect Dis. 2013;57(11):1648-1655. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24065320.
    14. Workowski KA, Berman S, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep. 2010;59(RR-12):1-110. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21160459.
    15. Agyemang E, Le QA, Warren T, et al. Performance of commercial enzyme-linked immunoassays for diagnosis of herpes simplex virus-1 and herpes simplex virus-2 infection in a clinical setting. Sex Transm Dis. 2017;44(12):763-767. Available at: https://www.ncbi.nlm.nih.gov/pubmed/28876290.
    16. Golden MR, Ashley-Morrow R, Swenson P, Hogrefe WR, Handsfield HH, Wald A. Herpes simplex virus type 2 (HSV-2) Western blot confirmatory testing among men testing positive for HSV-2 using the focus enzyme-linked immunosorbent assay in a sexually transmitted disease clinic. Sex Transm Dis. 2005;32(12):771-777. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16314775.
    17. Morrow RA, Friedrich D, Meier A, Corey L. Use of “biokit HSV-2 Rapid Assay” to improve the positive predictive value of Focus HerpeSelect HSV-2 ELISA. BMC Infect Dis. 2005;5:84. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16225691.
    18. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64(RR-03):1-137. Available at: http://www.ncbi.nlm.nih.gov/pubmed/26042815.
    19. Wald A, Krantz E, Selke S, Lairson E, Morrow RA, Zeh J. Knowledge of partners’ genital herpes protects against herpes simplex virus type 2 acquisition. J Infect Dis. 2006;194(1):42-52. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16741881.
    20. Wald A, Langenberg AG, Krantz E, et al. The relationship between condom use and herpes simplex virus acquisition. Ann Intern Med. 2005;143(10):707-713. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16287791.
    21. Martin ET, Krantz E, Gottlieb SL, et al. A pooled analysis of the effect of condoms in preventing HSV-2 acquisition. Arch Intern Med. 2009;169(13):1233-1240. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19597073.
    22. Corey L, Wald A, Patel R, et al. Once-daily valacyclovir to reduce the risk of transmission of genital herpes. N Engl J Med. 2004;350(1):11-20. Available at: https://www.ncbi.nlm.nih.gov/pubmed/14702423.
    23. Mujugira A, Magaret AS, Celum C, et al. Daily acyclovir to decrease herpes simplex virus type 2 (HSV-2) transmission from HSV-2/HIV-1 coinfected persons: a randomized controlled trial. J Infect Dis. 2013;208(9):1366-1374. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23901094.
    24. Abdool Karim Q, Abdool Karim SS, Frohlich JA, et al. Effectiveness and safety of tenofovir gel, an antiretroviral microbicide, for the prevention of HIV infection in women. Science. 2010;329(5996):1168-1174. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20643915.
    25. Celum C, Morrow RA, Donnell D, et al. Daily oral tenofovir and emtricitabine-tenofovir preexposure prophylaxis reduces herpes simplex virus type 2 acquisition among heterosexual HIV-1-uninfected men and women: a subgroup analysis of a randomized trial. Ann Intern Med. 2014;161(1):11-19. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24979446.
    26. Marrazzo JM, Rabe L, Kelly C, et al. Tenofovir gel for prevention of herpes simplex virus type 2 acquisition: findings from the VOICE trial. J Infect Dis. 2019;219(12):1940-1947. Available at: https://www.ncbi.nlm.nih.gov/pubmed/30753642.
    27. Celum C, Hong T, Cent A, et al. Herpes simplex virus type 2 acquisition among HIV-1-infected adults treated with tenofovir disoproxyl fumarate as part of combination antiretroviral therapy: results from the ACTG A5175 PEARLS Study. J Infect Dis. 2017;215(6):907-910. Available at: https://www.ncbi.nlm.nih.gov/pubmed/28453835.
    28. Tobian AA, Serwadda D, Quinn TC, et al. Male circumcision for the prevention of HSV-2 and HPV infections and syphilis. N Engl J Med. 2009;360(13):1298-1309. Available at: http://www.ncbi.nlm.nih.gov/pubmed/19321868.
    29. Sobngwi-Tambekou J, Taljaard D, Lissouba P, et al. Effect of HSV-2 serostatus on acquisition of HIV by young men: results of a longitudinal study in Orange Farm, South Africa. J Infect Dis. 2009;199(7):958-964. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19220143.
    30. Grund JM, Bryant TS, Jackson I, et al. Association between male circumcision and women’s biomedical health outcomes: a systematic review. Lancet Glob Health. 2017;5(11):e1113-e1122. Available at: https://www.ncbi.nlm.nih.gov/pubmed/29025633.
    31. Keating TM, Kurth AE, Wald A, Kahle EM, Barash EA, Buskin SE. Clinical burden of herpes simplex virus disease in people with human immunodeficiency virus. Sex Transm Dis. 2012;39(5):372-376. Available at: https://www.ncbi.nlm.nih.gov/pubmed/22504602.
    32. Meyers JD, Wade JC, Mitchell CD, et al. Multicenter collaborative trial of intravenous acyclovir for treatment of mucocutaneous herpes simplex virus infection in the immunocompromised host. Am J Med. 1982;73(1A):229-235. Available at: https://www.ncbi.nlm.nih.gov/pubmed/7048914.
    33. Posavad CM, Wald A, Kuntz S, et al. Frequent reactivation of herpes simplex virus among HIV-1-infected patients treated with highly active antiretroviral therapy. J Infect Dis. 2004;190(4):693-696. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15272395.
    34. Graham SM, Masese L, Gitau R, et al. Increased risk of genital ulcer disease in women during the first month after initiating antiretroviral therapy. J Acquir Immune Defic Syndr. 2009;52(5):600-603. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19648822.
    35. Tobian AA, Grabowski MK, Serwadda D, et al. Reactivation of herpes simplex virus type 2 after initiation of antiretroviral therapy. J Infect Dis. 2013;208(5):839-846. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23812240.
    36. Couppie P, Sarazin F, Clyti E, et al. Increased incidence of genital herpes after HAART initiation: a frequent presentation of immune reconstitution inflammatory syndrome (IRIS) in HIV-infected patients. AIDS Patient Care STDS. 2006;20(3):143-145. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16548710.
    37. Balfour HH Jr. Antiviral drugs. N Engl J Med. 1999;340(16):1255-1268. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10210711.
    38. Safrin S, Crumpacker C, Chatis P, et al. A controlled trial comparing foscarnet with vidarabine for acyclovir-resistant mucocutaneous herpes simplex in the acquired immunodeficiency syndrome. The AIDS Clinical Trials Group. N Engl J Med. 1991;325(8):551-555. Available at: https://www.ncbi.nlm.nih.gov/pubmed/1649971.
    39. Levin MJ, Bacon TH, Leary JJ. Resistance of herpes simplex virus infections to nucleoside analogues in HIV-infected patients. Clin Infect Dis. 2004;39 Suppl 5:S248-257. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15494896.
    40. Lascaux AS, Caumes E, Deback C, et al. Successful treatment of aciclovir and foscarnet resistant Herpes simplex virus lesions with topical imiquimod in patients infected with human immunodeficiency virus type 1. J Med Virol. 2012;84(2):194-197. Available at: https://www.ncbi.nlm.nih.gov/pubmed/22170537.
    41. Perkins N, Nisbet M, Thomas M. Topical imiquimod treatment of aciclovir-resistant herpes simplex disease: case series and literature review. Sex Transm Infect. 2011;87(4):292-295. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21406577.
    42. Lateef F, Don PC, Kaufmann M, White SM, Weinberg JM. Treatment of acyclovir-resistant, foscarnet-unresponsive HSV infection with topical cidofovir in a child with AIDS. Arch Dermatol. 1998;134(9):1169-1170. Available at: https://www.ncbi.nlm.nih.gov/pubmed/9762047.
    43. Kessler HA, Hurwitz S, Farthing C, et al. Pilot study of topical trifluridine for the treatment of acyclovir-resistant mucocutaneous herpes simplex disease in patients with AIDS (ACTG 172). AIDS Clinical Trials Group. J Acquir Immune Defic Syndr Hum Retrovirol. 1996;12(2):147-152. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8680885.
    44. Javaly K, Wohlfeiler M, Kalayjian R, et al. Treatment of mucocutaneous herpes simplex virus infections unresponsive to acyclovir with topical foscarnet cream in AIDS patients: a phase I/II study. J Acquir Immune Defic Syndr. 1999;21(4):301-306. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10428108.
    45. DeJesus E, Wald A, Warren T, et al. Valacyclovir for the suppression of recurrent genital herpes in human immunodeficiency virus-infected subjects. J Infect Dis. 2003;188(7):1009-1016. Available at: https://www.ncbi.nlm.nih.gov/pubmed/14513421.
    46. Lingappa JR, Baeten JM, Wald A, et al. Daily acyclovir for HIV-1 disease progression in people dually infected with HIV-1 and herpes simplex virus type 2: a randomised placebo-controlled trial. Lancet. 2010;375(9717):824-833. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20153888.
    47. Celum C, Wald A, Lingappa JR, et al. Acyclovir and transmission of HIV-1 from persons infected with HIV-1 and HSV-2. N Engl J Med. 2010;362(5):427-439. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20089951.
    48. Yi TJ, Walmsley S, Szadkowski L, et al. A randomized controlled pilot trial of valacyclovir for attenuating inflammation and immune activation in HIV/herpes simplex virus 2-coinfected adults on suppressive antiretroviral therapy. Clin Infect Dis. 2013;57(9):1331-1338. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23946220.
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    50. Erard V, Wald A, Corey L, Leisenring WM, Boeckh M. Use of long-term suppressive acyclovir after hematopoietic stem-cell transplantation: impact on herpes simplex virus (HSV) disease and drug-resistant HSV disease. J Infect Dis. 2007;196(2):266-270. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17570114.
    51. Stone KM, Reiff-Eldridge R, White AD, et al. Pregnancy outcomes following systemic prenatal acyclovir exposure: Conclusions from the international acyclovir pregnancy registry, 1984-1999. Birth Defects Res A Clin Mol Teratol. 2004;70(4):201-207. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15108247.
    52. Ahrens KA, Anderka MT, Feldkamp ML, et al. Antiherpetic medication use and the risk of gastroschisis: findings from the National Birth Defects Prevention Study, 1997-2007. Paediatr Perinat Epidemiol. 2013;27(4):340-345. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23772935.
    53. Pasternak B, Hviid A. Use of acyclovir, valacyclovir, and famciclovir in the first trimester of pregnancy and the risk of birth defects. JAMA. 2010;304(8):859-866. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20736469.
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    57. Chen KT, Segu M, Lumey LH, et al. Genital herpes simplex virus infection and perinatal transmission of human immunodeficiency virus. Obstet Gynecol. 2005;106(6):1341-1348. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16319261.

    Viral Skin Infection: Herpes gladiatorum (“Mat Herpes”)

    What is herpes gladiatorum?

    Herpes gladiatorum (“mat herpes”) is a skin infection caused by herpes simplex virus type 1 (HSV-1), the same virus that causes cold sores on the lips. HSV-1 infections are very common. In the United States, 30% to 90% of people are exposed to herpes by adulthood, although many people never develop symptoms.

    While herpes gladiatorum (HSV-1) can be treated, once infected with the virus, a person is infected for life. People with herpes gladiatorum can have periods where the virus is inactive and cannot be spread to others. However, the virus can reactivate at any time and be transmitted to others, even if there are no symptoms (such as sores). This is why prevention is so important.

    Herpes simplex virus type 1 (HSV-1) on lip

    What parts of the body can herpes gladiatorum (HSV-1 infection) affect?

    Athletes with herpes gladiatorum may develop lesions anywhere on the face or body. HSV-1 infection of the eye can be serious and requires immediate medical attention.

    HSV-1 on and around eye

    Is herpes gladiatorum only spread between athletes?

    No. HSV-1, the virus that causes herpes gladiatorum, can be spread to others through direct skin contact with lesions — this includes kissing or sharing beverage containers, eating utensils, cell phones, or lip balm with others.

    What are the symptoms of herpes gladiatorum (HSV-1 infection)?

    • Symptoms usually begin about 8 days after exposure to HSV-1.
    • Fever (especially during the first episode).
    • Swollen glands (enlarged lymph nodes).
    • A tingling feeling at the affected area.
    • A cluster (usually more than one) of clear, fluid-filled blisters that may be surrounded by redness — these blisters may or may not be painful.
    • Blisters and lesions usually heal within 7 to 10 days.
    • People with HSV-1 infection are infected for life, may have periodic outbreaks, and can transmit the virus to others.

    Herpes outbreak on arm

    How is herpes gladiatorum diagnosed and treated?

    • If you suspect you have HSV-1 infection, inform your coach immediately — early identification and treatment of skin infections is important for your health and the health of your teammates and opponents.
    • Some cases of herpes are mild and may not need treatment. However, athletes should not practice, play, or compete until a medical provider determines that the lesions are no longer infectious (contagious).
    • Athletes who have severe or prolonged outbreaks (especially if it is the first episode), immune system problems, or frequent outbreaks may be prescribed antiviral medications.

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    Herpes / Diseases / Clinic EXPERT

    Herpes is a common viral disease caused by the herpes simplex virus (HSV) and is characterized by the appearance of a blistering rash on the skin and mucous membranes of various organs.

    Almost all people in the world are carriers of HSV, but only 20% of them are infected.

    Usually herpes is manifested by damage to the following organs and structures of the body:

    • skin
    • mucous membranes of the face and genitals
    • eyes
    • central nervous system.

    The causes of herpes

    The development of herpes can be influenced by such factors as:

    • weakened immunity
    • the presence of certain diseases
    • overheating or hypothermia of the body
    • surgical procedures and other medical interventions (for example, the installation of an intrauterine device, abortion, etc.)
    • some psychological conditions and other factors.

    Infection with this disease occurs from a person already sick with herpes, in whom the rash is localized on the outer layer of the mucous membrane.

    Types of herpes

    In total, there are about two hundred varieties of the herpes virus. Of these, only eight types are distinguished that are dangerous to the human body:

    • herpes type 1: manifested by a rash in the face
    • herpes type 2: localized in the genital area
    • herpes type 3: provokes shingles and chickenpox
    • herpes 4 types (Epstein-Barr virus): causes the development of infectious mononucleosis
    • herpes type 5 (cytomegalovirus): provokes cytomegalia.

    Herpes virus types 6, 7 and 8 are currently not fully understood. They are thought to cause chronic fatigue and manifest as a blistering rash.

    Herpes Symptoms

    Herpes can manifest itself in different ways depending on the type of disease and the type of virus that caused it. The general symptoms of herpes are as follows:

    • itching and redness of the skin area
    • the appearance of neoplasms on the skin (blisters, crusts, ulcers)
    • general weakness of the body, pain in joints and muscles.

    Diagnostics of herpes

    For the diagnosis of herpes in the EXPERT Clinic, the following laboratory tests are carried out:

    • virological method for the determination of herpes simplex virus
    • polymerase chain reaction (PCR)
    • determination of herpes antigens
    • test for a simple immune response herpes
    • cytomorphological method
    • enzyme immunoassay
    • other analyzes.

    Treating herpes

    Since the herpes virus cannot be completely cured, treatment for this disease is aimed at reducing the number of relapses and alleviating symptoms.Treatment of herpes at the EXPERT Clinic is planned by an experienced immunologist after a thorough diagnosis and implies therapy with antiviral drugs according to various schemes. The dosage of the drug is calculated individually for each patient.

    Antiherpes therapy can be shown to the patient not only with exacerbation of herpes, but also during periods of remission of the disease for preventive purposes.

    Forecast

    Primary local herpes in a patient in the absence of concomitant pathologies, as a rule, goes away on its own in 7-14 days.A high risk of death is observed in newborns with disseminated herpes and in infants with severely impaired immune system functions. In the absence of adequate treatment, complications may appear: herpes eye disease can lead to scarring of the cornea and even complete loss of vision. An exacerbation of herpes with low immunity can also lead to serious complications.

    Timely diagnosis and treatment of herpes significantly improve the prognosis of the disease.

    Prevention of herpes

    In order to avoid contracting herpes, immunologists advise adhering to the following recommendations:

    • Limit contact with a person already sick with herpes
    • Use only personal hygiene items
    • Avoid promiscuous and unprotected sex in order to avoid genital herpes
    • careful use of public toilets, if possible, treat sitting with antiseptic agents
    • avoid overheating and hypothermia
    • adhere to a healthy lifestyle.

    In order to avoid negative consequences for your health, at the first signs of herpes, make an appointment with an immunologist. Your doctor will provide you with high-quality medical care and help you reduce the likelihood of further exacerbations of herpes.

    Urogenital herpes: symptoms and treatment

    Urogenital herpes is a viral disease that is an extremely urgent problem for society, since almost 80% of the population is infected with it. These statistics are based on the results of modern diagnostics, which allows for a thorough examination of patients.

    The causative agent of genital herpes is the herpes simplex virus of the first and / or second type (HSV1-2).

    The disease is transmitted primarily through sexual contact.

    Genital herpes can be caused by both HSV-1 (the causative agent of labial herpes) and HSV-2. The clinical manifestations of the disease are identical for both types of infections. At the same time, the symptomatology of a particular episode in a particular patient is determined by the presence of herpes in history (labial or genital), as well as by the primary focus of infection.

    Causes of exacerbation

    Exacerbations of genital herpes caused by HSV-2 occur more often than with HSV-1.
    The virus lives in the nerve ganglia. There he is at rest, but under the influence of unfavorable factors, general and local immunity is suppressed, as a result of which the virus is activated and the disease relapses. The main reasons for this are:

    • stress;
    • neuroses;
    • depression;
    • chronic fatigue;
    • intense physical activity;
    • the presence of foci of chronic infection in the body;
    • change of time zone or climate;
    • excessive insolation, hypothermia;
    • lack of vitamins and minerals;
    • alcohol abuse;
    • the use of certain medicines.

    HSV1-2 have the ability to create permanent colonies of viral particles inside the human body. When a relapse occurs, the pathogen moves along the nerve pathways to the skin and mucous membranes in the genital / perianal region, which is why the external symptoms of genital herpes appear there. They are characterized by painful rashes, accompanied by severe itching and paresthesias.

    Symptoms

    The classic manifestations of genital herpes include:

    • papular eruptions transforming into vesicles and then ulcers;
    • regional lymphadenitis;
    • Prodromal period before the appearance of the rash (with recurrent genital herpes).

    Primary episode of genital herpes caused by herpes simplex virus I (HSV-1) or II (HSV-2) can manifest manifestly with clinical manifestations localized at the site of infection in the human body. Herpes in men is more often manifested by rashes localized in the urethra. It can also be accompanied by pain when urinating. In women, with vaginal localization of rashes, mucopurulent vaginal discharge, an increase and soreness of regional lymph nodes are possible.

    General symptoms of intoxication occur more often with the first episode than with relapses. These include:

    • increase in body temperature;
    • headache;
    • nausea;
    • malaise;
    • myalgia;
    • Sleep disturbance.

    The severity and duration of clinical manifestations is also more pronounced during the first episode.
    Atypical forms of genital herpes are manifested by hyperemia and edema in the affected area in the absence of pathological rashes.Clinical manifestations may not occur. In this case, the infection remains unrecognized. In addition, systemic manifestations characteristic of many viral infections can be detected. Further, the herpes simplex virus enters a latent phase, localizing in the peripheral sensitive nerve ganglia. At the same time, it can cause periodic exacerbations (lesions of the skin and mucous membranes) or the disease remains asymptomatic, which, nevertheless, does not mean the impossibility of its transmission.

    Transmission of the virus

    The risk of infection with the virus is greatest during exacerbations with lesions of the mucous membranes and / or skin, as well as during the feeding period. For this reason, modern medicine recommends abstinence during these periods. In addition, transmission of the virus can occur in the absence of rashes as a result of subclinical viral shedding. There is no exact data on the effectiveness of condom use for the prevention of herpes.

    Despite the fact that the clinical manifestations of the disease are well recognized, it should not be forgotten that its manifestations can vary widely from patient to patient.In many people, lesions in the region of the urogenital tract can be mistaken for other genital dermatoses. Therefore, it is recommended to avoid making a diagnosis solely on the basis of the clinical picture, especially if atypical symptoms are detected.

    Treatment and prevention

    The nature of the primary episodes of genital herpes often determines the subsequent course of the infectious process. If left untreated, many patients can develop local or generalized complications.It is during the initial episode that therapy is most effective.

    Patients who seek help within 5 days from the onset of clinical manifestations (or later, but in the presence of fresh elements of rashes), it is necessary to select antiviral therapy both to eliminate symptoms and to reduce the duration of relapse. At the same time, none of the drugs prevents the further development of the infectious process. Local drugs are less effective than systemic ones. This means that their use is not enough to successfully treat genital herpes.

    Some patients relapse for more than 5 days. With prolonged exacerbations of genital herpes (with persisting general manifestations, the appearance of new rashes and the development of complications), the course of therapy should be extended.

    The diagnosis is established not only on the basis of clinical manifestations, but also according to the results of laboratory tests, which are used to clarify the etiology of the disease, as well as in atypical forms of the disease and for the purpose of differential diagnosis.Therefore, a doctor, not a patient, should make a diagnosis, relying on information on the Internet, which is only superficial, cognitive and informational.

    The specialist will tell the patient about the existence of a high risk of transmission of the virus (including periods of subclinical viral shedding) even with the use of condoms and the use of antiviral drugs. He will also point out the need to inform the sexual partner about the presence of genital herpes, report on preventive measures to reduce the risk of transmission of the virus.When confirming the diagnosis, it is necessary to examine the sexual partners and, if possible, establish the source of the infection, as well as develop treatment options.

    Given the high prevalence of the virus, it is very important to provide women and men with detailed information about the dangers of illness during pregnancy. Since there is a risk of intrapartum transmission, the patient should inform the obstetrician if she has urogenital herpes . As a rule, the first-heard diagnosis causes a stress response that continues during exacerbations, but can be reduced with the use of antiviral drugs.

    Urogenital herpes has an unpredictable course and is accompanied by complications. Therefore, in no case should you self-medicate when characteristic symptoms appear. It is important to seek professional medical help in specialized medical institutions so that it is the doctor who prescribes a competent laboratory examination and individually selects the treatment. In addition, the specialist will give valuable recommendations regarding the prevention of genital herpes, which will undoubtedly reduce the number of relapses and maintain a comfortable quality of life.

    HERPES OF THE SKIN AND MUCOSA

    Herpes of the skin and mucous membranes is a fairly common disease that has had more than 90% of the adult population.

    Herpes of the skin and mucous membranes is an infectious disease that is caused by herpes simplex viruses types 1 and 2. In everyday life, herpes is usually called “cold sores” or “fever”.

    According to statistics, herpes is ubiquitous. More than 90% of 40-year-old people have antibodies to this virus.This means that these people have had herpes at least once in their lives. Note that herpes infection occurs in different ways in different organisms. The severity of the disease depends on the state of the human immune system and susceptibility to herpes viruses. The herpes virus affects not only the skin and mucous membranes, but also the nervous system and internal organs.

    CAUSES OF DISEASE

    You can become infected with the herpes simplex virus from a patient with fresh herpes sores, as well as from carriers that release the virus into the environment.At the same time, for infection, it is enough only for a viral particle to hit the skin or mucous membranes. The virus can also be transmitted through contaminated items, such as dishes, toys, towels, bedding and other items.

    Genital herpes is sexually transmitted, which is why most people get herpes when they start having sex.

    Herpes can be congenital, when intrauterine infection of the fetus occurs. This can occur when the mother develops a primary herpes infection, when viruses enter the bloodstream.

    HERPES SYMPTOMS

    The incubation period after infection with the herpes virus can last from 1 to 26 days. Most often, with herpes simplex, the skin of the face in the area of ​​the lips, nose, and also the mucous membrane of the oral cavity is affected. In rare cases, herpes sores are found on the ears, forehead, cheeks, genitals, lower back, fingers and other parts of the body.

    About 10-12 days before the rash, there may be swelling, burning, flushing and itching of the skin and mucous membranes.After a while, bubbles appear on the affected area with transparent contents and an inflamed area at the base. After a few days, the contents of the vesicles become cloudy, the vesicles burst, which leads to the formation of ulcers covered with crusts.

    With herpes infection, general symptoms are also observed, such as weakness, malaise, and in rare cases, an increase in body temperature. Herpes infection usually lasts about 12 weeks.

    It is worth noting that the herpes virus can penetrate into nerve fibers and stay there for a long time in a “dormant” state.A relapse of the disease can occur with weakened immunity, hypothermia, stress and other negative factors.

    DIAGNOSTICS OF SKIN AND MUCOSA HERPES

    In the overwhelming majority of cases, herpes of the skin and mucous membranes does not need special studies, and the diagnosis can be made on the basis of an external examination of the patient.

    In some cases, a virological examination of the contents of the vesicles is carried out, as well as a blood test for the content of antibodies to the herpes simplex virus.

    HERPES TREATMENT

    Almost every adult has had herpes at least once in their life. At the same time, the overwhelming majority prefer not to seek medical help in view of the seeming frivolity of the disease. Doctors, nevertheless, strongly recommend contacting a specialist at the first manifestations of the disease, since competent treatment of herpes will help to avoid relapses in the future. Herpes in pregnant women requires special attention, so this category of patients must necessarily consult a doctor.

    In the treatment of herpes infection, antiherpetic drugs based on acyclovir are most often used. Various manifestations of the activity of the herpes virus are amenable to treatment with aminoglycosides (baneocin) and immunomodulatory drugs such as amixin and cycloferon. Depending on the specific form, the doctor prescribes the appropriate treatment regimen.

    Source Likar.info

    Herpes simplex – symptoms, treatment, causes of the disease, first signs

    Description

    Description of herpes simplex

    Herpes simplex is a common viral disease in which rashes appear on the mucous membranes or skin of a person in the form of multiple clusters of bubbles.

    According to medical statistics, at the moment about 90% of the world’s inhabitants are infected with herpes simplex virus types 1 and 2.

    The causative agent of this pathology is the herpes simplex virus type 1 or 2. After overcoming the skin barrier, the virus moves through the blood and lymphatic channels and thus reaches the tissues of internal organs. There the virus enters the nerve ganglia, invading the human genetic apparatus. After that, it is impossible to completely remove the virus from the body. The reproduction mechanisms of the herpes virus are the same as for any DNA-containing viruses.That is, a virus entering a cell triggers a productive or lytic type of disease. In this case, the infected areas can become inflamed, and after the body destroys the virus along with its cells, microscopic foci of necrosis are formed in the affected area.

    The incubation period for herpes simplex usually lasts 1-26 days.

    It is noteworthy that the reasons for the activation of herpes simplex are stress, chronic diseases, vitamin deficiency, etc.

    Herpes simplex is most common on the lips.

    This form of the disease is popularly called “labial cold”, although herpes simplex infection has nothing to do with a real cold. Often, herpes occurs on the human genitals.

    According to research carried out by scientists from Colombia, Alzheimer’s disease may be a consequence of herpes simplex. In 70% of patients, herpes simplex type 1 is found in the brain tissues. In addition, 90% of the plaques in the brain of patients contain antigens of the herpes simplex virus.

    Typically, herpes simplex virus type 1 causes the following diseases:

    • acute herpetic stomatitis. As a rule, a person encounters him in childhood at the first infection. The incubation period of the disease in this case can last up to 5 days. Damage to the mucous membranes, formed as a result of tissue damage by the virus, heal after 2-3 weeks;
    • Kaposi’s rash. The disease has symptoms similar to chickenpox. In some cases, it can be fatal;
    • keratoconjunctivitis.With simple recurrent herpes in this form of the disease, the patient may experience cloudy eyes, which in turn can lead to blindness;
    • herpes simplex virus encephalitis is a disease characterized by a high risk of death. If the patient recovers, some neurological disorders remain;
    • labialis is the most common form of type 1 herpes. The rash in this case is formed at the junction of the skin and mucous membranes.After healing, it does not leave scars on the body.

    In turn, the herpes simplex virus type 2 can creep as follows:

    • simple genital herpes, which is characterized by frequent relapses;
    • herpes simplex virus in a newborn – occurs when the mother of the child becomes infected during childbirth. In some cases, it can be fatal;
    • herpes simplex virus during pregnancy can provoke serious consequences.

    However, any type of herpes simplex virus can affect both areas of the human body (for example, after orogenital intercourse).

    It is important to note that the herpes simplex virus is not only dangerous for humans. It often causes various diseases in dogs, rabbits, mice, guinea pigs, etc.

    The choice of a specialist who will treat the disease depends largely on the area in which the tissue is damaged, and in what form the herpes simplex virus proceeds.So, simple and shingles of the skin is treated by a dermatologist, treatment of genital herpes is carried out by gynecologists, andrologists and urologists. With ophthalmic herpes, you may need the help of an ophthalmologist, and with herpes of the oral cavity, a dentist.

    Since herpes simplex usually manifests itself against the background of reduced immunity, it will not be superfluous to consult an immunologist. He will determine the reason for the decrease in the body’s defenses, and will give the necessary recommendations.

    Routes of infection

    Herpes simplex virus is transmitted by contact with rashes or natural fluids.However, in some cases, the virus is also transmitted through skin contact of a healthy person with a carrier of the virus. Often in the initial stages, the disease cannot be detected independently without the use of laboratory research methods. Most often, infection with type 1 of the virus occurs in childhood, while herpes simplex genital – only after the beginning of an intimate life.

    At a temperature of 23-26 degrees and an average humidity in the room, the herpes virus can be active throughout the day.At a temperature of 50-55 degrees, it dies in half an hour, and at a temperature of -70 degrees, it can live for about 5 days. The virus lives on metal objects (for example, money, doorknobs) for about 2 hours, while on pure medical wet cotton wool for up to 6 hours.

    Herpes immunity

    Children under 6 months of age have antibodies to the virus in their bodies, which were passed on to them from their mothers. However, during the first years of life, they will quickly be used up. Therefore, the child’s body becomes most susceptible to the effects of the virus at the age of 6 months to 2 years.

    In the blood and mucous membranes of patients who have had the herpes simplex virus, IgG and special antibodies are found, which drive the virus into a “dormant” state and prevent it from developing further.

    Herpes in pregnant women

    All types of viruses can pose a danger to a pregnant woman and her fetus. As you know, the herpes simplex virus is found in huge quantities in the environment, so it carries a special danger.

    Of both types of herpes, type 1 is considered less dangerous, since it has been in the body of patients since childhood.This means that the body has developed IgG and natural killer cells for herpes simplex, which help the body to protect the fetus from the virus and keep its amount at a low level.

    Herpes simplex type 2 is more dangerous. So, if a woman has a primary infection, then she has a risk of intrauterine infection of the fetus. If she has been sick with this type of virus for a long time, and she has frequent exacerbations, then there is a possibility of infection of the baby during childbirth. That is why women with herpes simplex virus are advised to have a caesarean section.

    The greatest threat is the herpes simplex virus type 2 if it entered the body of a woman when she was already pregnant. After all, it is not for nothing that this virus is classified as having a sharply negative effect on the fetus.

    So, herpes simplex during pregnancy less than 13 weeks can lead to miscarriage, in the second trimester – to fetal malformations, and before childbirth can cause severe inflammation of the pelvic organs.

    However, the herpes virus does not interfere with conception, provided that the intimate organs have not been damaged due to the disease, and this has not led to infertility.

    In order to avoid various complications before planning pregnancy, a woman is recommended to do a PCR for the herpes simplex virus.

    Symptoms

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    Herpes simplex is one of the most common viral diseases caused by 2 serotypes of the pathogen.

    A person has been in contact with the first type of virus with herpes simplex from birth, and by the age of 18 months, almost everyone has it in a latent form in the body.Herpes simplex shows symptoms on the skin and mucous membranes of the lips, nose, eyelids, and oral mucosa. The virus of the second type can only be infected through sexual contact, while rashes on the genitals are observed, after which it also goes into a latent form.

    Knowledge of the symptoms manifested in herpes simplex is necessary in order to identify this disease as early as possible and begin its treatment. Usually, herpes simplex shows symptoms due to a decrease in the body’s defenses. Often this occurs against the background of hypothermia, which gives rise to the common speech to identify the virus of the first type with the “cold”.Overheating, stress, various infectious diseases that weaken the immune system (including HIV) are also provoking factors.

    In the typical development of herpes simplex, 4 stages can be distinguished, which correspond to local symptoms of the disease:

    • 1 stage. Itching, tingling sensations appear on the lips, tongue, corners of the mouth, in other areas, then redness of the skin and mucous membranes appears.
    • Stage 2. The next day, in the area of ​​redness, in the absence of adequate treatment, small bubbles appear (first transparent, then with unclear contents), the itching decreases.The number of bubbles can reach 10 or more.
    • Stage 3. The bubble ruptures, the fluid with the multiplied herpes simplex virus flows out and an ulcer forms. The site of injury becomes painful.
    • Stage 4. The sores are covered with a crust, skin damage is combined with pain.

    All stages and symptoms of the virus multiplication in herpes simplex can be repeated many times, and the bubbles can merge into one larger size. In this case, the area of ​​the rash becomes edematous.

    Symptoms are more pronounced with primary infection with herpes simplex virus. The period after communication with a sick person usually lasts from one to eight days, after which chills, headaches, malaise are noted, the temperature in some cases reaches 39-40 ° C. Redness, then a rash appears on the surface of the lips, tongue, it is unlikely in the palate. tonsils and arches. Lymph nodes in the submandibular regions may enlarge. In children with significantly reduced immunity, the virus can also damage internal organs.On average, the duration of the disease is seven to ten days, but in the presence of a bacterial infection, it is prolonged.

    Relapses occurring in herpes simplex occur with similar symptoms, but in a milder form. The incidence of the disease is different: from once in several years, to three to four times in one month. The herpes simplex virus is not contagious without the development of external symptoms.

    Herpes simplex virus in the mouth, called herpetic stomatitis, has different symptoms.A specific rash appears on the inner surface of the lips, cheeks, gums, palate. Within an hour or two, superficial ulcers open and appear. The next day, a whitish bloom appears on their surface. In the oral cavity, one of the symptoms of the development of herpes simplex against the background of rashes is soreness and increased production of saliva.

    When the foci of inflammation are infected, the symptoms of herpes simplex after the vesicles dry out are aggravated by the appearance of large crusts with a layered brown structure.The process of treatment with this course of the disease is delayed; if symptoms persist for more than 2 weeks, scar formation is possible.

    Sometimes an edematous form can develop, in which severe edema occurs at the site of the herpes simplex virus (more often on the lips, eyelids, genitals) against the background of usual symptoms. This form, with frequent relapses, creates a state of persistent swelling of the lesion sites.

    The combination of manifestations of the disease in different parts of the body often occurs with a pronounced decrease in immunity.

    In women, symptoms of recurrence of herpes simplex are often combined with the menstrual cycle. Frequent relapses of genital herpes simplex can cause difficulties in maintaining a normal sex life with the onset of symptoms of neuropsychiatric disorders.

    Penetration of the herpes simplex virus can occur in places of damage with skin diseases: pemphigus, ichthyosis, with thermal burns of the skin. In this case, the main symptom is extensive skin erosion, and with the addition of a secondary infection, abscesses.

    Symptoms of the erosive and ulcerative form of herpes simplex are characterized by the appearance of long non-healing ulcers that do not have seals, after opening the vesicles with typical polycyclic outlines. Pronounced painful sensations are noted.

    One of the rare forms of herpes simplex is herpetic folliculitis, which develops against the background of HIV infection. Symptoms include multiple vesicles, which quickly break open and become brownish crusted.It occurs only in men in the area of ​​the lips and chin.

    At the same time, forms of herpes simplex are distinguished, in which the disease stops at the initial stage. Symptoms in this case may be limited to:

    • itchy red spots with close to rounded contours, disappearing in 3-4 days
    • single bubbles
    • short-term itching that disappears in 1-2 days.

    In case of doubtful symptoms of herpes simplex, especially with genital localization, PCR (polymerase chain reaction technique) or RIF (immunofluorescence reaction) are used to detect the virus.However, these techniques are not cheap and are only used when needed.

    Antiviral drugs are used for treatment, which reduce the symptoms of herpes simplex, but do not completely destroy the virus. Also, immunity enhancement and treatment of major diseases are carried out.

    Treatment of herpes simplex in order to obtain a lasting result, as soon as possible relief of symptoms, should be comprehensive and carried out by a specialist doctor. This is also true because more serious health problems can be hidden behind the manifestations of herpes.

    Diagnostics

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    If you suspect you have a disease similar to herpes, immediately go to the hospital, where you will be prescribed to do the necessary tests and get the correct diagnosis.

    Diagnosis of herpes simplex consists of anamnesis (survey), examination and laboratory diagnosis.

    Anamnesis is collected by a doctor. During the examination, an element (vesicle, or vesicle) is found that rises above the level of the skin, containing a transparent liquid (hemispherical in shape with rounded outlines).When dry, the bubbles form crusts. If the vesicle is damaged, a small superficial defect remains, which disappears without a trace over time. The herpes virus of the first type, as a rule, affects the mucous membrane of the oral cavity and pharynx, eyes, and can cause encephalitis. Herpes virus of the second type is localized in the genital area. Nowadays, due to the diversity of people’s sexual life, there are cases of detection of HSV-2 in places characteristic of HSV-1 and vice versa. These mutated viruses are more resistant and difficult to treat.

    After examination by a doctor, the tests necessary for delivery to the laboratory are prescribed. None of the modern methods for diagnosing viral diseases gives a complete guarantee about this disease. Therefore, it is necessary to resort to the use of at least two diagnostic methods or to conduct repeated studies.

    For laboratory diagnosis of herpes simplex, it is necessary to take the following materials for tests: blood, saliva, the contents of herpetic vesicles, smears from the mucous membranes of the oral cavity, pharynx, cervical canal and urethra.

    Later, the obtained fluids are examined for the content of herpes simplex virus. Diagnostics can be carried out by the following methods: microscopic, molecular biological, cultural and serological.

    Microscopic method. The resulting smears are stained with special dyes. In the presence of the herpes simplex virus, giant multinucleated cells are found. The amount of cytoplasm in them is increased, in the nuclei there are Caudi inclusions, which are lumps of marginal chromatin.However, this study has a low diagnostic specificity, since this method cannot distinguish HSV from other types of herpes. The sensitivity is about 60%. In our time, this study is not reliable.

    Cultural method. This type of research consists of several stages. First, material is taken from the patient (mainly the contents of the vesicles), presumably containing a virus. Then either a laboratory animal is infected with it, or (most often) it is introduced into a special cell culture or chicken embryo.After a day, the infected animals show symptoms of the disease. After 2-3 days, changes begin to occur in the layers of cells: they round up, form huge cells with atypical inclusions in the nucleus and many nucleoli. On the second day, plaques of 2-3 mm in size are formed in the chicken embryo. For better visibility, they are painted with neutral red. In the presence of the above changes, the analysis for the herpes simplex virus is considered positive. This method is accurate, however, it is time consuming and expensive.

    Molecular biological method. This method includes the polymerization chain reaction (PCR). With the help of this reaction, it is possible to identify the pathogen in the analysis of blood, sputum, saliva, urine, contents of vesicles, cerebrospinal fluid. DNA is separated from the material obtained from the patient. Then the fragments specific to this virus are copied many times and the results obtained are recorded. This study is the method of choice due to its high accuracy. PCR is able to distinguish HSV-1 and HSV-2 and to determine the amount of herpes simplex virus, which makes it possible to use this method both for diagnosis and for evaluating the effectiveness of treatment.

    In the presence of even a minimal amount of HSV in the material obtained, the reaction becomes positive, in the absence – negative.

    Serological method. Used more often than others. As a research material, blood serum is mainly taken. Diagnosis is based on the detection of antigens (specific viral proteins) and antibodies (specific immune complexes of the body) to the herpes simplex virus. Antibodies are protein complexes that are produced by blood cells.When a pathogen enters the body, antibodies bind to it and after a while it is activated.

    In HSV disease, the focus is on three types of antibodies: M, G to early proteins and G to late proteins. Antibody M appears in the blood a week after contracting the herpes virus and indicates an acute, first-onset infection. In some people, this protein may be found when an old infection reappears. Antibody G – an indicator of chronic disease, appears in the body 14-21 days after the disease.Its different concentrations indicate either the transition of the disease to the chronic stage, or about the low resistance of the body, or about recovery.

    The serological method allows you to determine the amount of the virus and control the increase in its titers in the blood, which makes it possible to assess the effectiveness of treatment. To do this, examine the sera taken at intervals of 7-14 days. This diagnostic method is based on RNIF and ELISA.

    The reaction of indirect immunofluorescence (RNIF) is a highly sensitive and specific method.It is based on the binding of antigen + antibody complexes and the subsequent attachment to them of fluorochrome-labeled antibodies specific to specific antibodies to antigens of herpes viruses. Subsequently, when glowing with ultraviolet light, complexes that can be calculated are determined.

    Enzyme-linked immunosorbent assay (ELISA) has high accuracy and specificity, about 100%. To diagnose HSV, two methods of ELISA are used: with a labeled antigen and with a labeled antibody.

    In a labeled antigen assay, a labeled herpes antigen is added to the available serum.If there were antibodies in the serum, antigen + antibody complexes are formed. After the instrumentation is washed and specific enzymes are added to them that can react with these complexes. Then the reaction takes place, and the samples are colored. The brightness of the colored substance is judged on the titer of antibodies in the blood.

    The reaction with a labeled antibody is more complex. Labeled antibodies are added after the unlabeled antigen + antibody substrate has already formed. In this case, a new complex is formed, where the antigen is surrounded by two antibodies.This arrangement improves the quality of the ELISA reaction, which helps to detect antibodies even with their low content.

    If the test is positive for antibodies M, G to primary proteins and G to secondary proteins, this indicates an initial acute form of the disease. If the analysis is negative for these types of antibodies, the person has never had a simple herpes virus. If the test is positive for antibodies M and negative for antibodies G to primary proteins and G to secondary proteins, it can be concluded that the disease is very recent.If the analysis is negative for antibodies M and positive for antibodies G to primary proteins and G to secondary proteins – either the second half of the initial acute infection, or exacerbation (relapse) of herpes disease. If the analysis for antibodies M and antibodies G to primary proteins is negative, and antibodies G to secondary proteins are positive, a strong immunity against the herpes simplex virus has been developed.

    The disease can be judged by the percentage of antibodies G. The presence of antibodies G more than 60% indicates that a person is a carrier of the infection, and the disease has passed into a chronic stage.If the amount of G antibodies is 50-60% – the transition of the disease from the acute stage to the chronic one, it is necessary to repeat the study after two weeks. The absence of these antibodies suggests that the person has never had the herpes simplex virus.

    Decoding of the analysis is carried out in the laboratory. Diagnosis and diagnosis is carried out exclusively by a physician.

    Treatment

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    Therapeutic tactics are determined by the type of virus, the nature and severity of the lesion.The main targets are:

    • reduction of the period of exacerbation of the disease;
    • decrease in the severity of symptoms;
    • reduction in the number of relapses;
    • prevention of fetal infection during pregnancy;
    • preventive measures aimed at reducing the risk of complications in children born to an infected mother.

    Treatment of herpes simplex (with the exception of complicated and severe course) is carried out on an outpatient basis.All drugs can be roughly divided into 2 groups:

    • Influencing the etiological factor (virus) – the most important link in the treatment.
    • Influencing the pathogenetic and symptomatic factor – NSAIDs, dehydration, glucocorticosteroids.

    Complex therapy with the simultaneous use of antiviral and immunomodulatory agents is considered the best option during an exacerbation. Drug therapy is complemented by non-drug methods.

    Ozone therapy

    In the treatment of herpes type 2, doctors often use ozone therapy.This allows you to improve the patient’s condition, shorten the period of taking medications. With a slight severity of symptoms, the technique can replace the course of immunostimulants and antiviral drugs. Ozone-oxygen mixture is administered by subcutaneous microinjection.

    It is possible to carry out autohemoozonotherapy. The essence of the manipulation is the collection of venous blood and its further enrichment with an ozone-oxygen mixture. After that, the patient’s blood is again injected into the vein. To eliminate the symptoms caused by herpes infection, on average, 8-10 autohemoozonotherapy procedures are required, which should be performed at intervals of 2-3 times a week.

    Laser therapy

    Laser therapy is effective for herpes simplex virus type 1. During the procedure, the doctor acts on the affected tissues with a special apparatus with infrared radiation. Laser therapy is used at any stage of herpes treatment, however, the best results can be achieved in the initial stages. When itching and burning appear, the development of the pathological process stops after the first procedure. Regeneration of the skin occurs in the shortest possible time.

    Treatment of herpes in children

    Treatment of herpes simplex in children is recommended to start at the first signs of the disease. Antiviral drugs are used for external and internal use. With general hyperthermia, insufficient effectiveness of therapy, human immunoglobulins are additionally prescribed. With frequent recurrence, consultation with an immunologist is required.

    Parents should monitor the implementation of hygiene measures. With a herpetic lesion of the oral cavity, the child should not injure the sores with his tongue.

    Medicines

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    Antiviral therapy

    Antiviral agents are the drugs of choice in the treatment of herpes simplex. Acyclovir, interacting with DNA polymerase, leads to suppression of viral DNA synthesis, which disrupts its replication (reproduction). The medication has few side effects, is practically non-toxic to the body in adequate doses. With herpes simplex, it can be applied topically, orally and parenterally.

    Topically, the medicine is applied in the form of an ointment, treating the affected skin area 4-5 times a day until the symptoms disappear.Inside, the agent is prescribed 4-5 times a day for 8-9 days. With frequent relapses against a background of decreased immunity and other infections, the drug can be used for prophylaxis.

    Intravenous administration is indicated for the complicated course of herpes simplex and herpetic encephalitis, it is not required for the normal course of the disease. The dose is determined by the doctor individually, the average duration of the course of treatment is 10 days.

    Other antiviral agents are used less frequently.Valacyclovir has greater bioavailability compared to acyclovir, but less pronounced anti-herpes effects. Penciclovir is applied only topically.

    Vidarabine has the same spectrum of activity as acyclovir. The most effective for herpetic keratitis, it is a “reserve” drug for herpetic encephalitis. Differs in higher toxicity, possible side effects in the form of dizziness, lack of coordination, seizures.

    Long-term use of antiviral drugs and the use of ointments are contraindicated.The terms of treatment established by the doctor should be observed.

    Correction of immunity

    In the treatment of herpes simplex, endogenous interferon inducers are used – amiksin, polidan. Improves the general well-being of the patient. Immunomodulators are often used – immunofan, polyoxidonium. The principle of action of all immunomodulators is to correct immunity disorders in diseases accompanied by its decrease. The dosage and course of treatment are set individually by the doctor.

    After relief is achieved, intradermal administration of herpes inactivated vaccine is recommended for patients in permanent remission.Thus, the patient will be able to reliably record the achieved result.

    Symptomatic therapy

    A special place is occupied by non-steroidal anti-inflammatory drugs, which alleviate the course of the disease, eliminate pain and fever, improve the general condition and well-being of the patient. Drugs such as ketorolac, ketans can be used, ibuprofen is effective at elevated temperatures.

    In severe cases, synthetic glucocorticosteroids are prescribed, such as dexamethasone, dexazone, usually together with dehydration therapy in case of central nervous system virus damage (including generalization of the disease).For infusion, use a 5% dextrose solution.

    Folk remedies

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    First of all, you need to ask your doctor if there are any components in the composition of the chosen folk recipe that can negatively affect the course of the disease. After that, together with a specialist, you can draw up a treatment plan and select the appropriate traditional medicine.

    Sage-based decoction

    For cooking you will need:

    • 1 tablespoon of sage leaves or 1 sachet of crushed pharmacy.
    • Glass of water.

    Bring water to a boil and simmer the sage. After 30-40 minutes, strain the broth and cool to room temperature. Use as a gargle for the first type of herpes. With the second type, add a decoction to the bath. It is recommended to lie in water with the addition of a decoction for no more than 15 minutes.

    Essential oils

    The following essential oils will help cure herpes:

    • fir;
    • tea tree oil;
    • almond.

    These oils have antibacterial properties. During treatment, add a few drops to the bath or apply oil to the affected skin. The method is equally good in the case of “cold sores” and genital herpes.

    The information is for reference only and is not a guide to action. Do not self-medicate. At the first symptoms of the disease, see your doctor.

    Sources

    1. Herpesvirus infection / Filatova T.G. – 2014.
    2. Herpesviruses. Textbook / Litusov N.V. – 2018.
    3. Herpes simplex. Cytomegalovirus infection. Methodical recommendations / Potekaev N.N. and others – 2016.
    4. Herpetic infection: etiology, pathogenesis, clinical picture and diagnosis / Zubritskiy M.G. and others // Journal of the State Medical University – 2009 – №3.

    Your comments on symptoms and treatment

    How to treat herpes on the lips and oral mucosa in adults and children

    Herpes simplex infection is very common.Herpes simplex virus type 1 (HSV-1) primarily causes infection in or around the mouth (oral herpes). According to the World Health Organization, in 2012 the number of people infected with the HSV-1 virus was about 3.7 billion people under the age of 50, or 67% of the world’s population. Herpes can also appear on the gums, causing discomfort. But the dentist will help you deal with the problem.

    Transmission

    Infection occurs through airborne droplets or through oral contact.This often happens already in childhood. The virus is transmitted to a child through contact with family members, even by touching or sharing cutlery. If a child has not become infected at home, it is possible through contact with the body fluids of other children at school, for example, sneezing or eating together.

    People who managed to avoid infection during childhood can get the virus during adolescence or youth. Transmission occurs by kissing a carrier of the virus, or using lip balm, razor blades, or other personal care products together.

    Symptoms

    Primary herpes occurs in a person who has not been sick before. Usually, several round papules appear in the corner of the mouth, they are accompanied by gingivostomatitis – an infection of the mouth and gums. In children and adults, gums are red, swollen, and sore. Bubbles form on the gums. They are filled with fluid and painful to open. In addition, painful sores develop on the gums. In addition to these symptoms, sore throat and increased salivation are possible.

    Diagnostics

    Often, the dentist diagnoses herpes in the mouth without special tests, by examining the oral cavity. But sometimes tests are recommended to distinguish herpes simplex from other conditions with similar symptoms, such as an STD. In this case, a small tissue sample is taken from the lesions and analyzed for viral or bacterial infections of other types. If the dentist suspects that the ulcers may be cancerous, they will also perform a biopsy.

    Treatment

    Herpes sores usually take 7 to 14 days to heal. Your dentist may recommend taking over-the-counter pain relievers and prescribing an antiviral medication. According to the WHO, the most effective drugs for herpes simplex are antiviral drugs such as acyclovir, famciclovir, and valacyclovir. They help reduce the severity and frequency of symptoms, but the infection will not cure.

    If you find it difficult to brush your teeth due to sensitive gums, try switching to a toothbrush with very soft bristles. This brush is designed for gentle cleaning of sensitive gums. Even if you have cold sores in your mouth, it is important to keep brushing your teeth and gums, and choosing the right hygiene products will significantly improve your well-being.