What is the etiology of herpes simplex type 2. How is herpes simplex type 2 diagnosed. What are the treatment options for herpes simplex type 2. How can herpes simplex type 2 be prevented. What are the epidemiological trends of herpes simplex type 2. How does herpes simplex type 2 affect pregnancy. What are the pathophysiological mechanisms of herpes simplex type 2.

Understanding Herpes Simplex Virus Type 2 (HSV-2)

Herpes simplex virus type 2 (HSV-2) is a prevalent sexually transmitted infection that affects millions of adults worldwide. This article delves into the various aspects of HSV-2, including its etiology, epidemiology, pathophysiology, and management strategies.

Etiology and Transmission of HSV-2

HSV-2 is primarily transmitted through sexual contact with an infected individual. The virus is present in bodily fluids, particularly saliva and genital secretions. Direct contact with these fluids, especially during sexual intercourse, is the main route of transmission.

Can HSV-2 be transmitted through non-sexual means? While sexual contact is the primary mode of transmission, HSV-2 can theoretically remain infectious on moist surfaces for a short period. However, transmission through non-sexual means is generally considered insignificant due to the virus’s low stability outside the body.

Risk Factors for HSV-2 Infection

• Multiple sexual partners
• Unprotected sexual intercourse
• Early onset of sexual activity
• History of other sexually transmitted infections
• Compromised immune system

Epidemiology of Herpes Simplex Type 2

HSV-2 remains one of the most common sexually transmitted infections globally. In the United States, approximately 16% of individuals aged 14 to 49 were reported to be seropositive for HSV-2 between 2005 and 2010.

Are there demographic differences in HSV-2 prevalence? Yes, several demographic factors influence HSV-2 prevalence:

• Gender: Women have higher infection rates than men
• Age: Prevalence increases with age, correlating with sexual activity
• Ethnicity: Non-Hispanic African Americans show higher rates compared to non-Hispanic whites
• Sexual behavior: Prevalence increases with the number of sexual partners

Alarmingly, 85% to 90% of HSV-2 infections remain unrecognized and undiagnosed, contributing to its continued spread. Globally, more than 23 million new cases are reported annually, making HSV-2 a significant public health concern.

Pathophysiology of HSV-2 Infection

The pathophysiology of HSV-2 infection involves a complex interplay between the virus and the host’s immune system. Understanding this process is crucial for developing effective treatment and prevention strategies.

Initial Infection and Viral Replication

How does HSV-2 initially infect the body? The virus enters the body through breaks in the skin or mucous membranes. Upon entry, HSV-2 invades epithelial cells and begins replicating intracellularly. This initial phase typically lasts 10 to 14 days and is often accompanied by visible symptoms.

Latency and Reactivation

After the initial infection resolves, HSV-2 establishes latency in the sensory nerve ganglia. The virus can remain dormant in the periaxonal sheath of sensory nerves, including the trigeminal, cervical, lumbosacral, or autonomic ganglia.

What triggers HSV-2 reactivation? Various factors can trigger viral reactivation, including:

• Stress
• Hormonal changes
• Immune system suppression
• Concurrent infections
• Exposure to UV light

During reactivation, the virus travels back along the nerve fibers to the skin or mucous membranes, causing recurrent outbreaks of lesions or asymptomatic viral shedding.

Clinical Presentation of HSV-2 Infection

The clinical presentation of HSV-2 infection can vary widely, ranging from asymptomatic cases to severe, painful outbreaks. Understanding the spectrum of symptoms is essential for accurate diagnosis and timely treatment.

Primary Infection

What are the symptoms of primary HSV-2 infection? Primary infection with HSV-2 may present with the following symptoms:

• Painful genital or anal lesions
• Fever
• Body aches
• Swollen lymph nodes
• Headache
• Painful urination

These symptoms typically appear 2 to 12 days after exposure and can last up to 3 weeks. However, it’s important to note that many individuals experience milder symptoms or no symptoms at all during primary infection.

Recurrent Outbreaks

Recurrent outbreaks of HSV-2 are generally less severe and shorter in duration compared to the primary infection. Symptoms may include:

• Localized tingling or burning sensation before lesion appearance
• Painful genital or anal lesions
• Itching or irritation in the genital area
• Mild flu-like symptoms

The frequency and severity of recurrent outbreaks tend to decrease over time, but the virus remains in the body indefinitely.

Diagnosis of Herpes Simplex Type 2

Accurate diagnosis of HSV-2 infection is crucial for appropriate management and prevention of transmission. Several diagnostic methods are available, each with its own advantages and limitations.

Clinical Diagnosis

Can HSV-2 be diagnosed based on symptoms alone? While experienced clinicians may suspect HSV-2 based on characteristic symptoms and lesion appearance, clinical diagnosis alone is not always reliable. Many HSV-2 infections present with atypical or minimal symptoms, making laboratory confirmation essential.

Laboratory Tests

Several laboratory tests can be used to confirm HSV-2 infection:

1. Viral Culture: This test involves taking a sample from an active lesion and attempting to grow the virus in a laboratory setting. While highly specific, its sensitivity decreases as lesions begin to heal.
2. Polymerase Chain Reaction (PCR): PCR detects HSV DNA in clinical specimens. It is highly sensitive and specific, making it the preferred test for diagnosing HSV infections, especially in cases of suspected herpes meningitis or encephalitis.
3. Serological Tests: These blood tests detect HSV-2 antibodies, indicating past or current infection. They are particularly useful for diagnosing asymptomatic infections or when lesions are not present.

Which test is most appropriate for diagnosing HSV-2? The choice of test depends on various factors, including the presence of active lesions, the time since potential exposure, and the clinical presentation. PCR is generally considered the gold standard for diagnosing active HSV-2 infections, while serological tests are useful for identifying asymptomatic carriers.

Treatment and Management of HSV-2 Infection

While there is no cure for HSV-2 infection, several antiviral medications can effectively manage symptoms, reduce the frequency of outbreaks, and lower the risk of transmission.

Antiviral Medications

What are the primary antiviral medications used to treat HSV-2? The most commonly prescribed antiviral medications for HSV-2 include:

• Acyclovir
• Valacyclovir
• Famciclovir

These medications can be used in different regimens:

1. Episodic Therapy: Short-term treatment initiated at the first sign of an outbreak to reduce its severity and duration.
2. Suppressive Therapy: Daily medication to reduce the frequency of outbreaks and lower the risk of transmission to sexual partners.

Supportive Care

In addition to antiviral medications, supportive care measures can help manage symptoms and promote healing:

• Keep affected areas clean and dry
• Wear loose-fitting clothing to reduce friction
• Apply cool compresses to soothe irritated skin
• Use over-the-counter pain relievers for discomfort
• Avoid touching or scratching lesions to prevent secondary bacterial infections

Prevention and Risk Reduction Strategies

Preventing HSV-2 transmission is crucial for public health. Several strategies can help reduce the risk of acquiring or transmitting the virus.

Safe Sex Practices

How can individuals reduce their risk of HSV-2 infection? Practicing safe sex is the most effective way to prevent HSV-2 transmission:

• Use condoms or dental dams consistently during sexual activity
• Avoid sexual contact during active outbreaks
• Communicate openly with sexual partners about HSV-2 status
• Consider suppressive antiviral therapy to reduce asymptomatic viral shedding

Vaccination Research

While there is currently no approved vaccine for HSV-2, researchers are actively working on developing effective vaccines. Some promising candidates are in various stages of clinical trials, offering hope for future prevention strategies.

Impact of HSV-2 on Pregnancy and Neonatal Health

HSV-2 infection during pregnancy poses significant risks to both the mother and the fetus. Understanding these risks and implementing appropriate management strategies is crucial for ensuring optimal outcomes.

Risks to the Fetus

What are the potential consequences of maternal HSV-2 infection for the fetus? Maternal HSV-2 infection can lead to several adverse outcomes:

• Neonatal herpes: A potentially life-threatening condition if the infant is exposed to the virus during delivery
• Miscarriage or preterm birth
• Intrauterine growth restriction
• Congenital abnormalities (rare)

Management During Pregnancy

Proper management of HSV-2 during pregnancy is essential to minimize risks to the fetus:

1. Antiviral suppressive therapy: Recommended for women with a history of genital herpes, starting from 36 weeks gestation
2. Cesarean delivery: Recommended for women with active genital lesions or prodromal symptoms at the time of delivery
3. Regular monitoring: Frequent check-ups to detect and manage any outbreaks promptly
4. Partner education: Counseling partners about the risks and prevention strategies

How effective is antiviral therapy in preventing neonatal herpes? Antiviral suppressive therapy has been shown to significantly reduce the risk of HSV-2 outbreaks at the time of delivery and decrease the need for cesarean sections. However, it does not completely eliminate the risk of neonatal herpes, emphasizing the importance of comprehensive management strategies.

Psychosocial Aspects of Living with HSV-2

The impact of HSV-2 infection extends beyond physical symptoms, often affecting individuals’ mental health and social relationships. Addressing these psychosocial aspects is crucial for comprehensive patient care.

Psychological Impact

How does HSV-2 diagnosis affect mental health? Receiving an HSV-2 diagnosis can lead to various psychological reactions:

• Anxiety and depression
• Feelings of shame or guilt
• Fear of rejection by sexual partners
• Concerns about future relationships and fertility
• Stress related to managing outbreaks and medication regimens

Support and Counseling

Providing adequate support and counseling is essential for helping individuals cope with an HSV-2 diagnosis:

1. Patient education: Accurate information about the infection, its management, and transmission risks
2. Psychological counseling: Professional support to address emotional concerns and develop coping strategies
3. Support groups: Connecting with others living with HSV-2 can provide valuable peer support and reduce feelings of isolation
4. Relationship counseling: Guidance on discussing HSV-2 status with current or potential partners

What strategies can healthcare providers use to address the psychosocial impact of HSV-2? Healthcare providers should adopt a holistic approach that includes:

• Providing non-judgmental, empathetic communication
• Offering resources for mental health support and counseling
• Addressing misconceptions and stigma surrounding HSV-2
• Empowering patients with knowledge and tools for self-management

Future Directions in HSV-2 Research and Management

The field of HSV-2 research is continually evolving, with promising developments in various areas that may significantly impact future management and prevention strategies.

Novel Therapeutic Approaches

What new treatments are being developed for HSV-2? Several innovative therapeutic approaches are under investigation:

• Gene editing techniques to target latent viral DNA
• Immunomodulatory therapies to enhance the body’s natural defenses against HSV-2
• Novel antiviral compounds with improved efficacy and reduced side effects
• Therapeutic vaccines to boost immune response and reduce outbreak frequency

Advances in Diagnostic Technologies

Improvements in diagnostic technologies aim to enhance the accuracy and accessibility of HSV-2 testing:

1. Point-of-care tests for rapid diagnosis in clinical settings
2. More sensitive and specific serological assays to differentiate between HSV-1 and HSV-2
3. Advanced molecular techniques for detecting drug-resistant HSV strains

Prevention Strategies

How might future prevention strategies change the landscape of HSV-2 management? Ongoing research focuses on developing more effective prevention methods:

• Prophylactic vaccines to prevent initial infection
• Microbicides and other topical products to reduce transmission risk
• Improved barrier methods with antiviral properties
• Public health interventions targeting high-risk populations

As research progresses, these advancements hold the potential to revolutionize HSV-2 management, reducing its prevalence and impact on global health.

Herpes Simplex Type 2 – StatPearls

Continuing Education Activity

This activity reviews the evaluation and management of herpes simplex type 2 and highlights the role of the primary care provider in managing patients with this condition. In addition to providing basic knowledge of the condition and clinical presentation of herpes genitalis, this review will highlight important aspects of the diagnostic interventions, antiviral therapy (both current and future), and prophylaxis. This activity covers the interprofessional team managing patients with herpes genitalis and with the potential of being exposed to herpes genitalis.

Objectives:

• Identify the etiology of herpes simplex type 2.

• Outline the appropriate evaluation of herpes simplex type 2.

• Review the treatment and management options available for herpes simplex type 2.

• Describe interprofessional team strategies for improving care coordination and communication to advance herpes simplex type 2 and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

Herpes genitalis can be caused by the herpes simplex virus type 1 or type 2 and manifests as either a primary or recurrent infection.[1]  Most commonly, viral replication occurs in epithelial tissue and establishes dormancy in sensory neurons, reactivating periodically as localized recurrent lesions.[2]  It remains one of the most common sexually transmitted infections (STI) but continues to be underestimated, given the vague presentation of its symptoms.[3] In addition to providing the reader with basic knowledge of the pathogen and clinical presentation of herpes genitalis, this review article discusses important aspects of the laboratory diagnostics, antiviral therapy, and prophylaxis. This article is aimed at all health-care providers managing patients with herpes genitalis and attempts to improve the often suboptimal counseling, targeted use of laboratory diagnostics, treatment, and preventive measures provided to patients.

Herpes simplex virus type 2 (HSV-2) continues to be a common infection, affecting approximately 22% of adults ages 12 and older, representing 45 million adults in the United States alone.[4] While HSV-1 often affects the perioral region and can be known to cause genital lesions, HSV-2 is more commonly the consideration when patients present with genital lesions. Despite this, most outbreaks of the infection will present with nonspecific symptoms such as genital itching, irritation, and excoriations, which may cause diagnosis and treatment to be delayed.[4] As a result, further exposure to uninfected individuals may occur.

Etiology

Risk factors for acquiring HSV-2 infection revolve around direct exposure to fluids (i.e., saliva) from a seropositive individual containing viral products most often during sexual intercourse.[3] HSV-2 is mainly transmitted through sexual intercourse, attributing to its predominant rise starting at puberty.[3] Due to its low stability outside the body, HSV can only remain infectious for days on moist surfaces. Therefore modes of transmission other than sexual intercourse are often insignificant.[3] Both primary and recurrent HSV infections in pregnant women can lead to intrauterine transmission and resultant congenital HSV infection.[5]

Epidemiology

Herpes genitalis remains one of the most common sexually transmitted infections (STI).[3] While the majority of cases are due to HSV-2, rare but increasing cases have been found due to herpes simplex virus type 1 (HSV-1).[3] The primary mode of transmission of both HSV-1 and HSV-2 is via direct contact of open lesions. Sixteen percent of patients aging 14 to 49 were reported to be seropositive for HSV-2 from 2005 to 2010.[6] Antibodies to HSV-2 are often present by the time of puberty, and their presence often correlates with the degree of sexual activity of that individual. More women than men have been reported to be infected, and as expected, the prevalence increases with an increasing number of sexual partners. [7] Ethnically, non-Hispanic African Americans have greater rates of infection than non-Hispanic whites. About 85% to 90% of infections are unrecognized and remain undiagnosed.[8]

In the United States, HSV remains one of the most common causes of genital ulcers, and internationally, more than 23 million new cases are reported annually.[9] 

Pathophysiology

HSV-2 is transmitted through direct contact of sections in a seropositive individual who is actively shedding the virus. The virus preferentially affects the skin and mucous membranes with the virus invading epithelial cells on initial exposure and ultimately replicating intracellularly at that site. After the initial exposure and symptoms resolve, in 10 to 14 days, on average, the virus then lays dormant in the periaxonal sheath of the sensory nerves of either the trigeminal, cervical, lumbosacral, or autonomic ganglia. In these locations, the viral replication is often controlled by the patient’s immune system and remains in a dormant state only to later reactive later in life.[9] When reactivation does occur, the virus travels through the sensory nerves until it reaches the mucocutaneous sites where replication then takes place and leads to vesicular clusters at the dermatological site of that sensory neuron.

Histopathology

Histological presentations of HSV-2 include the presence of dense lymphoid infiltrates with atypical lymphocytes.[10] Diagnosis is often made based on the clinical exam, but if the pathological analysis is performed, it is consistent with dense and deep infiltrates of lymphocytes near adnexal structures along with individual necrotic keratinocytes. When looking at the surface of cells, it is common to see epidermal ballooning and acantholysis, which leads to the classic vesiculation seen on the clinical exam.[11]

History and Physical

Genital symptoms are commonly seen in the outpatient primary care setting, despite many going without a clear diagnosis. HSV-2, in particular, may present as a primary infection with painful genital ulcers, sores, crusts, tender lymphadenopathy, and dysuria.[4] The classical features are of macular or papular skin and mucous membrane lesions progressing to vesicles and pustules that often last for up to 3 weeks. Genital lesions can be especially painful, leading to swelling of the vulva in women, burning pain, and dysuria. [12]

It is important to note that HSV-2 does not typically present with painless ulcers. Systemic symptoms can occur to include fever, headache, and malaise and are often due to concurrent viremia, which has been reported in up to 24% of patients in one study.[13]

Evaluation

 Recommended Laboratory Assessments[14][15]

• A direct swab of vesicular lesions (within 72 hours of onset) is ideal but avoid lesions that have evidence of crusting or healing. Do not clean area with topical alcohols before acquiring material

• Swab locations include: skin via unroofing vesicles with a sterile needle, urethra via sterile swab, the cervix through the vaginal speculum, urine, swabbing of the conjunctiva, and rectal swabs through proctoscopes [16]

• HSV serotyping

• HSV PCR (if direct swab not possible, PCR is the test of choice)

• Tzank smear – low sensitivity and cannot decipher between HSV serotypes

 Given symptoms can mimic acute urinary tract infection, consider urinalysis and culture.

 Given HSV is an STI, consider further STI work up to include:

• Gonorrhea/chlamydia testing (urine)

• HIV (known interaction between HSV-2 and HIV in which concurrent infection may occur faster than if HSV-2 was not present)

• RPR

Treatment / Management

Management of genital herpes centers around preventing its transmission and suppressing viral shedding through antiviral therapy and counseling regarding the risk of sexual transmission. 

Primary Treatment

Primary infections with multiple ulcerating lesions will resolve after approximately 19 days, regardless of treatment interventions.[12] Treatments typically categorize as either primary or non-primary. Primary infection is when the individual is experiencing their first outbreak (previously seronegative for HSV). Secondary (or non-primary) refers to an infection in a patient with preexisting immunity. Treatment is similar for both patient populations.  

Antiherpesviral agents include those that act as nucleoside analog-polymerase inhibitors and pyrophosphate analog–polymerase inhibitors. The mainstay of therapy remains acyclovir, which has antiviral activity against all herpesviruses and has been FDA approved for the treatment and suppression of both HSV and VZV.[17] Other treatments include penciclovir (which is more often used as a topical therapy for HSV labialis) and ganciclovir (which has suppression activity against CMV). These medications are preferentially taken up by those cells already infected with the virus and stop viral replication. [17] Treatment should be offered to all patients to prevent a prolonged duration of their symptoms, ideally immediately after the appearance of the first lesion.[1] 

• Acyclovir: available in topical, oral, and IV formulations. The oral formulation has quite a poor bioavailability, which has been improved with valacyclovir (see below). The benefits of acyclovir include its low side effect profile, which allows it to be tolerated for long periods. Suppressive treatment with acyclovir can prevent or delay up to 80% of recurrences, thus reducing shedding by greater than 90%.[18] Reported side effects include kidney toxicity and neutropenia when given at high doses.[17] Given its chronicity of use, resistance has been reported in immunocompromised patients and those who are immunocompetent taking acyclovir as suppressive therapy for genital herpes.[17]

• • Primary herpes genitalis: 3 x 400 mg tablets PO daily for 7 to10 days

  • Severe primary herpes genitalis: 3 x 5 mg/kg IV daily for 5 to 7 days

  • Recurrent herpes genitalis (less than 5 to 6 episodes/year): 2 x 800 mg PO daily for 5 days 

  • Prophylaxis: 2 x 400 mg PO daily for 6 months

• Valacyclovir is another formulation option that is attractive to patients

• Recurrent herpes genitalis (less than 5 to 6 episodes/year): 2 x 500mg PO daily for 3 days

• or

Prophylaxis: 1 x 500 mg PO daily for 6 months

Treatments on the Horizon

Standard therapy for herpes simplex virus type 2 infections include acyclovir and valacyclovir. Medications on the horizon include brincidofovir and maribavir (both against CMV) and valomaciclovir (activity against HSV, VZV, and EBV). As patients seek alternative treatments that have a smaller side effect profile, essential oils have been a focus of interest.[19] HSV has demonstrated susceptibility to many essential oils and their constituents through both direct virucidal activity and inhibition of intracellular replication.[19] Topical peppermint oil has been studied due to its virucidal component, with antiviral activity reported at 99% after only 3 hours of exposure.[20] The stipulation of use and activity, however, was that peppermint oil was only effective against the virus before absorption into the host cell. As a result, it may be of particular benefit from a chronic suppressive treatment rather than post-infectious symptoms. Other oils that have been found to have antiviral effects against HSV include Australian tea tree oil and eucalyptus oil.[21]

Vaccinations

HSV vaccines are being studied to reduce the severity of symptoms and to help expedite visible lesion healing. Furthermore, by reducing shedding, the severity may be reduced, as has been seen with the Varicella-zoster vaccination.[2] No current vaccine is available for HSV.

Differential Diagnosis

 Infectious genital ulcerative conditions 

 Genital HSV-2 infection is associated with an increased risk of HIV infection. As a result, be aware that testing for HIV infection may alter the treatment of HSV-2.[22]

Prognosis

There is no cure for HSV-2, early identification of symptoms, and prompt institution of pharmacotherapy can lead to early suppression of viral replication. Abstinence during known viral shedding can decrease the risk of transmission to a seronegative partner. The Herpes viruses as a family are responsible for significant neurological morbidity, and unfortunately, HSV-2 persists in the seropositive individual for a lifetime.

Complications

• Genital HSV-2 infection is known to be associated with an increased risk of HIV infection. As a result, be aware that testing for HIV infection may alter the treatment of HSV-2. [22] 

• Untreated HSV-2 can cause meningitis; however, any part of the nervous system may be affected by this virus.

• • Aseptic meningitis occurs in 36% of women and 13% of men leading to the hospitalization of a percentage of inflicted persons. During the prodrome of genital herpes and herpetic eruption, as discussed above, affected individuals may experience more systemic symptoms such as headaches, neck stiffness, and low-grade fever. Such symptoms should lead to immediate lumbar puncture with an analysis of the CSF, often revealing a lymphocytic pleocytosis. While the CSF can be sent for viral culture, PCR is the recommended diagnostic modality.[8] 

• Acute retinal necrosis – presents with a unilateral or bilateral red eye(s), periorbital pain, and impaired visual acuity. Examination reveals episcleritis or scleritis and necrosis with retinal detachment. May occur with HSV-2 meningoencephalitis.[8]

Deterrence and Patient Education

•  Condom use recommended

• Abstain from sexual activity during periods of known active viral shedding (visible lesions)

• Consider prophylactic suppressive therapy if frequent sexual activity is likely to occur [23]

Pearls and Other Issues

• HSV cannot be cured, but suppressive therapy can help prevent spread to seronegative individuals.

• HSV has been associated with HIV infection, and thus patients with a new diagnosis of HSV should have full STI workups performed.

Enhancing Healthcare Team Outcomes

The primary care physician or provider will often be the first one to diagnose and treat HSV-2 infections. However, an interprofessional team approach is the optimal means to address this condition. [Level 5]

• Early identification of the classical vesicular lesions can lead to prompt treatment and potentially prevent spread to seronegative individuals

• The interprofessional healthcare team, to include the medical assistants and nursing staff, are pivotal in providing medical education to the patient on how to prevent unnecessary spread. This should be documented and communicated to the treating physician.

• Utilizing network public health officials can help dispense information as well as track STIs in the area leading to early identification in patients who may be otherwise asymptomatic.

• Pharmacists review medications, verify dosing, check for interactions, inform patients about use and potential side effects. They also may be involved in the purchase of condoms and can make patient recommendations.

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

Figure

Herpes Simplex. Contributed by DermNetNZ

Figure

This photograph depicted a close view of a patient’s vagina, revealing evidence of an outbreak of herpes genitalis, which had manifested as pustular-vesicular rash around the vaginal introitus, due to the herpes simplex virus type-2 (HSV-2) virus. (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

This was an outbreak of herpes genitalis, which had manifested as blistering on the underside of the penile shaft, just proximal to the corona of the glans, which was due to the herpes simplex 2 (HSV-2) virus, otherwise referred to as genital herpes. (more…)

Figure

This image depicts a close view of a female’s perineum, revealing what had been an outbreak of herpes genitalis, which had manifested as blistering around the vaginal introitus due to the herpes simplex 2 (HSV-2) virus, otherwise referred to as (more…)

References

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Whitley R, Baines J. Clinical management of herpes simplex virus infections: past, present, and future. F1000Res. 2018;7 [PMC free article: PMC6213787] [PubMed: 30443341]

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Sauerbrei A. Herpes Genitalis: Diagnosis, Treatment and Prevention. Geburtshilfe Frauenheilkd. 2016 Dec;76(12):1310-1317. [PMC free article: PMC5177552] [PubMed: 28017972]

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Anzivino E, Fioriti D, Mischitelli M, Bellizzi A, Barucca V, Chiarini F, Pietropaolo V. Herpes simplex virus infection in pregnancy and in neonate: status of art of epidemiology, diagnosis, therapy and prevention. Virol J. 2009 Apr 06;6:40. [PMC free article: PMC2671497] [PubMed: 19348670]

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Bradley H, Markowitz LE, Gibson T, McQuillan GM. Seroprevalence of herpes simplex virus types 1 and 2–United States, 1999-2010. J Infect Dis. 2014 Feb 01;209(3):325-33. [PubMed: 24136792]

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Centers for Disease Control and Prevention (CDC). Seroprevalence of herpes simplex virus type 2 among persons aged 14-49 years–United States, 2005-2008. MMWR Morb Mortal Wkly Rep. 2010 Apr 23;59(15):456-9. [PubMed: 20414188]

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Berger JR, Houff S. Neurological complications of herpes simplex virus type 2 infection. Arch Neurol. 2008 May;65(5):596-600. [PubMed: 18474734]

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Fatahzadeh M, Schwartz RA. Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management. J Am Acad Dermatol. 2007 Nov;57(5):737-63; quiz 764-6. [PubMed: 17939933]

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Leinweber B, Kerl H, Cerroni L. Histopathologic features of cutaneous herpes virus infections (herpes simplex, herpes varicella/zoster): a broad spectrum of presentations with common pseudolymphomatous aspects. Am J Surg Pathol. 2006 Jan;30(1):50-8. [PubMed: 16330942]

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Böer A, Herder N, Winter K, Falk T. Herpes folliculitis: clinical, histopathological, and molecular pathologic observations. Br J Dermatol. 2006 Apr;154(4):743-6. [PubMed: 16536821]

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Corey L, Adams HG, Brown ZA, Holmes KK. Genital herpes simplex virus infections: clinical manifestations, course, and complications. Ann Intern Med. 1983 Jun;98(6):958-72. [PubMed: 6344712]

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Singh A, Preiksaitis J, Ferenczy A, Romanowski B. The laboratory diagnosis of herpes simplex virus infections. Can J Infect Dis Med Microbiol. 2005 Mar;16(2):92-8. [PMC free article: PMC2095011] [PubMed: 18159535]

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Slomka MJ. Current diagnostic techniques in genital herpes: their role in controlling the epidemic. Clin Lab. 2000;46(11-12):591-607. [PubMed: 11109508]

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Brown EL, Gardella C, Malm G, Prober CG, Forsgren M, Krantz EM, Arvin AM, Yasukawa LL, Mohan K, Brown Z, Corey L, Wald A. Effect of maternal herpes simplex virus (HSV) serostatus and HSV type on risk of neonatal herpes. Acta Obstet Gynecol Scand. 2007;86(5):523-9. [PubMed: 17464578]

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Poole CL, James SH. Antiviral Therapies for Herpesviruses: Current Agents and New Directions. Clin Ther. 2018 Aug;40(8):1282-1298. [PMC free article: PMC7728158] [PubMed: 30104016]

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Paz-Bailey G, Ramaswamy M, Hawkes SJ, Geretti AM. Herpes simplex virus type 2: epidemiology and management options in developing countries. Sex Transm Infect. 2007 Feb;83(1):16-22. [PMC free article: PMC2598582] [PubMed: 17098770]

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Schnitzler P. Essential Oils for the Treatment of Herpes Simplex Virus Infections. Chemotherapy. 2019;64(1):1-7. [PubMed: 31234166]

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Schuhmacher A, Reichling J, Schnitzler P. Virucidal effect of peppermint oil on the enveloped viruses herpes simplex virus type 1 and type 2 in vitro. Phytomedicine. 2003;10(6-7):504-10. [PubMed: 13678235]

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Schnitzler P, Schön K, Reichling J. Antiviral activity of Australian tea tree oil and eucalyptus oil against herpes simplex virus in cell culture. Pharmazie. 2001 Apr;56(4):343-7. [PubMed: 11338678]

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Disclosure: Jacob Mathew Jr declares no relevant financial relationships with ineligible companies.

Disclosure: Amit Sapra declares no relevant financial relationships with ineligible companies.

Herpes Simplex Virus Infection

Herpes simplex virus (HSV) is a very common and easily transmitted virus. In fact, 80% or more of people have been infected with herpes simplex virus-1. Most of us acquire the virus early in childhood from our parents, relatives, or childhood contacts through normal kissing, etc. Most of the time, the first infection is associated with few or no symptoms, but sometimes primary herpes simplex virus infection can produce mild to severe pain and difficulty in swallowing. Lesions resolve and pain decreases usually after 8 to 16 days.

After initial infection, the virus remains dormant deep inside the nerves. Many individuals go their entire life without realizing they carry HSV. However, around 20% of those with HSV will have a recurrent infection. Outside the mouth these are known as “cold sores” and are most commonly seen on the lips. It is also possible to have recurrent HSV infections around the nose, eyes, and inside the mouth. In the mouth, these infections appear as small painful ulcers on the hard palate, gums, and the top of the tongue.

Cold sores usually begin as a small cluster of blisters or fluid-filled swellings (Picture 1). These quickly rupture to leave behind open “weeping” sores or ulcers. In a few days, these will begin to crust over and scab (Picture 2). After a week or a little more, the cold sores will heal completely and usually there is no scarring or known long-term effect.

Q: When do people acquire a primary herpes simplex virus infection?
A: Usually in infancy or childhood. However, many people acquire the disease later on when they kiss an infected person during adolescence or adulthood. 

Q: What does the initial primary herpes simplex virus outbreak look like?
A: The initial outbreak is most common in children, but can be seen in adults. The initial infection is accompanied by painful sores on the lips, cheeks, gums, and tongue. The presence of lesions can be accompanied by fever and swollen glands under the neck. Swallowing can be difficult and if liquids are not taken, dehydration can result. 

Q: What is the treatment for primary herpes?
A. The best treatment is (as with any virus infection) is to ensure adequate nutrition and hydration while it runs its course (usually around a week). If this is diagnosed very early your doctor may be able to prescribe an antiviral medication to shorten this process.

Q: Are cold sores contagious?
A: Yes. They can easily be transmitted by contact from one person to another, including through oral-genital contact. It is also possible to spread the virus from one site to another, such as the eyes, nose, or around the fingernails. You should minimize any contact with the sores. After contact with a cold sore you should wash your hands and be careful not to accidentally touch your eyes or wipe your nose. 

Q: What can cause a cold sore breakout?
A: Common causes are exposure to sunlight, cold, wind, stress, trauma, and medications or conditions that impair the immune system such as prednisone, Enbrel or cancer therapy. If you know what triggers a cold sore for you, you should tell your doctor. It may be possible to apply a cream or ointment or take an antiviral pill that can either prevent or abort cold sores in these circumstances.

Q: Is there a cure for herpes simplex?
A: Not yet. The virus remains in nerve cells in the body even between breakouts. In this hiding place, it is difficult to eliminate.

Q: Can anything prevent cold sores if I am getting a lot of them?
A: Sunscreen applied before sun exposure can help prevent the development of cold sores on the lips. It is possible for your doctor to prescribe antiviral medications that may help to reduce the number of cold sore episodes that you experience. Most of these medications are taken by mouth on a regular basis. 

Q: Are medications available?
A: Nonprescription agents such as lysine, Carmex, and Docosanol (Abreva) can help reduce virus replication and may speed healing. Lip emollients can help keep the lips moist, but should only be used after the lesion is no longer weeping fluid (i.e., in the scab phase or between episodes). Antiviral medications can be prescribed by your doctor or dentist. These medicines help to reduce the severity and duration of lesions and can prevent the formation of lesions. Prescription antiviral medicines include:

• Acyclovir (Zovirax) 
• Valacyclavir (Valtrex)
• Famciclovir (Famvir)

Prepared by the AAOM Web Writing Group 
Updated 22 January 2015

The information contained in this monograph is for educational purposes only. This information is not a substitute for professional medical advice, diagnosis, or treatment. If you have or suspect you may have a health concern, consult your professional health care provider. Reliance on any information provided in this monograph is solely at your own risk.

Herpes simplex virus I, II types (H simplex 1/2, Herpes I/II, HSV 1 and 2) (IgG class antibodies), (semi-quantitative)

Description
Preparation

Most often, the first and second type of virus occurs. They are contagious and contribute to the formation of small bubbles on the mucous membranes that burst, forming open wounds. In HSV-1, vesicles appear mainly around the mouth and in the oral cavity, while HSV-2 usually affects areas in the genital area.
The herpes simplex virus can be transmitted through skin contact, contact with blisters, and sometimes even in the absence of visible lesions.
Sexually transmitted HSV-2 is more common, however, infection with herpes HSV-1 can also occur, for example, during oral sex. According to WHO, from 50% to 80% of the adult population of developed countries is infected with herpes of the first type and about 20% of herpes of the second type. Since the symptoms are often subtle, 90% may not even be aware of their infection.
In the case of primary infection, painful blisters usually form at the site of infection after two weeks, which usually disappear after four weeks. They appear on the genitals, around the anus, on the buttocks or on the thighs, after which they can burst. You may also have flu-like symptoms, such as chills and sore throat.
However, vesicles with herpes are not always formed. Sometimes the manifestations of the disease are so mild that they go unnoticed or are mistaken for something else, such as insect bites or allergies. After entering the body and spreading, the herpes virus is in a latent form. With stress or other diseases that lead to a decrease in immunity, it can be activated again. In most cases, herpes simplex is not dangerous to health, but it can cause serious illnesses: neonatal herpes (if a child becomes infected during childbirth from a mother infected with genital herpes) and encephalitis. They can lead to serious incurable neurological diseases and even death.

The following factors increase the risk of contracting herpes:

• diseases in which the immune system is suppressed (for example, HIV/AIDS),
• organ transplant.

There are antiviral drugs that suppress the spread of herpes, as well as shorten the duration of the acute phase of a viral infection and alleviate the symptoms of the disease.

Antibodies are produced to fight infection. The formation of IgG to the herpes simplex virus begins a few days after the appearance of IgM. The concentration of IgG in the blood first increases for several weeks, then falls, and then stabilizes. With repeated infection with herpes, it increases much faster – already in the first days of infection. After a disease, small amounts of IgG remain in a person until the end of life, which, however, does not provide one hundred percent protection against re-infection.

What is analysis used for?

• As an auxiliary study to confirm the diagnosis with symptoms of herpetic lesions (ulcers, vesicles on the mucous membranes) or neonatal herpes.
• To screen certain groups of people, such as those who are sexually active, potential recipients infected with the AIDS virus, or those who have previously been exposed to HSV infection.

When is the test ordered?

• When examining persons who have been in contact with patients with HSV.
• During preparation for pregnancy and in monitoring it.

What do the results mean?

Reference values ​​
S/CO ratio (signal/cutoff): 0 – 0. 9.
A positive result indicates the presence of IgG antibodies to HSV-1 or HSV-2, indicating either an active or past herpes virus infection.

A negative result indicates a low probability of an acute herpes virus infection, and also that the body has not previously come into contact with the herpes simplex virus. However, immediately after infection, when a sufficient amount of antibodies has not yet been developed, the result may be false negative. In this case, an additional IgM test and a second IgG test after a few weeks is recommended.

What can influence the result?
Reduce the concentration of antibodies capable of:

• antiviral therapy,
• immunodeficiency.

It is necessary to refrain from eating for 2-3 hours.

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PCR analysis of semen for herpes simplex virus type 1

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Molecular-biological Analysis of sperm Using of the PCR method, which allows you to detect genetic material of the Herpes 1 Serotype (HSV-1) , is carried out to diagnose herpetic infection and evaluate the success of its treatment.

Herpes simplex virus (HSV) type 1 is considered the most common of the herpes virus family – human infection most often occurs in childhood. The most typical localization of the causative agent of the infectious process is the skin of the nasolabial triangle, lips, mucous membranes of the eye cavity, nose and mouth. That is why HSV-1 is called oral or labial herpes.

The incubation period for is approximately four days. The reproduction of the virus occurs in the cell nucleus – it invades the cell, affects its morphological components and subjugates them, “forcing” them to produce the necessary substances for the structure of new viruses. However, the human immune system stops this process and the virus moves into clusters of nerve endings, where it becomes latent. Practitioners distinguish between the following phases of a herpes infection:

1. Primary – most often the virus causes vesicular lesions of the skin and mucous membranes, accompanied by:

• fever;
• headache, muscle and joint pain;
• general weakness.

2. Latent – HSV is found in the tissues of the nervous system.
3. Manifest – virus reactivation.

Modern medicine has indisputable evidence that the resumption of herpetic infection contributes to the weakening of the immune system, intoxication of the body and hormonal disorders.

Primary infection with HSV-1 is especially dangerous for pregnant women – the virus can penetrate the placental barrier and cause damage to the nerve cells of the developing fetus and the formation of birth defects in it.

When analysis is done

Conducting semen analysis for herpes simplex virus type 1 by PCR is necessary for:

• diagnosis of urogenital infectious and inflammatory processes;
• the patient has herpetiform blisters;
• planning the birth of a child;
• immunodeficiency states;
• lymphoproliferative pathologies.

Method of analysis

The collection of a sample of biological material (sperm) is carried out in the morning, before urination, by masturbation in a special sterile container. Complicated preparation for the procedure is not required, however, 2 days before the study, the patient should not drink alcohol, take hot baths, visit a sauna or bath.