How does the structure of herpes simplex virus DNA affect its infectivity. What is the role of nicks and gaps in the HSV genome. How does HSV interact with cellular DNA damage response mechanisms. What are the key features of HSV DNA replication and organization.

The Complex Structure of Herpes Simplex Virus DNA

The herpes simplex virus (HSV) genome is a marvel of viral engineering, with a structure that plays a crucial role in its infectivity and replication. The DNA of HSV is double-stranded and linear, but its organization is far from simple.

How is HSV DNA structured? The genome contains unique and repeated sequences, with nicks and gaps that are strategically positioned. These interruptions in the DNA strands are not flaws, but rather essential features that contribute to the virus’s life cycle.

Nicks and Gaps: Key Players in HSV Infectivity

What purpose do nicks and gaps serve in the HSV genome? These structural elements are critical for viral infectivity. Research has shown that manipulating these nicks and gaps can significantly alter the virus’s ability to infect host cells. The presence of these discontinuities allows for the efficient unpacking of viral DNA upon entry into the host cell nucleus.

Can the infectivity of HSV be altered by manipulating its DNA structure? Indeed, studies have demonstrated that modifying the nicks and gaps can abrogate infectivity, highlighting their importance in the viral life cycle.

HSV Genome Replication: A Complex Orchestration

The replication of HSV DNA is a sophisticated process that involves both viral and host cellular machinery. During replication, the linear genome forms concatemers – long chains of repeated viral genome units.

How does HSV DNA replication differ from typical cellular DNA replication? Unlike cellular DNA, HSV replication involves the formation of branched structures and the incorporation of ribonucleotides into newly synthesized DNA. This unique replication strategy contributes to the rapid production of viral progeny.

Concatemers: The Building Blocks of Viral Progeny

What are concatemers and why are they important for HSV? Concatemers are long, multimeric forms of the viral genome produced during replication. These structures are essential for the efficient packaging of viral DNA into new virus particles.

How do concatemers form? The process involves the continuous replication of viral DNA without immediate cleavage into individual genome units. This strategy ensures the production of multiple genome copies in a single replication cycle.

The Interplay Between HSV and Host DNA Damage Response

HSV infection triggers a complex interaction with the host cell’s DNA damage response (DDR) machinery. This interplay is crucial for successful viral replication and evasion of host defenses.

How does HSV manipulate the host DNA damage response? The virus has evolved multiple strategies to both activate and inhibit different aspects of the DDR. This manipulation allows the virus to create an environment conducive to its replication while preventing the cell from mounting an effective antiviral response.

Viral Proteins: Modulators of Host DNA Repair

Which viral proteins are involved in modulating the host DDR? Several HSV proteins, including ICP0, play key roles in this process. ICP0, for instance, has been shown to induce the degradation of certain DDR components, effectively altering the cellular response to viral infection.

How does ICP0 affect DNA-dependent protein kinase? Studies have demonstrated that ICP0 can attenuate the activity of DNA-dependent protein kinase (DNA-PK), a crucial enzyme in DNA repair pathways. This inhibition helps the virus evade host defense mechanisms.

The Role of Host Cellular Factors in HSV Infection

Host cellular factors play a significant role in both facilitating and restricting HSV infection. The virus must navigate a complex landscape of cellular proteins to successfully replicate.

Which host factors are involved in restricting HSV infection? Several cellular proteins, including PML, Sp100, ATRX, and hDaxx, have been identified as restrictive factors against HSV. These proteins are part of nuclear structures called ND10 bodies, which play a role in intrinsic antiviral defense.

The Inflammasome Response to HSV

How does HSV interact with the cellular inflammasome? The virus has been shown to both activate and subsequently inhibit inflammasome components such as IFI16 and NLRP3. This dual action allows the virus to modulate the inflammatory response to its advantage.

What is the role of IFI16 in HSV infection? IFI16 acts as a DNA sensor, triggering antiviral signaling pathways. However, HSV has evolved mechanisms to degrade IFI16, thereby dampening this response.

HSV and Epigenetic Modifications

Epigenetic modifications play a crucial role in regulating gene expression, and HSV has evolved mechanisms to manipulate these processes to its advantage.

How does HSV affect histone modifications? The virus can alter histone ubiquitination patterns through its interaction with cellular proteins. For instance, the viral E3 ligase targets cellular proteins RNF8 and RNF168, which are involved in histone ubiquitination and DNA damage responses.

Chromatin Remodeling During HSV Infection

What changes occur in host chromatin during HSV infection? HSV infection leads to significant changes in chromatin structure, including the disruption of nucleosomes and alterations in histone modifications. These changes facilitate viral gene expression and replication.

How does HSV overcome the repressive effects of cellular chromatin? The virus employs multiple strategies, including the use of viral proteins that interact with and modify cellular chromatin remodeling complexes.

Antiviral Defense Mechanisms Against HSV

The host cell employs various intrinsic and innate immune mechanisms to combat HSV infection. Understanding these defenses is crucial for developing new antiviral strategies.

What are the primary intrinsic antiviral defenses against HSV? Key components include nuclear domain 10 (ND10) bodies, DNA sensors like IFI16 and DAI/ZBP1, and various DNA repair proteins. These factors work together to create an inhospitable environment for viral replication.

The Role of DNA Repair in Antiviral Defense

How do DNA repair mechanisms contribute to antiviral defense? Certain DNA repair proteins are involved in recognizing and responding to viral DNA. This response can lead to the silencing of viral gene expression or the triggering of innate immune signaling pathways.

Can HSV evade DNA repair-mediated antiviral responses? Yes, the virus has evolved mechanisms to counteract these defenses. For example, the viral protein ICP0 can induce the degradation of certain DNA repair proteins, thereby neutralizing their antiviral effects.

Future Directions in HSV Research

As our understanding of HSV biology continues to grow, new avenues for research and therapeutic intervention are emerging.

What are some promising areas for future HSV research? Areas of interest include:

• Further elucidation of the complex interactions between HSV and host cellular factors
• Development of novel antiviral strategies targeting viral manipulation of host processes
• Investigation of the long-term effects of HSV infection on host cell epigenetics
• Exploration of potential links between HSV infection and other diseases

Emerging Therapeutic Approaches

What new therapeutic approaches are being explored for HSV? Some promising areas include:

1. Gene editing techniques to target viral DNA
2. Immunomodulatory therapies to enhance natural antiviral responses
3. Novel drug delivery systems for improved treatment of HSV infections
4. Combination therapies targeting multiple aspects of the viral life cycle

The complex interplay between HSV and its host continues to fascinate researchers and offers numerous opportunities for scientific discovery and therapeutic intervention. As we unravel the intricacies of HSV biology, we move closer to developing more effective treatments and potentially even a cure for this ubiquitous viral infection.

Structure of the Herpes Simplex Virus 1 Genome: Manipulation of Nicks and Gaps Can Abrogate Infectivity and Alter the Cellular DNA Damage Response

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Herpes Simplex Virus (HSV) Infections – Infectious Diseases

By

Kenneth M. Kaye

, MD, Harvard Medical School

Reviewed/Revised Sep 2021 | Modified Sep 2022

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Topic Resources

Herpes simplex viruses (human herpesviruses types 1 and 2) commonly cause recurrent infection affecting the skin, mouth, lips, eyes, and genitals. Common severe infections include encephalitis, meningitis, neonatal herpes, and, in immunocompromised patients, disseminated infection. Mucocutaneous infections cause clusters of small painful vesicles on an erythematous base. Diagnosis is clinical; laboratory confirmation by culture, polymerase chain reaction, direct immunofluorescence, or serologic testing can be done. Treatment is symptomatic; antiviral therapy with acyclovir, valacyclovir, or famciclovir is helpful for severe infections and, if begun early, for recurrent or primary infections.

Eight types of herpesviruses infect humans, two of which are herpes simplex viruses (HSV). Both types of herpes simplex virus, HSV-1 and HSV-2, can cause oral or genital infection. Most often, HSV-1 causes gingivostomatitis, herpes labialis, and herpes keratitis. HSV-2 usually causes genital lesions.

Transmission of HSV results from close contact with a person who is actively shedding virus. Viral shedding occurs from lesions but can occur even when lesions are not apparent.

After the initial infection, HSV remains dormant in nerve ganglia, from which it can periodically emerge, causing symptoms. Recurrent herpetic eruptions are precipitated by

Generally, recurrent eruptions are less severe and occur less frequently over time.

(See Overview of Herpesvirus Infections Overview of Herpesvirus Infections Eight types of herpesviruses infect humans ( see Table: Herpesviruses That Infect Humans). After initial infection, all herpesviruses remain latent within specific host cells and may subsequently… read more .)

Diseases include

• Mucocutaneous infection (most common), including genital herpes Genital Herpes Genital herpes is a sexually transmitted infection caused by human herpesvirus 1 or 2. It causes ulcerative genital lesions. Diagnosis is clinical with laboratory confirmation by culture, polymerase… read more

• Ocular infection (including herpes keratitis Herpes Simplex Keratitis Herpes simplex keratitis is corneal infection with herpes simplex virus. It may involve the iris. Symptoms and signs include foreign body sensation, lacrimation, photophobia, and conjunctival… read more )

• Central nervous system (CNS) infection

• Neonatal herpes Neonatal Herpes Simplex Virus (HSV) Infection Neonatal herpes simplex virus infection is usually transmitted during delivery. A typical sign is vesicular eruption, which may be accompanied by or progress to disseminated disease. Diagnosis… read more

HSV rarely causes fulminant hepatitis in the absence of cutaneous lesions.

In patients with HIV infection Human Immunodeficiency Virus (HIV) Infection Human immunodeficiency virus (HIV) infection results from 1 of 2 similar retroviruses (HIV-1 and HIV-2) that destroy CD4+ lymphocytes and impair cell-mediated immunity, increasing risk of certain… read more , herpetic infections can be particularly severe. Progressive and persistent esophagitis, colitis, perianal ulcers, pneumonia, encephalitis, and meningitis may occur.

HSV outbreaks may be followed by erythema multiforme Erythema Multiforme Erythema multiforme is an inflammatory reaction, characterized by target or iris skin lesions. Oral mucosa may be involved. Diagnosis is clinical. Lesions spontaneously resolve but frequently… read more , possibly caused by an immune reaction to the virus.

Eczema herpeticum Complications of atopic dermatitis is a complication of HSV infection in which severe herpetic disease develops in skin regions with eczema.

Lesions may appear anywhere on the skin or mucosa but are most frequent in the following locations:

Generally, after a prodromal period (typically

Vesicles typically persist for a few days, then rupture and dry, forming a thin, yellowish crust.

Healing generally occurs within 10 to 19 days after onset in primary infection or within 5 to 10 days in recurrent infection. Lesions usually heal completely, but recurrent lesions at the same site may cause atrophy and scarring. Skin lesions can develop secondary bacterial infection. In patients with depressed cell-mediated immunity due to HIV infection or other conditions, prolonged or progressive lesions may persist for weeks or longer. Localized infections can disseminate, particularly—and often dramatically—in immunocompromised patients.

Acute herpetic gingivostomatitis usually results from primary infection with HSV-1, typically in children. Herpetic pharyngitis can occur in adults as well as children. Occasionally, through oral-genital contact, the cause is HSV-2. Intraoral and gingival vesicles rupture, usually within several hours to 1 or 2 days, to form ulcers. Fever and pain often occur. Difficulty eating and drinking may lead to dehydration. After resolution, the virus resides dormant in the semilunar ganglion.

Herpes labialis is usually a recurrence of HSV. It develops as ulcers (cold sores) on the vermilion border of the lip or, much less commonly, as ulcerations of the mucosa of the hard palate.

Genital herpes Genital Herpes Genital herpes is a sexually transmitted infection caused by human herpesvirus 1 or 2. It causes ulcerative genital lesions. Diagnosis is clinical with laboratory confirmation by culture, polymerase… read more is the most common ulcerative sexually transmitted infection in developed countries. Genital HSV can be caused by HSV-1 or HSV-2.

Herpes simplex keratitis Herpes Simplex Keratitis Herpes simplex keratitis is corneal infection with herpes simplex virus. It may involve the iris. Symptoms and signs include foreign body sensation, lacrimation, photophobia, and conjunctival… read more (HSV infection of the corneal epithelium) causes pain, tearing, photophobia, and corneal ulcers that often have a branching pattern.

Herpetic whitlow Herpetic Whitlow Herpetic whitlow is a cutaneous infection of the distal aspect of the finger caused by herpes simplex virus. (See also Overview and Evaluation of Hand Disorders. ) Herpetic whitlow may cause… read more , a swollen, painful, erythematous lesion of the finger, results from inoculation of HSV through the skin and is most common among health care practitioners.

Neonatal HSV infection Neonatal Herpes Simplex Virus (HSV) Infection Neonatal herpes simplex virus infection is usually transmitted during delivery. A typical sign is vesicular eruption, which may be accompanied by or progress to disseminated disease. Diagnosis… read more develops in neonates, including those whose mothers have no suggestion of current or past herpes infection. It is most commonly transmitted during birth through contact with vaginal secretions containing HSV and usually involves HSV-2.

Neonatal HSV infection usually develops between the 1st and 4th week of life, often causing mucocutaneous vesicles or central nervous system involvement. It causes major morbidity and mortality.

Herpes encephalitis Encephalitis Encephalitis is inflammation of the parenchyma of the brain, resulting from direct viral invasion or occurring as a postinfectious immunologic complication caused by a hypersensitivity reaction. .. read more occurs sporadically and may be severe. Multiple early seizures are characteristic.

Viral meningitis Viral Meningitis Viral meningitis tends to be less severe than acute bacterial meningitis. Findings include headache, fever, and nuchal rigidity. Diagnosis is by cerebrospinal fluid (CSF) analysis. Treatment… read more may result from HSV-2. It is usually self-limited.

Lumbosacral myeloradiculitis, typically caused by HSV-2, can occur during primary infection or reactivation of HSV-2 infection and can result in urinary retention or obstipation.

Diagnosis of HSV infection is often clinical based on characteristic lesions.

Laboratory confirmation can be helpful, especially if infection is severe, the patient is immunocompromised or pregnant, or lesions are atypical. A Tzanck test (a superficial scraping from the base of a freshly ruptured vesicle stained with Wright-Giemsa stain) often reveals multinucleate giant cells in HSV or varicella-zoster virus infection.

Definitive diagnosis is with culture, seroconversion involving the appropriate serotype (in primary infections), PCR, and antigen detection. Fluid and material for culture should be obtained from the base of a vesicle or of a freshly ulcerated lesion. HSV can sometimes be identified using direct immunofluorescence assay of scrapings of lesions. PCR of CSF and MRI are used to diagnose HSV encephalitis.

HSV should be distinguished from herpes zoster Herpes Zoster Herpes zoster is infection that results when varicella-zoster virus reactivates from its latent state in a posterior dorsal root ganglion. Symptoms usually begin with pain along the affected… read more , which rarely recurs and usually causes more severe pain and larger groups of lesions that are distributed along a dermatome and typically do not cross the midline.

Clusters of vesicles or ulcers on an erythematous base are unusual in genital ulcers other than those due to HSV infection.

If herpes infections recur frequently, do not resolve, or do not respond to antiviral drugs as expected, immunocompromise, possibly due to HIV infection Human Immunodeficiency Virus (HIV) Infection Human immunodeficiency virus (HIV) infection results from 1 of 2 similar retroviruses (HIV-1 and HIV-2) that destroy CD4+ lymphocytes and impair cell-mediated immunity, increasing risk of certain. .. read more , should be suspected.

• Usually acyclovir, valacyclovir, or famciclovir

• For keratitis, topical trifluridine (typically in consultation with an ophthalmologist)

Treating primary HSV infection with drugs, even if done early, does not prevent the possibility of recurrence.

Isolated infections often go untreated without consequence.

Acyclovir, valacyclovir, or famciclovir can be used to treat infection, especially when it is primary. Infection with acyclovir-resistant HSV is rare and occurs almost exclusively in immunocompromised patients. Foscarnet may be effective for acyclovir-resistant infections.

Secondary bacterial infections are treated with topical antibiotics (eg, mupirocin or neomycin-bacitracin) or, if severe, with systemic antibiotics (eg, penicillinase-resistant beta-lactams). Systemic analgesics may help.

Gingivostomatitis and pharyngitis may require symptom relief with topical anesthetics (eg, dyclonine, benzocaine, viscous lidocaine). (NOTE: Lidocaine must not be swallowed because it anesthetizes the oropharynx, the hypopharynx, and possibly the epiglottis. Children must be watched for signs of aspiration.) Severe cases can be treated with acyclovir, valacyclovir, or famciclovir.

Herpes labialis responds to oral and topical acyclovir. The duration of a recurrent eruption may be decreased by about a day by applying penciclovir 1% cream every 2 hours while awake for 4 days, beginning during the prodrome or when the first lesion appears. Toxicity appears to be minimal. Famciclovir 1500 mg as one dose or valacyclovir 2 g orally every 12 hours for 1 day can be used to treat recurrent herpes labialis. Acyclovir-resistant strains are resistant to penciclovir, famciclovir, and valacyclovir. Docosanol 10% cream may be effective when used 5 times a day.

Herpetic whitlow heals in 2 to 3 weeks without treatment. Topical acyclovir has not been shown to be effective. Oral or IV acyclovir can be used in immunosuppressed patients and those with severe infection.

Pearls & Pitfalls

Treatment of herpes simplex keratitis Treatment Herpes simplex keratitis is corneal infection with herpes simplex virus. It may involve the iris. Symptoms and signs include foreign body sensation, lacrimation, photophobia, and conjunctival… read more involves topical antivirals, such as trifluridine, and should be supervised by an ophthalmologist.

Acyclovir 20 mg/kg IV every 8 hours for 14 days should be used if renal function is normal. A dose of 20 mg/kg IV every 8 hours for at least 21 days is indicated for CNS and disseminated HSV disease.

Encephalitis is treated with acyclovir 10 mg/kg IV every 8 hours for 14 to 21 days if renal function is normal. Treatment for 14 to 21 days is preferred to prevent potential relapse. Higher doses up to 20 mg/kg IV every 8 hours are used in children.

Viral meningitis is usually treated with IV acyclovir. Acyclovir is generally very well-tolerated. However, adverse effects can include phlebitis, renal dysfunction, and, rarely, neurotoxicity (lethargy, confusion, seizures, coma).

• HSV usually causes mucocutaneous infection but sometimes causes keratitis, and serious CNS infection can occur in neonates and in adults.

• After initial infection, HSV remains dormant in nerve ganglia, from which it can periodically emerge, causing symptoms.

• Diagnose mucocutaneous infections clinically, but do viral culture, PCR, or antigen detection if patients are neonates, immunocompromised, or pregnant or have a CNS infection or severe disease.

• Give IV acyclovir to patients with serious infections.

• For mucocutaneous infections, consider oral acyclovir, valacyclovir, or famciclovir; for herpes labialis, an alternative is topical penciclovir or docosanol.

Drug Name	Select Trade
acyclovir	SITAVIG, Zovirax, Zovirax Cream, Zovirax Ointment, Zovirax Powder, Zovirax Suspension
valacyclovir	Valtrex
famciclovir	Famvir
trifluridine	Viroptic
foscarnet	Foscavir
mupirocin	Bactroban, Centany, Centany AT
neomycin	Neo-Fradin
bacitracin	AK-Tracin, Baciguent, BaciiM, Baci-Rx, Ocu-Tracin
benzocaine	Advocate Pain Relief Stick, Americaine, Anbesol, Anbesol Baby , Anbesol Jr , Banadyne-3, Benzodent, Benz-O-Sthetic, Boil-Ease, Cepacol Sensations, Chloraseptic, Comfort Caine , Dry Socket Remedy, Freez Eez, Little Remedies for Teethers, Monistat Care, Orabase, Orajel, Orajel Baby, Orajel Denture Plus, Orajel Maximum Strength, Orajel P. M., Orajel Protective, Orajel Severe Pain, Orajel Swabs, Orajel Ultra, Oral Pain Relief , Oticaine , Otocain, Outgro, Pinnacaine, Pro-Caine, RE Benzotic, Topex, Topicale Xtra, Zilactin-B
lidocaine	7T Lido, Akten , ALOCANE, ANASTIA, AneCream, Anestacon, Aspercreme with Lidocaine, Astero , BenGay, Blue Tube, Blue-Emu, CidalEaze, DermacinRx Lidogel, DermacinRx Lidorex, DERMALID, Ela-Max, GEN7T, Glydo, Gold Bond, LidaMantle, Lidocare, Lidoderm, LidoDose, LidoDose Pediatric, Lidofore, LidoHeal-90, LIDO-K , Lidomar , Lidomark, LidoReal-30, LidoRx, Lidosense 4 , Lidosense 5, LIDO-SORB, Lidotral, Lidovix L, LIDOZION, Lidozo, LMX 4, LMX 4 with Tegaderm, LMX 5, LTA, Lydexa, Moxicaine, Numbonex, ReadySharp Lidocaine, RectaSmoothe, RectiCare, Salonpas Lidocaine, Senatec, Solarcaine, SUN BURNT PLUS, Tranzarel, Xylocaine, Xylocaine Dental, Xylocaine in Dextrose, Xylocaine MPF, Xylocaine Topical, Xylocaine Topical Jelly, Xylocaine Topical Solution, Xylocaine Viscous, Zilactin-L, Zingo, Zionodi, ZTlido
penciclovir	Denavir
docosanol	Abreva

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Herpes, Cytomegalovirus, Epstein-Barr virus

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Treatment of herpes, cytomegalovirus, Epstein-Barr virus depends on the form of the infection:

• latent,
• subclinical,
• manifest,

and the state of the immune system. A decrease in immunity that spontaneously occurs in urban residents as a result of exposure to stress, unfavorable ecology, disruption of sleep, nutrition, etc. viral infections.

Herpes viruses, along with other opportunistic infections, are called clinical markers of immunodeficiency states. Mucocutaneous manifestations of herpes 1, 2 types are known to almost everyone.

Cytomegalovirus infection and Epstein-Barr virus infection in an adult can occur as a common acute respiratory disease with a characteristic enlargement of the posterior cervical lymph nodes, which resolve with recovery. However, with violations in the immune system, the course of these infections often takes a latent or subclinical form. A characteristic clinical sign in this case is an increase in lymph nodes located near the entrance gates of infections (submandibular, cervical, inguinal). According to their parameters, these lymph nodes correspond to the concept of “viral lymphadenitis”: their size does not exceed 1. 5 cm, they are not soldered to the skin, they have a round or oval shape, elastic, mobile, differ in density.

The fact of enlarged lymph nodes is associated with the ability of herpetic viruses to infect cells of the immune system : Epstein-Barr viruses, herpes type 6 viruses are found in B-lymphocytes, herpesviruses types 1, 6 and 7 – in T-lymphocytes, cytomegaloviruses – in macrophages / monocytes, etc. . cells.

When a herpes infection is activated, patients may complain of:

• sore throat,
• nasal congestion,
• dyspeptic disorders,

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  What you need to know about herpes? Herpes virus: its types and symptoms

  The source of infection is sick people who transmit the virus through shared objects or through direct contact. The causative agent of herpes is also transmitted by airborne droplets and from mother to fetus.

  Herpes virus (Herpesviridae) is a DNA-containing virus consisting of three subfamilies – alpha, beta, gamma.

  Diseases caused by the herpes virus (Herpesviridae) are divided into:

  • herpes simplex
  • genital herpes
  • Kaposi’s eczema herpetiformis
  • chickenpox and herpes zoster.

  Herpes simplex (blister lichen, Herpes simplex)

  After entering the body, the herpes simplex virus spreads through the lymph and nerve fibers, penetrates into the lymphatic and circulatory systems, and internal organs.

  Accumulates in the ganglia (aggregation of nerve cells) of the nervous system, where it lives in a dormant state for a long time. After the virus enters the body, antibodies to the causative agent of herpes simplex are formed, which remain at approximately the same level throughout life, regardless of the clinical manifestations of the disease. When activated, the herpes simplex virus (during the acute period of the disease) reproduces its copies, which causes the death of the infected cell.

  The first episode of illness usually occurs in childhood after infection. The incubation period lasts from 1-2 days to 2 weeks. Small blisters appear on the skin of the lips or nose. Patients report soreness and itching. The disease can occur in the form of herpetic stomatitis, with fever, headache and malaise, swollen lymph nodes. Grouped vesicles appear on the mucous membrane of the cheeks, the inner surface of the lips, tongue, tonsils, and palate against the background of specific reddening of the skin. Then painful erosions form.

  Relapses of herpes simplex virus (HSV) can occur up to several times a year, and there are cases of a continuous course of the disease for several years. Burning, pain, itching are felt before the appearance of a blistering rash on the skin. The size of the bubbles is 1-2 mm, with transparent contents. Over time, the contents of the bubbles become cloudy, they burst with the formation of painful erosions.
  In the process of healing, erosions become covered with crusts. When the bacterial flora is attached, the defects heal more slowly, ulcers form.

  Herpes simplex virus usually manifests as a rash on the skin of the cheeks, lips, nose, but can occur on the skin of the genitals, buttocks, sacrum, thighs, hands2.

  Kaposi’s eczema herpetiformis (Exzema hertipetiformis)

  Predisposing dermatological background – the presence of eczema, atopic dermatitis and other diseases in which the integrity of the skin is disturbed.

  The incubation period is up to 7 days. There is a deterioration in well-being, an increase in lymph nodes and an increase in body temperature up to 40 ° C. After a few days, multiple grouped small vesicles appear on the affected areas of the skin. Pustules form. Elements shrink into a brown crust. The mucous membrane of the mouth, genitals, conjunctiva of the eyes may be affected. The disease can be complicated by a bacterial infection, a state of shock. In severe cases, it can lead to the death of the patient.

  Genital herpes (Herpes progenitalis)

  Herpetic rash occurs on the skin of the genitals and in the anus (anus). The main route of transmission is sexual or orogenital, through contact with a patient with or without symptoms, that is, when carrying the virus. The household route through contaminated common items is also possible. The risk of infection of a child neonatally from a mother when a woman becomes infected closer to childbirth is up to 50%2.

  Herpes zoster

  At the beginning of the disease, there is pain along the affected nerves, then a rash appears: redness and vesicles with clear and cloudy contents. Bubbles shrink into brown crusts. The disease lasts up to 3 weeks.

  In atypical cases, the rash may present with only redness without vesicles or large blistering. Sometimes sores are formed, healing with the formation of scars.

  Varicella (chickenpox)

  The incubation period lasts up to 3 weeks. At the onset of the disease, body temperature rises, headache occurs, and a widespread small-spotted rash appears. Then the spot turns into a knot, on which a bubble appears. Bubbles first appear on the trunk, face, scalp. Bubbles shrink into crusts. In a severe form of the course of the disease, a rash can occur on the skin of the palms and feet. A characteristic feature of the disease is a false variety of forms (polymorphism) – on one part of the body there may be spots, nodules and vesicles, since the rashes appear jerkily.

  The mild form of the disease is characterized by an increase in temperature
  up to 38.5°C for several days. The rash is not numerous, there are several days.