ICD variantCongenital herpesviral [herpes simplex] infection is a specific ICD-10 coded subtype of Herpes Simplex Infection. The clinical content below covers Herpes Simplex Infection in general.
NeonatologymoderateICD-10 · P35.2
Congenital herpesviral [herpes simplex] infection.Care & specialists in Brazil
In Brazil, congenital herpesviral [herpes simplex] infection is managed by neonatologists. Herpes simplex infection is a lifelong viral condition caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2), which establish latency in sensory ganglia and reactivate periodically. WHO estimates 3.7 billion people under 50 carry HSV-1 (67% global seroprevalence) and 491 million adults aged 15-49 carry HSV-2.
Herpes simplex infection (ICD-10: B00 for HSV non-genital; A60 for anogenital herpesviral infection) is caused by two closely related double-stranded DNA alphaherpesviruses: HSV-1 (Human alphaherpesvirus 1) and HSV-2 (Human alphaherpesvirus 2). After primary infection at mucosal or skin sites, the virus travels retrograde along sensory nerve axons to neuronal cell bodies in regional ganglia — the trigeminal ganglion for orofacial HSV-1, the sacral dorsal root ganglia for anogenital HSV-2. There, the viral genome persists as an episome in a latent state, expressing only latency-associated transcripts. Reactivation, triggered by ultraviolet light, fever, trauma, immune suppression, menstruation, or psychological stress, drives anterograde transport of new virions back to mucocutaneous sites, producing recurrent vesicular eruptions.
key facts
Prevalence
HSV-1: 67% of people under 50 globally; HSV-2: 13% of adults aged 15-49 (WHO 2016 estimates)
Demographics
HSV-2 affects women nearly twice as often as men due to mucosal vulnerability; sub-Saharan Africa has the highest HSV-2 burden (44% in women)
Avg. age
HSV-1 acquired in childhood (median age 5-10) when orally transmitted; HSV-2 acquired after sexual debut, typically ages 15-35
Global cases
3.7 billion HSV-1 infections; 491 million HSV-2 infections worldwide (WHO)
Specialist
Neonatology
ICD-10
§ 02
How you might notice it
The key symptoms of Congenital herpesviral [herpes simplex] infection are: Tingling, itching, or burning at the site 12-48 hours before any visible lesion appears — the prodrome that signals imminent outbreak and the optimal window for antiviral treatment., Clusters of small fluid-filled vesicles on an erythematous base, most often on the lip vermilion, perioral skin, or anogenital region; vesicles typically number 3-10 and feel sharply painful., Vesicles rupture within 24-48 hours to form shallow painful ulcers that gradually crust over and re-epithelialize over 7-14 days in recurrent disease (longer in primary infection)., Primary genital HSV often produces fever, headache, malaise, and tender bilateral inguinal lymphadenopathy in addition to widespread genital ulcers — symptoms peak around day 7 and last 2-3 weeks., Dysuria and urinary retention are common in primary genital herpes, especially in women, due to ulcers near the urethral meatus and a transient sacral radiculitis., Recurrent outbreaks are typically milder than the primary episode, more localized, shorter (5-7 days), and often unilateral on the same site each time., Asymptomatic viral shedding occurs on approximately 10-20% of days in HSV-2 carriers and accounts for most sexual transmissions; carriers are infectious without any visible lesion..
01Tingling, itching, or burning at the site 12-48 hours before any visible lesion appears — the prodrome that signals imminent outbreak and the optimal window for antiviral treatment.
02Clusters of small fluid-filled vesicles on an erythematous base, most often on the lip vermilion, perioral skin, or anogenital region; vesicles typically number 3-10 and feel sharply painful.
03Vesicles rupture within 24-48 hours to form shallow painful ulcers that gradually crust over and re-epithelialize over 7-14 days in recurrent disease (longer in primary infection).
§ 03
How it’s diagnosed
diagnosis
Diagnosis of herpes simplex infection rests on the clinical appearance of typical grouped vesicles or ulcers in a recognizable distribution, supported by laboratory confirmation in any unclear, severe, or potentially transmissible case. The CDC 2021 STI Treatment Guidelines (Workowski et al.) recommend that all suspected genital herpes be virologically confirmed — empirical diagnosis is unreliable because syphilis, chancroid, and aphthous ulcers can mimic HSV. The diagnostic test of choice is nucleic acid amplification testing (NAAT, usually PCR) of a swab taken from an unroofed vesicle or moist ulcer. PCR detects 11-71% more cases than viral culture, distinguishes HSV-1 from HSV-2, and remains positive longer in the lesion. Viral culture is an acceptable alternative where PCR is unavailable but has limited sensitivity (35-50% in recurrent lesions). Type-specific serology (glycoprotein G-based HSV-1 and HSV-2 IgG antibodies) is used to confirm past infection in asymptomatic patients, to counsel a partner of a known carrier, or to clarify whether a primary outbreak is truly primary (seronegative) versus a recurrent first-recognized episode (seropositive). Serology takes 12 weeks after exposure to become reliably positive. Tzanck smears showing multinucleated giant cells are nonspecific and inferior to PCR. In suspected HSV encephalitis, CSF PCR for HSV DNA has 96% sensitivity and 99% specificity and should be sent immediately along with MRI, which classically shows temporal lobe hyperintensity. In neonatal herpes, surface swabs, CSF PCR, blood PCR, and LFTs are obtained simultaneously, and IV acyclovir is begun empirically before results return. Differential diagnosis includes syphilis, chancroid, lymphogranuloma venereum, candidiasis, aphthous ulcers, Behçet disease, and fixed drug eruption.
Key tests
01
HSV PCR from lesion swabGold-standard diagnostic test — detects viral DNA and types as HSV-1 or HSV-2 with 95% sensitivity in active vesicular lesions. Distinguishes the two types, which guides counseling and prognosis.
02
Type-specific HSV-1 and HSV-2 IgG serology (gG-based)
§ 04
Treatment & cost
medical treatments
✓Acyclovir (oral 400 mg three times daily for 7-10 days; IV 10 mg/kg every 8 hours for severe disease; topical 5% cream for orolabial)
✓Valacyclovir (1 g twice daily for 7-10 days for primary; 500 mg twice daily for 3 days for recurrence; 500 mg daily for suppression)
✓Famciclovir (250 mg three times daily for 7-10 days for primary; 1 g twice daily for 1 day for episodic recurrence; 250 mg twice daily for suppression)
✓Topical antivirals for herpes simplex keratitis (ganciclovir 0.15% gel five times daily, or trifluridine 1% drops every 2 hours)
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Causes & risk factors
known causes
Direct mucocutaneous contact with infected secretions or lesions
The dominant transmission route. HSV enters through breaks in skin or via intact mucosal surfaces during kissing, oral sex, vaginal or anal sex, and contact sports. The virus replicates locally in epithelial cells, then enters sensory nerve endings to reach ganglia within days.
Asymptomatic viral shedding from the index partner
Most genital HSV transmissions occur when the source partner has no visible lesion. Genital HSV-2 carriers shed virus on roughly 10-20% of days; HSV-1 oral shedding occurs on 9% of days. This is why condoms and suppressive therapy matter even when no outbreak is present.
Vertical transmission during birth
Neonatal HSV is acquired in 85% of cases during vaginal delivery from a mother shedding virus from genital lesions. Risk is highest (30-50%) when the mother acquires primary HSV in the third trimester — she has not yet developed protective IgG to transfer.
Autoinoculation to new body sites
Patients with active orolabial or genital herpes can transfer virus on their fingers to eyes, fingertips (whitlow), or other broken skin. Strict handwashing during outbreaks reduces this risk.
Reactivation from latent infection in sensory ganglia
Recurrent disease is not new infection — it is virus traveling down sensory axons from the ganglion where it has lived since primary infection. Reactivation is triggered by UV light, fever, hormonal change, immunosuppression, trauma, dental procedures, and stress.
Iatrogenic exposure in healthcare settings
Herpetic whitlow historically affected dentists, nurses, and respiratory therapists handling oral secretions without gloves. Universal precautions have largely eliminated occupational HSV transmission, but cases still occur with breached barriers.
risk factors
§ 06
Living with it
01Use latex condoms consistently to reduce HSV-2 transmission by approximately 30% — partial protection because perineal and pubic skin is not covered
02Avoid sexual contact during prodromal symptoms and visible outbreaks, when shedding and infectivity peak
03Take daily suppressive antiviral therapy if you have HSV-2 and a non-infected partner — reduces transmission by approximately 50%
04Apply SPF 30+ lip balm during sun exposure if you are prone to recurrent cold sores
05Avoid sharing utensils, lip products, towels, and razors during active orolabial outbreaks
06Disclose HSV status before sex with a new partner so they can make informed decisions and consider pre-exposure suppression
recommended foods
•Balanced diet rich in vegetables, lean protein, and whole grains — supports general immune function
•Adequate hydration, particularly during outbreaks of oral or genital HSV with dysphagia or dysuria
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When to seek help
why see a neonatology
See an infectious disease physician, sexual health specialist, or dermatologist when outbreaks are frequent (>6 per year) despite suppression, when ulcers are chronic or atypical, when immunosuppression complicates management, when acyclovir-resistant HSV is suspected, or when pregnancy requires careful peripartum risk assessment. Most uncomplicated HSV is managed in primary care or by sexual health clinics. Ophthalmology referral is mandatory for any suspected herpes simplex keratitis; suspected HSV encephalitis is a neurological emergency that warrants immediate hospital admission.
01Herpes simplex encephalitis — the most common cause of sporadic fatal viral encephalitis; mortality 70%+ untreated, 15-20% with acyclovir; survivors often have memory and behavioral deficits
02Neonatal herpes (skin-eye-mouth, CNS, or disseminated) — disseminated form has 29% mortality despite high-dose IV acyclovir; up to half of CNS survivors have neurological impairment
03Herpes simplex keratitis — repeated reactivations cause stromal scarring and is the leading infectious cause of corneal blindness in high-income countries
04Eczema herpeticum — disseminated cutaneous HSV in a patient with atopic dermatitis; can be life-threatening without IV acyclovir
05Aseptic meningitis (Mollaret meningitis) — recurrent benign HSV-2 lymphocytic meningitis that may persist for years
Orolabial herpes (HSV-1 in most cases)Recurrent cold sores on the lip vermilion border or perioral skin. Primary infection in children may present as gingivostomatitis with extensive intraoral ulcers, fever, and lymphadenopathy.
Anogenital herpes (HSV-2 or HSV-1)Painful vesicles and ulcers on the genitalia, perineum, buttocks, or thighs. First episodes can be severe with fever, dysuria, and inguinal lymphadenopathy lasting 2-3 weeks.
Herpetic whitlowHSV infection of the finger, classically acquired by dental and healthcare workers from oral secretions before universal glove precautions; now seen mostly in children who suck thumbs during a primary oral infection.
Herpes gladiatorumCutaneous HSV-1 infection spread by skin-to-skin contact in wrestlers, rugby players, and other contact-sport athletes; lesions appear on the face, neck, and arms.
Herpes simplex keratitisHSV-1 corneal infection producing dendritic ulcers — the leading infectious cause of corneal blindness in high-income countries. Repeated reactivation causes stromal scarring.
Neonatal herpesAcquired peripartum from a mother with active genital shedding; classified as skin-eye-mouth (SEM), CNS disease, or disseminated disease. Mortality reaches 30% in disseminated cases despite treatment.
Herpes simplex encephalitisHSV-1 reactivation in the temporal lobe, the most common cause of sporadic viral encephalitis in adults. Untreated mortality exceeds 70%; with acyclovir, mortality falls below 20%.
Living with Congenital herpesviral [herpes simplex] infection
Timeline
Primary genital herpes lesions heal over 2-3 weeks; primary orolabial gingivostomatitis in children lasts 7-14 days. Recurrent outbreaks last 5-10 days untreated and 3-7 days with early antiviral treatment. Suppressive therapy benefits accumulate over 3-6 months as outbreak frequency falls. HSV encephalitis treatment continues for 14-21 days IV; neurological recovery can take months and may be incomplete. Neonatal HSV requires 14-21 days IV acyclovir plus 6 months of oral suppression to reduce neurological sequelae (Kimberlin 2011).
Lifestyle
01Identify and avoid personal outbreak triggers — keep a brief diary noting sun exposure, illness, menstruation, stress, and outbreak dates
02Manage stress through regular exercise, adequate sleep (7-9 hours), and evidence-based techniques such as mindfulness or CBT
04Maintain meticulous hand hygiene during outbreaks to prevent autoinoculation to eyes or fingers
05Inform dentists of HSV history before procedures — dental trauma can trigger reactivation, and prophylactic valacyclovir can be considered for major work
06If immunocompromised or transplant recipient, discuss long-term suppressive therapy with your specialist
Daily management
01
Complementary approaches
Sunscreen on the lips (SPF 30+ lip balm)Reduces UV-triggered recurrent orolabial outbreaks. Randomized data show approximately 65% reduction in experimentally UV-induced cold sore recurrence when daily SPF lip protection is used.
L-lysine supplementation (1-3 g daily)Limited evidence — some small trials report reduced recurrence frequency, but meta-analyses are inconclusive. Cheap and safe enough to try as an adjunct, but not a replacement for prescription antivirals in frequent recurrers.
Choosing a doctor
For genital herpes, sexual health clinics are typically free or low-cost and have rapid PCR testing. For frequent or atypical recurrences, look for an infectious disease physician or dermatologist comfortable with type-specific serology, suppression decisions, and discordant-couple counseling. In pregnancy, the obstetric team plus a maternal-fetal medicine consultant should coordinate management. Ask about access to acyclovir-resistance testing if you are immunocompromised with chronic ulcers.
Patient support resources
CDC — Genital Herpes Fact Sheet →Authoritative US patient education with up-to-date statistics, transmission, and treatment information.
No, herpes simplex is lifelong because the virus stays dormant in nerve ganglia. No cure exists, but daily antiviral medication reduces outbreaks by 70-80% and transmission risk by about 50%. Most people manage HSV with minimal day-to-day impact.
What is the difference between HSV-1 and HSV-2?▾▴
HSV-1 typically causes cold sores; HSV-2 typically causes genital herpes. HSV-1 now causes over half of new genital herpes cases via oral sex. Genital HSV-1 recurs less often (about 1 outbreak per year) than HSV-2 (median 4 per year).
How is herpes transmitted?▾▴
Herpes spreads through direct skin or mucosal contact during kissing, oral sex, vaginal or anal sex, and contact sports. Most genital transmissions occur when no sore is visible — carriers shed virus asymptomatically on 10-20% of days. Condoms reduce but do not eliminate risk.
Can I have herpes without knowing?▾▴
Yes. Over 80% of HSV-2 carriers are unaware because outbreaks are mild, atypical, or absent. Asymptomatic carriers still shed virus and can transmit to partners. Type-specific HSV IgG blood testing identifies prior infection but is not part of routine screening.
Does a condom prevent herpes?▾▴
Condoms reduce HSV-2 transmission by approximately 30% but do not eliminate risk because the virus also sheds from skin not covered by the condom — labia, perineum, scrotum, thighs. Combining condom use with daily suppressive therapy in the carrier partner reduces transmission by roughly 70-75%.
What triggers a herpes outbreak?▾▴
Common triggers: ultraviolet sunlight (especially for cold sores), fever or illness, menstruation, sexual activity, friction or trauma, immunosuppression, dental procedures, and psychological stress. A brief trigger diary helps anticipate outbreaks.
How long does a herpes outbreak last?▾▴
A primary outbreak lasts 2-3 weeks; a recurrent outbreak typically lasts 5-10 days untreated, or 3-7 days with antivirals started within 24 hours of the first prodromal tingling. Lesions go through stages: prodrome, papule, vesicle, ulcer, crust, healing.
Should I take daily antivirals or treat outbreaks?▾▴
Daily suppression is recommended for 6+ outbreaks per year, severe outbreaks, immunosuppression, or a susceptible sexual partner. Episodic treatment is appropriate for occasional mild outbreaks. Many patients switch between strategies over time.
Can I have a normal sex life with herpes?▾▴
Yes. Disclose your status to partners, use condoms, take daily suppressive antiviral therapy if you have a long-term partner without HSV, and avoid sexual contact during prodromal symptoms or visible outbreaks. Many discordant couples remain partnered for decades without transmission when these steps are followed.
Can I have children if I have genital herpes?▾▴
Yes. Most women with genital HSV have uncomplicated pregnancies and vaginal deliveries. The key concern is acquiring a new primary infection in the third trimester. Pregnant women with known HSV are offered suppressive valacyclovir from 36 weeks; cesarean delivery is recommended only if active genital lesions or prodromal symptoms are present at labor.
Is herpes dangerous?▾▴
In healthy adults, HSV is mostly a nuisance, not a danger. Serious complications — encephalitis, neonatal disease, ocular keratitis, eczema herpeticum, disseminated disease — are uncommon and treatable with IV acyclovir. Prompt treatment dramatically improves outcomes.
What is herpes simplex encephalitis?▾▴
HSV-1 occasionally reactivates in the temporal lobe of the brain rather than the skin, causing severe encephalitis with fever, headache, confusion, and seizures. Untreated mortality exceeds 70%; with prompt IV acyclovir, mortality drops below 20%. Suspect HSV encephalitis with any cold-sore patient who develops new confusion or seizures.
Can babies catch herpes?▾▴
Yes. Neonatal HSV is mostly acquired during birth from a mother shedding genital HSV. Risk peaks (30-50%) when mothers acquire HSV in the third trimester. Cesarean and maternal suppressive therapy reduce risk. Newborns with vesicles, fever, or seizures need urgent IV acyclovir.
Will I pass herpes to my partner?▾▴
Transmission risk depends on viral type, time since infection, frequency of outbreaks, condom use, and suppressive therapy. Without precautions, an HSV-2 positive partner transmits to a susceptible partner at approximately 10% per year. Combining condoms, abstinence during outbreaks, and daily valacyclovir reduces this to roughly 1-2% per year.
Does herpes affect fertility?▾▴
Herpes simplex does not impair fertility or affect the ability to conceive. The only fertility-related consideration is timing of conception around active outbreaks. Genital HSV does not cause tubal scarring (unlike untreated chlamydia or gonorrhea) and is not a structural cause of infertility.
Can I get herpes from a toilet seat?▾▴
No. HSV is fragile outside the body and does not survive on dry surfaces long enough to transmit through toilet seats, towels (once dry), doorknobs, or swimming pools. Transmission requires direct skin-to-skin or mucosal contact with infected secretions.
How is herpes diagnosed if I have a sore?▾▴
A clinician swabs the sore for PCR, which detects HSV DNA and distinguishes type 1 from type 2 with 95% sensitivity. Results take 1-3 days. Blood antibody tests identify past infection but cannot determine whether the current sore is herpes.
Are cold sores and genital herpes the same disease?▾▴
Both are caused by herpes simplex virus but typically by different types: HSV-1 for cold sores, HSV-2 for genital herpes. HSV-1 can cause genital herpes through oral sex, and HSV-2 can cause oral herpes through the reverse. The behavior, treatment, and antibody pattern differ slightly, but they are the same family of virus.
How much does herpes treatment cost?▾▴
Generic acyclovir, valacyclovir, and famciclovir are inexpensive — typically under USD 20 per month for daily suppression in most countries, often much less. Episodic treatment for an outbreak costs a few dollars. Generics are available in India, the US, and Europe. Prescription savings programs further lower costs.
Is there a herpes vaccine?▾▴
No HSV vaccine is currently licensed despite decades of research. Several candidates have failed phase 3 trials. Active research continues on mRNA-based vaccines and therapeutic vaccines aimed at reducing recurrence in already-infected people. Until one is approved, daily suppressive antivirals are the closest equivalent.
04Primary genital HSV often produces fever, headache, malaise, and tender bilateral inguinal lymphadenopathy in addition to widespread genital ulcers — symptoms peak around day 7 and last 2-3 weeks.
05Dysuria and urinary retention are common in primary genital herpes, especially in women, due to ulcers near the urethral meatus and a transient sacral radiculitis.
06Recurrent outbreaks are typically milder than the primary episode, more localized, shorter (5-7 days), and often unilateral on the same site each time.
07Asymptomatic viral shedding occurs on approximately 10-20% of days in HSV-2 carriers and accounts for most sexual transmissions; carriers are infectious without any visible lesion.
08Outbreak triggers reported by patients include sunlight exposure (orolabial), febrile illness, menstruation, sexual activity, immunosuppression, and emotional stress.
09In primary herpetic gingivostomatitis (children) extensive painful intraoral ulcers, drooling, halitosis, fever to 39-40°C, and cervical lymphadenopathy can lead to dehydration from refusal to eat.
10Herpes simplex keratitis presents with unilateral red painful eye, photophobia, watering, and decreased vision — slit-lamp exam shows a branching dendritic ulcer staining with fluorescein.
early warning signs
•Tingling, itching, or burning sensation at the typical lesion site 12-48 hours before vesicles appear
•Persistent painful crack at the corner of the mouth that does not heal within a week (atypical HSV presentation)
•Recurrent unilateral red painful eye with photophobia — suggests herpes simplex keratitis and warrants urgent ophthalmology review
•Multiple painful genital ulcers within 2-12 days of a new sexual contact — primary genital herpes is high on the differential
•Fever, headache, and confusion in an adult with cold sores — herpes simplex encephalitis must be excluded urgently
● emergency signs
•Fever, headache, behavioral change, seizure, or focal neurological deficit — herpes simplex encephalitis requires immediate empirical IV acyclovir and lumbar puncture for HSV PCR
•Newborn with vesicles, fever, lethargy, poor feeding, or seizures in the first 6 weeks of life — neonatal herpes is a medical emergency with mortality reaching 30%
•Unilateral red painful eye with vision loss, photophobia, or dendritic corneal ulcer — herpes simplex keratitis can scar the cornea permanently if treatment is delayed
•Widespread vesicular rash in a patient with eczema (eczema herpeticum) — disseminated HSV in damaged skin requires hospital admission and IV acyclovir
•Severe genital pain with urinary retention in primary genital herpes — may require catheterization and admission
•Disseminated HSV with multi-organ involvement in immunocompromised patients (transplant recipients, advanced HIV, neonates) — life-threatening and requires IV antivirals
Documents past infection when no lesion is available, helps interpret an unclear first episode (true primary versus newly recognized), and supports counseling of asymptomatic partners.
03
CSF HSV PCR in suspected encephalitisHighly sensitive (96%) and specific (99%) for HSV encephalitis. Combined with MRI brain showing temporal lobe involvement and CSF lymphocytic pleocytosis, it confirms the diagnosis.
04
Viral culture of lesion fluidAlternative when PCR unavailable. Allows antiviral susceptibility testing in immunocompromised patients with suspected acyclovir-resistant HSV.
05
Slit-lamp examination with fluorescein stainingDiagnoses herpes simplex keratitis by visualizing the characteristic branching dendritic corneal ulcer that stains green under cobalt-blue light.
06
MRI brain in suspected HSV encephalitisDemonstrates asymmetric temporal lobe hyperintensity on T2/FLAIR sequences, a hallmark of HSV-1 encephalitis. Helps localize disease and exclude alternative pathology.
07
HIV testing in any newly diagnosed genital HSVHIV co-infection materially changes HSV management — more severe and prolonged outbreaks, higher antiviral doses, longer prophylaxis. CDC recommends co-testing.
Outlook
Herpes simplex infection is a lifelong condition with an excellent long-term prognosis in immunocompetent patients. Recurrence frequency naturally declines with time — outbreak frequency falls by roughly 50% over a decade in HSV-2 carriers, and many patients become outbreak-free by middle age. Daily suppressive therapy reduces clinical outbreaks by 70-80%, reduces asymptomatic shedding by approximately 80%, and cuts transmission to a susceptible partner by about 50%. Genital HSV-1 recurs less often than HSV-2 (median 1 recurrence per year vs 4). Serious complications — encephalitis, neonatal disease, ocular disease, eczema herpeticum, disseminated disease — are uncommon but carry meaningful mortality if untreated; with prompt antiviral therapy, encephalitis mortality drops from over 70% to under 20%, and neonatal disseminated HSV mortality drops from 85% to about 30%. The principal long-term burden is psychological — stigma, anxiety, and relationship impact often outweigh the medical impact. Patients given accurate information, type-specific serology, and the option of suppression typically resume normal sexual and reproductive lives.
Multiple sexual partners or new sexual partnermodifiable
Each additional lifetime sexual partner roughly doubles HSV-2 acquisition risk. Inconsistent condom use, anal sex, and partner with known HSV-2 are independent risk drivers.
Female sexnon-modifiable
Women have approximately twice the seroprevalence of HSV-2 as men at any age. The thinner vulvar and vaginal mucosa offer easier viral entry than penile skin.
Lower socioeconomic status and limited healthcare accessenvironmental
HSV-2 seroprevalence is 2-3 times higher in low-income populations, partly due to earlier sexual debut, higher prevalence in sexual networks, and reduced access to suppressive therapy and counseling.
HIV infection or other immunosuppressionmodifiable
HIV-positive patients shed HSV more frequently, have more severe and prolonged outbreaks, and develop chronic non-healing ulcers. Transplant recipients on calcineurin inhibitors face similar risks.
Agenon-modifiable
HSV-1 seroprevalence rises through childhood and adolescence; HSV-2 rises after sexual debut and peaks around age 40. Each year of additional exposure adds incremental risk.
Atopic dermatitis or eczemamodifiable
Disrupted skin barrier allows widespread cutaneous HSV spread — eczema herpeticum — which can be severe. Patients with active eczema should avoid contact with anyone showing cold sores.
Contact-sport participationmodifiable
Wrestlers, rugby players, and mixed martial artists are at risk for herpes gladiatorum from skin-to-skin contact. NCAA and similar bodies require lesion-free clearance before competition.
Healthcare or dental occupation without barriersmodifiable
Direct contact with oral secretions causes herpetic whitlow. Universal glove use has nearly eliminated occupational HSV among modern dental and medical workers.
Sub-Saharan African residenceenvironmental
WHO estimates HSV-2 prevalence reaches 44% in adult women in sub-Saharan Africa, compared to 12% in the Americas, driven by sexual network density and limited testing.
•
Foods rich in lysine (legumes, fish, poultry, dairy) — theoretically reduce arginine/lysine ratio relevant to viral replication
•Vitamin D-sufficient diet or supplementation — deficiency is associated with more frequent recurrences in observational studies
foods to avoid
•There are no foods that reliably trigger outbreaks; restrictive diets are not evidence-supported
•Excessive alcohol — disrupts sleep and immune function, anecdotally associated with reactivation
•Sharing food or drinks during active orolabial outbreaks to avoid spreading HSV to family members
•Heavily processed, high-arginine snacks (only if dietary lysine therapy is being trialed; evidence is weak)
06Increased HIV acquisition risk — genital HSV-2 ulcers double the per-act risk of HIV transmission to a susceptible partner
07Acyclovir-resistant HSV in immunocompromised patients — chronic non-healing ulcers requiring foscarnet or cidofovir
08Psychosocial impact — anxiety, depression, and relationship strain documented in multiple cohort studies; targeted counseling improves outcomes
If on suppressive therapy, take antivirals at the same time each day — adherence determines outbreak reduction
02Keep a small emergency supply of valacyclovir or famciclovir at home for episodic treatment at first prodrome
03Wash hands thoroughly after touching any active lesion
04Avoid touching eyes during oral or genital outbreaks to prevent ocular HSV
05Note prodromal symptoms early and start antiviral within the 24-hour window for maximum benefit
Exercise
Regular moderate exercise is encouraged and does not trigger outbreaks. During active genital herpes, avoid activities that cause sweat and friction in the affected area (cycling, tight athletic wear) until lesions are crusted. Athletes with herpes gladiatorum must be lesion-free and on suppressive therapy before returning to contact sports — most governing bodies require 5-7 days of suppression and complete crusting.