Herpes PCR (HSV-1 and HSV-2): Diagnosis, Interpretation, and Treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"HSV PCR is the gold standard test for diagnosing herpes simplex (HSV-1 and HSV-2). Genital herpes, cold sores, encephalitis, meningitis, antiviral treatment, and management in Quebec.\">\n<meta name=\"keywords\" content=\"PCR herp\u00e8s HSV, herp\u00e8s simplex diagnostic, HSV-1 HSV-2 traitement, herp\u00e8s g\u00e9nital PCR, enc\u00e9phalite herp\u00e9tique PCR LCR, aciclovir valaciclovir herp\u00e8s, herp\u00e8s r\u00e9current suppressif, herp\u00e8s Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap*{font-family:'Poppins',sans-serif;box-sizing:border-box}\n.co-wrap{max-width:1100px;margin:0 auto;padding:30px 0 60px}\n.co-label{font-family:'Cinzel',serif;font-size:14px;font-weight:bold;letter-spacing:1px;text-transform:uppercase;color:#4D6577;margin-bottom:14px;display:block}\n.co-wrap h1{font-size:32px;font-weight:500;color:#323C52;margin:0 0 22px;line-height:1.2}\n.co-intro{font-size:16px;line-height:1.75;color:#4D6577;margin-bottom:36px;padding-bottom:32px;border-bottom:1px solid rgba(77,101,119,.2)}\n.co-wrap h2{font-size:20px;font-weight:600;color:#323C52;margin:32px 0 12px}\n.co-wrap p{font-size:15px;color:#4D6577;line-height:1.7;margin-bottom:14px}\n.co-list{list-style:none;padding:0;margin:12px 0 24px}\n.co-list li{font-size:15px;color:#4D6577;padding:10px 14px 10px 38px;margin-bottom:8px;border-radius:6px;position:relative;background:rgba(77,101,119,.06);border-left:3px solid #4D6577}\n.co-list li::before{content:\"\u2713\";position:absolute;left:12px;font-weight:700;color:#4D6577}\n.co-table{width:100%;border-collapse:collapse;margin:14px 0 22px;font-size:14px;border-radius:8px;overflow:hidden;table-layout:fixed}\n.co-table thead tr{background:#323C52;color:#fff}\n.co-table thead th{padding:11px 16px;text-align:left;font-weight:600;font-size:13px}\n.co-table tbody tr:nth-child(even){background:rgba(77,101,119,.06)}\n.co-table tbody tr:nth-child(odd){background:#fff}\n.co-table td{padding:10px 16px;color:#4D6577;border-bottom:1px solid rgba(77,101,119,.12);font-size:14px;vertical-align:top}\n.co-table td:first-child{font-weight:600;color:#323C52}\n.co-infobox{display:flex;gap:12px;background:rgba(77,101,119,.06);border-radius:8px;border-left:4px solid #4D6577;padding:14px 18px;margin:18px 0 28px;font-size:14px;color:#4D6577;line-height:1.65}\n.co-infobox .ico{font-size:18px;flex-shrink:0}\n.co-urgence{background:#fff8f8;border-left:5px solid #c0392b;border-radius:6px;padding:20px 26px;margin:24px 0 32px}\n.co-urgence .co-urgence-titre{font-size:13px;font-weight:700;color:#c0392b;letter-spacing:1.5px;text-transform:uppercase;margin-bottom:10px}\n.co-urgence p{color:#5a2020;font-size:14px;margin:0 0 10px;line-height:1.7}\n.co-urgence p:last-child{margin-bottom:0}\n.co-disclaimer{font-size:13px;color:#8a9aaa;font-style:italic;border-top:1px solid rgba(77,101,119,.15);padding-top:24px;margin-top:40px;line-height:1.6}\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Infectious Diseases & Dermatology & Neurology & Family Medicine<\/span>\n <h1>Herpes PCR (HSV-1 and HSV-2)<\/h1>\n\n <div class=\"co-intro\">\n Herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2) are double-stranded DNA viruses of the Herpesviridae family, characterized by their ability to establish a lifelong latent infection in sensory ganglia after primary infection, with periodic symptomatic or asymptomatic reactivations. PCR (polymerase chain reaction) has become the reference test for the diagnosis of all forms of HSV infection - definitively supplanting viral culture, Tzanck cytology and serology in most clinical contexts - due to its far superior sensitivity (90-100 %), near-absolute specificity (99-100 %), rapidity (results in 2-6 hours for multiplex panels) and ability to differentiate HSV-1 from HSV-2. HSV PCR on cerebrospinal fluid (CSF) is indispensable in the diagnosis of herpes encephalitis - the most frequent cause of fatal sporadic viral encephalitis in developed countries - where one hour's delay in IV aciclovir can definitively compromise the neurological prognosis. PCR on genital, urethral, cervical or anal swabs is the method of choice for diagnosing genital herpes, replacing Vero cell culture, whose sensitivity fell to 30-50 % in the healing phase. Type-specific serology (gG-based serology) has a distinct place in partner screening and management, but should not be used as a replacement for PCR for the diagnosis of an active clinical episode.\n <\/div>\n\n <h2>Virology, epidemiology, and pathophysiology<\/h2>\n <ul class=\"co-list\">\n <li><strong>Viral biology and mechanisms of latency and reactivation:<\/strong> structure and biology : HSV-1 and HSV-2 = enveloped viruses with 152 kb linear double-stranded DNA \u2192 family Herpesviridae (subfamily Alphaherpesvirinae) \u2192 11 envelope glycoproteins (gB + gC + gD + gE + gG + gH + gI + gJ + gK + gL + gM) \u2192 gD = main fusion protein and target of neutralizing antibodies \u2192 gG = glycoprotein type-specificity \u2192 gG-1 vs gG-2 \u2192 basis for type-specific serological tests \u2192 replication cycle : attachment via gB\/gC to heparan sulfates + binding of gD to entry receptors (nectin-1 + nectin-2 + HVEM + 3-O-sulfate HS) \u2192 envelope fusion \u2192 internalization of nucleocapsid \u2192 transport to nucleus \u2192 viral DNA replication \u2192 budding release + retrograde axonal transport to sensory ganglia \u2192 latency; latency mechanisms in sensory ganglia: retrograde axonal transport of virion along axons \u2192 trigeminal ganglion (HSV-1) or sacral ganglion S2-S4 (HSV-2) \u2192 circularization of viral DNA \u2192 formation of episomes in neuronal nuclei \u2192 limited transcription of LATs (Latency-Associated Transcripts) \u2192 non-coding RNAs \u2192 inhibit neuronal apoptosis \u2192 maintain latency \u2192 reactivation mechanisms: triggering stimuli: psychological stress + immunosuppression + UV (herpes labialis) + fever + microtrauma (sexual intercourse \u2192 genital herpes) + menstruation + trigeminal ganglion surgery \u2192 anterograde axonal transport \u2192 replication in skin or mucosal epithelia \u2192 symptomatic or asymptomatic viral shedding \u2192 Spruance 1977 - Lancet: pathophysiological model of the HSV latency-reactivation cycle \u2192 Bloom 2010 - Journal of Neurovirology: molecular mechanisms of HSV latency + role of LATs; global and Canadian epidemiology: HSV-1 seroprevalence: 67 % of world population (Looker 2015 - PLOS ONE: WHO meta-analysis \u2192 3.7 billion people under 50 years of age HSV-1 carriers) \u2192 genital HSV-1: 30-50 % of genital primary infections in high-income countries \u2192 increase in young adults (decrease in oral exposure in childhood) \u2192 HSV-2 seroprevalence: 11 % worldwide (Looker 2015 - PLOS ONE) \u2192 491 million carriers aged 15-49 \u2192 Canada: HSV-2 seroprevalence \u2248 14-16 % adults \u2192 HSV-1 seroprevalence \u2248 60-67 % adults \u2192 asymptomatic viral shedding (AVE): key mechanism of transmission \u2192 Tronstein 2011 - JAMA: 9 % of days \u2192 HSV-2 excreted asymptomatically \u2192 76 % of excretion is asymptomatic \u2192 up to 5 daily micro-short (<6h) episodes \u2192 responsible for the majority of transmissions because the source partner is asymptomatic \u2192 Schiffer 2010 - PLOS Medicine: modeling asymptomatic excretion \u2192 fountain model (fountain model) \u2192 multiple daily reactivations of short duration \u2192 biological differences HSV-1 vs HSV-2: HSV-2 \u2192 frequency of genital recurrences 5.1 recurrences\/year vs genital HSV-1 1.3 recurrences\/year (Langenberg 1999 - Annals of Internal Medicine) \u2192 HSV-2 \u2192 more frequent asymptomatic excretion \u2192 HSV-1 \u2192 more frequent in encephalitis + recurrent herpes labialis \u2192 different neurotropism + different antiviral resistances (TK-mutations for aciclovir - more frequent under immunosuppression)<\/li>\n <li><strong>Clinical manifestations by type and location:<\/strong> orofacial herpes (HSV-1 predominant): primary infection (herpetic gingivostomatitis): children 1-5 years + young adults \u2192 vesicles + painful erosions on gingiva + oral mucosa + palate + lips + cervical adenopathies + fever + dysphagia + duration: 7-14 days + 10-15 % of symptomatic primary infections \u2192 recurrent herpes labialis (cold sore): vesicles clustered at labial mucocutaneous junction \u2192 5 phases: prodrome (1-2d) + vesicular (2-3d) + pustular + ulcerative + healing \u2192 total duration: 8-10 days + recurrences: 1-6\/year on average \u2192 triggers: UV + stress + fever + menstruation + local trauma \u2192 ocular herpes: dendritic keratitis (fern-leaf corneal ulcer) + conjunctivitis + uveitis \u2192 HSV-1 = leading cause of infectious corneal blindness in developed countries (Wilhelmus 2008 - Cochrane) \u2192 herpetic panariasis (herpetic whitlow): finger \u00b1 in caregivers or nail-drinkers; genital herpes (HSV-2 predominant but HSV-1 increasing): genital primary infection: often asymptomatic (60-80 %) or not very typical \u2192 if symptomatic: vesicles + painful erosions on penis + vulva + vagina + cervix + perineal + anorectal region + aseptic meningitis (15-30 % of HSV-2 primary infections) \u2192 urinary retention syndrome + 20-40 days resolution \u2192 prolonged viral excretion + recurrences : HSV-2 genital \u2192 5-7 recurrences\/year on average in the first few years \u2192 HSV-1 genital \u2192 1-3 recurrences\/year + prodromes (burning + tingling) 12-24h before \u2192 prevalence of atypical manifestations (fissure + erythematous papule + pain without visible lesion) \u2192 frequent underdiagnosis; severe forms and complications: herpetic encephalitis: HSV-1 involved in 90 % of cases + life-threatening neurological emergency \u2192 fever + behavioral disorders + olfacto-gustatory hallucinations + headaches + disorientation \u2192 temporal localization (temporal gyrus + insula + cingulate) \u2192 Whitley 1982 - NEJM: IV aciclovir vs vidarabine in herpetic encephalitis \u2192 mortality reduced by 70 % \u2192 28 % (aciclovir) vs 54 % (vidarabine) \u2192 time to treatment = major prognostic factor \u2192 if treatment within first 4 days: mortality 1 month = AIDS criterion) <\/ul>\n\n <h2>Diagnostic by PCR, serology, and treatment<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Domain<\/th><th>Data, modalities, and criteria<\/th><th>Key studies and recommendations<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>PCR HSV \u2014 methods, sample collection, and diagnostic performance<br><small style=\"font-weight:400;color:#7a8fa0;\">Real-time PCR \u2014 multiplex \u2014 LCR \u2014 genital sample \u2014 swabbing \u2014 HSV-1\/HSV-2 differentiation \u2014 false negatives \u2014 sensitivity\/specificity<\/small><\/td>\n <td>HSV PCR methods available: quantitative or qualitative real-time PCR (qPCR): reference method \u2192 amplification of a conserved region of the HSV genome (glycoprotein B genes or DNA polymerase - UL30) \u2192 TaqMan or SYBR Green probes \u2192 results in 2-4h \u2192 sensitivity: 95-100 % \u2192 specificity: 99-100 % \u2192 HSV-1\/HSV-2 differentiation by type-specific probes \u2192 viral load quantification possible (useful in encephalitis and monitoring of the immunocompromised) \u2192 multiplex PCR on CSF (example: BioFire FilmArray Meningitis\/Encephalitis Panel): simultaneous detection of 14 agents (HSV-1 + HSV-2 + CMV + HHV-6 + EBV + VZV + enterovirus + parechovirus + meningeal bacteria) \u2192 results in 1h \u2192 very useful in emergencies \u2192 but: sensitivity slightly lower than conventional PCR for some rare agents \u2192 high cost \u2192 viral culture (historical method): Vero cells or human diploid cells \u2192 EPC (cytopathogenic effect) visible in 2-7d \u2192 sensitivity: 70-85 % in vesicular phase \u2192 30-50 % in healed ulcer phase \u2192 abandoned in practice in favor of PCR \u2192 useful if antiviral resistance suspected (viral antibiogram) \u2192 Tzanck cytology: multinucleated giant cells (Cowdry type A intranuclear inclusion) \u2192 sensitivity: 50-70 % \u2192 very unspecific (does not differentiate HSV from VZV) \u2192 only in limited resources \u2192 direct immunofluorescence (DIF): fluorescent monoclonal antibodies + sensitivity: 70-85 % + gradual abandonment in favor of PCR; types of samples and preanalytical conditions: lesion sampling (mucocutaneous herpes) : dacron or nylon swab (no cotton - PCR inhibitors) \u2192 rub the base of the lesion vigorously (ruptured blister or active ulcer) \u2192 place in Universal Transport Medium (UTM) or PBS \u2192 store at +4\u00b0C \u2192 analyze within 48-72h \u2192 sensitivity decreases sharply if lesion is healing \u2192 frequent false negatives if : crusty lesion + delay between sampling and analysis + poor technique (insufficient superficial sampling) + insufficient volume \u2192 CSF sampling (meningitis + herpetic encephalitis): lumbar puncture \u2192 CSF in a sterile tube \u2192 HSV PCR on CSF: reference method \u2192 sensitivity: 96-98 % + specificity: 99 % \u2192 Aurelius 1993 - Lancet: PCR on CSF \u2192 diagnostic revolution in herpetic encephalitis \u2192 replaces brain biopsy as gold standard \u2192 do not delay aciclovir while waiting for PCR \u2192 result may be falsely negative if: sampling <72h after onset of symptoms + rare but documented early false negative \u2192 repeat LP at 48-72h if strong clinical suspicion and first negative result \u2192 genital sampling: urethral swab (male) + cervical or vaginal swab (female) + swab of visible lesions \u2192 PCR on desquamated cells \u2192 do not use lubricating gel (PCR inhibitor) + rectal or anal swab if anal herpes suspected \u2192 PCR on oral or pharyngeal lesions \u2192 direct swabbing; comparative sensitivity of methods according to lesion stage: vesicular phase: PCR = 100 % + culture = 85 % + Tzanck = 70 % \u2192 ulcerative phase: PCR = 95 % + culture = 60 % \u2192 scabby phase: PCR = 70 % + culture = 30 % \u2192 healed lesion: PCR = 40 % (residual DNA) + culture = 0 % \u2192 PCR is 3-5\u00d7 more sensitive than culture on lesions in regression phase \u2192 saliva sample \/ genital secretion without visible lesion: EVA (asymptomatic viral excretion) \u2192 PCR detects EVA \u2192 does not immediately predict contagiousness as quantities are small \u2192 epidemiological value + useful in serodiscordant couple workup + Wald 2001 - JAMA: asymptomatic HSV-2 excretion \u2192 detected in 28 % of specimens in HSV-2 seropositive women without symptoms \u2192 antiviral resistance workup: culture + antibiogram (IC50 aciclovir) \u2192 mutations in the TK gene (UL23) or DNA polymerase (UL30) \u2192 indication: clinical resistance (persistent lesions on aciclovir after 14-21d in the immunocompromised) \u2192 alternative treatment: foscarnet + cidofovir<\/td>\n <td>Fundamental data on diagnostic performance: Aurelius 1993 - Lancet: CSF PCR in herpetic encephalitis \u2192 sensitivity 96 % + specificity 99 % \u2192 diagnostic revolution \u2192 abandons brain biopsy as gold standard \u2192 Corey 1992 - Sexually Transmitted Diseases: PCR vs culture for diagnosis of genital herpes \u2192 PCR 3-5\u00d7 more sensitive on lesions in regression phase \u2192 Wald 1995 - Annals of Internal Medicine: lesion PCR = reference method for genital herpes \u2192 sensitivity 98 % in active phase \u2192 Wald 2001 - JAMA: asymptomatic HSV-2 shedding \u2192 28 % of PCR-positive specimens in symptomless HIV-positive women \u2192 serodiscordant couple workup \u2192 Tronstein 2011 - JAMA (prospective cohort): 9 % of HSV-2 days excreted + 76 % asymptomatic excretion \u2192 PCR is the essential tool for VAS measurement + IDSA 2015: PCR = test of choice for all HSV syndromes \u2192 replaces culture + CDC 2021 STI Guidelines: PCR on genital lesion or swab \u2192 reference test for genital herpes \u2192 type-specific (gG) serology reserved for asymptomatic screening + STI national guidelines Canada 2022 (PHAC): HSV PCR = test of choice in Canada<\/td>\n <\/tr>\n <tr>\n <td>HSV Type-Specific Serology (gG-based) \u2014 Role and Limitations<br><small style=\"font-weight:400;color:#7a8fa0;\">IgG HSV-1 \u2014 IgG HSV-2 \u2014 reactivity index \u2014 serological window \u2014 false positives \u2014 asymptomatic screening \u2014 serodiscordant couple<\/small><\/td>\n <td>Type-specific gG-based serology - principles: detects IgG against the glycoprotein G of HSV-1 (gG-1) and HSV-2 (gG-2) \u2192 the two antigens are sufficiently different to allow reliable distinction between serotypes \u2192 methods: ELISA (HerpeSelect 2 Focus Diagnostics + Captia Herpes Select + Trinity Biotech) \u2192 immunoblot (Kalon HSV-2) \u2192 results expressed as index of reactivity (IR): for HerpeSelect ELISA \u2192 IR \u22651,10 = positive \u2192 IR 1,10-3,49 = gray area \u2192 IR \u22653,50 = strong positive \u2192 problem of false positives in the gray area (IR 1,10-3,49) \u2192 confirmations recommended by Western blot or immunoblot (Johnston 2016 - Sexually Transmitted Infections: false positive in 50-80 % of IRs between 1.10 and 3.49 if low prevalence) \u2192 HSV-2 serology does not provide information on site of infection or active nature \u2192 serological window: anti-HSV IgG appear 2-12 weeks after primary infection \u2192 a negative result within the first 12 weeks does not exclude infection \u2192 do not use serology to diagnose an acute episode + current role of type-specific serology: asymptomatic screening in high-risk individuals (MSM + UDIV + multiple partners + history of STI) \u2192 assessment of serodiscordant couple: identify source partner + adapt prevention measures \u2192 pregnant woman with HSV-2 seropositive partner: screening to assess risk of periconceptional acquisition \u2192 patients with atypical picture whose diagnosis of genital herpes is suspicious but without active lesion \u2192 decision on suppressive therapy \u2192 USPSTF 2023: routine screening for HSV-2 by serology is not recommended in the asymptomatic general population without risk factors \u2192 serology is recommended in the clinical contexts listed above \u2192 HSV IgM: not recommended \u2192 does not reliably distinguish primary infection and reactivation \u2192 often false positive by cross-reactivity + not type-specific \u2192 to be avoided; interpretation of common serological profiles: HSV-1 IgG + \/ HSV-2 IgG - : HSV-1 seropositivity only \u2192 oral infection in childhood in most cases \u2192 an episode of genital herpes in this context \u2192 genital HSV-1 primary infection possible + HSV-2 IgG + : HSV-2 infection (most often genital) \u2192 suppressive therapy to be considered + preventive measures \u2192 both positive : double seropositivity \u2192 very frequent (50-60 % of sexually active adults in certain populations) + HSV-1 IgG - \/ HSV-2 IgG - : uninfected \u2192 susceptible \u2192 preventive counseling + HSV-2 IgG in the gray area (IR 1.10-3.49) \u2192 confirm by Western immunoblot before concluding<\/td>\n <td>Fundamental data on serology: Johnston 2016 - Sexually Transmitted Infections: HerpeSelect ELISA in IR 1.10-3.49 \u2192 false positives 50-80 % if low prevalence \u2192 confirmation by immunoblot recommended \u2192 Looker 2015 - PLOS ONE (WHO meta-analysis): worldwide HSV-1 seroprevalence: 67 % + HSV-2: 11 % \u2192 3.7 billion and 491 million carriers respectively \u2192 Wald 2005 - NEJM: suppressive treatment with valaciclovir \u2192 reduction of HSV-2 transmission to serodiscordant partners by 48 % \u2192 demonstration that serology + suppression are a prevention strategy + Tronstein 2011 - JAMA: HSV-2 VAS \u2192 9 % days + 76 % asymptomatic \u2192 serology identifies asymptomatic carriers \u2192 preventive measures \u2192 USPSTF 2023: no routine HSV-2 screening by serology in general population \u2192 but in high-risk settings + Langenberg 1999 - Annals of Internal Medicine: HSV-2 genital recurrences 5.1\/year vs HSV-1 genital 1.3\/year \u2192 basis for suppressive therapy decision according to type \u2192 CDC 2021 STI Guidelines + STI Canada 2022 (PHAC): serology algorithm in STI \u2192 validated contexts of use<\/td>\n <\/tr>\n <tr>\n <td>Antiviral Treatment \u2014 Acyclovir, Valacyclovir, Famciclovir, and Special Situations<br><small style=\"font-weight:400;color:#7a8fa0;\">Acyclovir \u2014 Valacyclovir \u2014 Famciclovir \u2014 Encephalitis \u2014 Neonatal \u2014 Genital \u2014 Suppressive \u2014 Pregnancy \u2014 Immunocompromised \u2014 Resistance \u2014 Foscarnet<\/small><\/td>\n <td>Mechanism of action of anti-HSV antivirals: aciclovir (aciclovir = ACV + valaciclovir = aciclovir prodrug \u00d7 3-5 best oral bioavailability + famciclovir = penciclovir prodrug) : viral TK (thymidine kinase) phosphorylates aciclovir to aciclovir monophosphate \u2192 cellular kinases add 2nd and 3rd phosphates \u2192 aciclovir triphosphate \u2192 guanosine triphosphate (GTP) competitor \u2192 incorporation into growing viral DNA by viral DNA polymerase (UL30) \u2192 DNA chain termination (absence of the 3'-OH group) \u2192 viral DNA polymerase is 10-30\u00d7 more sensitive to inhibition by aciclovir triphosphate than cellular DNA polymerase \u2192 very good therapeutic index \u2192 no toxicity on uninfected cells + resistance : TK gene mutation (UL23) \u2192 non-functional TK \u2192 no phosphorylation \u2192 resistance \u2192 or DNA polymerase mutation (UL30) \u2192 less frequent \u2192 treatment of resistance : foscarnet (direct inhibitor of viral DNA polymerase - no need for TK phosphorylation) + or cidofovir (nephrotoxic); treatment of herpetic encephalitis - absolute emergency: aciclovir IV 10 mg\/kg \u00d7 3\/d \u00d7 14-21 days (in immunocompetent adults) \u2192 adjustment according to renal function (longer interval if CKD) \u2192 Whitley 1986 - NEJM : IV aciclovir vs vidarabine \u2192 mortality 28 % vs 54 % \u2192 aciclovir = standard of care since 1986 \u2192 Raschilas 2002 - Annals of Neurology: prognostic factors in herpetic encephalitis \u2192 time to treatment + age + Glasgow score on admission \u2192 treatment before D4 = major protective factor \u2192 if strong clinical suspicion + inflammatory CSF \u2192 start IV aciclovir WITHOUT waiting for PCR result (early treatment takes priority over confirmation) \u2192 assess response at D7 by control CSF PCR \u2192 duration 21 days if severe or immunocompromised \u2192 oral relay (valaciclovir 2 g \u00d7 3\/d \u00d7 3 months in some postencephalitis protocols); treatment of genital herpes: primary infection: aciclovir 400 mg \u00d7 3\/d \u00d7 7-10d OR valaciclovir 1 g \u00d7 2\/d \u00d7 7-10d OR famciclovir 250 mg \u00d7 3\/d \u00d7 7-10d \u2192 Mertz 1984 - NEJM: aciclovir in primary genital infection \u2192 reduction in duration of symptoms from 5 to 8 days + reduction in duration of viral excretion \u2192 standard of care since the 1980s \u2192 symptomatic recurrence (episodic treatment): valaciclovir 500 mg \u00d7 2\/d \u00d7 3-5d OR aciclovir 800 mg \u00d7 3\/d \u00d7 2d (short regimen) OR famciclovir 1,000 mg \u00d7 2\/d \u00d7 1d (single dose) \u2192 to be initiated within 24 h of prodrome or appearance of lesions \u2192 continuous suppressive therapy: valaciclovir 500 mg\/d \u00d7 12 months (or indefinite) \u2192 indicated if: \u22656 recurrences\/year + or reduction in transmission to HIV-negative partner + or anxiety related to recurrences + or pregnancy \u2192 Reitano 1998 - Journal of Infectious Diseases: valaciclovir 500 mg\/d \u2192 reduction in recurrences by 80 % + reduction in VAS \u2192 Wald 2005 - NEJM (PARTNERS study): valaciclovir 500 mg\/d in serodiscordant couple \u2192 reduced transmission by 48 % + reduced recurrences by 79 % \u2192 dual role (suppressive + transmission preventive) \u2192 Strauss 1984 - NEJM: first trial suppressive aciclovir in genital \u2192 reduction in recurrences + feasibility; recurrent herpes labialis (topical + oral aciclovir): topical aciclovir (Zovirax cream): reduces duration from \u00bd to 1 day \u2192 modest efficacy + Spruance 2003 - Antimicrobial Agents and Chemotherapy: valaciclovir 2 g \u00d7 2 taken 12h apart \u2192 single dose \u2192 reduction in lesion duration by 1.5 days + abortive effect of the episode in 40 % of cases \u2192 taken as soon as prodrome \u2192 famciclovir 1,500 mg single dose (Spruance 2006 - JAMA) \u2192 penciclovir cream (Denavir): Spruance 1997 - JAMA \u2192 reduced duration; neonatal herpes (Kimberlin 2001 - NEJM CASG 103): aciclovir IV 60 mg\/kg\/d divided into 3 doses \u00d7 14-21 days \u2192 depending on form \u2192 disseminated or CNS form: 21 days \u2192 after IV: suppressive oral aciclovir 300 mg\/m\u00b2\/dose \u00d7 3\/d \u00d7 6 months \u2192 significant improvement in survival + neurological development; pregnancy and herpes \u2192 prevention of neonatal transmission: woman with primary HSV infection in late pregnancy (3rd trimester): aciclovir 400 mg \u00d7 3\/d from 36 SA \u2192 reduction of viral excretion at the time of delivery \u2192 or Caesarean section if active lesions in labor + woman with recurrence of genital HSV herpes in late pregnancy: aciclovir 400 mg \u00d7 3\/d from 36 SA \u2192 ACOG 2020 + SOGC 2008 \u2192 recommendation to reduce the risk of neonatal transmission + woman with active lesions at the time of labor \u2192 cesarean section recommended \u2192 no contraindication to breastfeeding if no lesions in the breast; immunocompromised (HIV + transplant patients + chemotherapy): high-dose IV or oral aciclovir \u2192 valaciclovir 1 g \u00d7 2\/d \u2192 antiviral prophylaxis indicated if CD4 <200 or profound immunosuppression \u2192 Gnann 2012 - NEJM: aciclovir IV + immunosuppressed with disseminated herpes \u2192 reduced mortality + Kimberlin 1996 - Journal of Infectious Diseases: resistance to aciclovir in immunosuppressed patients \u2192 foscarnet 40-60 mg\/kg \u00d7 3\/d IV \u2192 cidofovir 5 mg\/kg IV qwk \u00d7 2 with hydration and probenecid<\/td>\n <td>Fundamental data on treatment: Whitley 1982 - NEJM: aciclovir IV vs vidarabine in herpetic encephalitis \u2192 mortality 28 % vs 54 % \u2192 aciclovir = absolute standard + Whitley 1986 - NEJM: confirmation of superiority \u2192 therapeutic revolution \u2192 Raschilas 2002 - Annals of Neurology (n=93 encephalitis): treatment delay <4d \u2192 major prognostic factor \u2192 treatment without waiting for PCR if strong suspicion + Mertz 1984 - NEJM: aciclovir in genital primary infection \u2192 reduction in duration from 5-8 days \u2192 founder + Reitano 1998 - JID: valaciclovir 500 mg\/d suppressive \u2192 -80 % recurrences + Wald 2005 - NEJM (PARTNERS trial): valaciclovir 500 mg\/d + serodiscordant couple \u2192 -48 % transmission \u2192 demonstration of preventive role + Spruance 2003 - AAC: valaciclovir 2 g \u00d7 2 doses \u2192 abortion 40 % labial episode \u2192 Kimberlin 2001 - NEJM (CASG 103): aciclovir IV 60 mg\/kg\/d neonatal \u2192 reduced disseminated mortality + better neurological development + 6-month suppression \u2192 ACOG 2020 + SOGC 2008: suppressive aciclovir from 36 SA if history of genital herpes + CDC 2021 STI Guidelines + STI Canada 2022 ASPC: recommendations for episodic + suppressive + pregnancy prophylaxis treatment<\/td>\n <\/tr>\n <tr>\n <td>Prevention, partner screening, and special situations<br><small style=\"font-weight:400;color:#7a8fa0;\">Condom \u2014 HSV PrEP \u2014 Transmission \u2014 Serodiscordant Couple \u2014 HIV + HSV \u2014 Mollaret's Meningitis \u2014 Ocular Herpes \u2014 Informed Consent<\/small><\/td>\n <td>Prevention of HSV transmission: condom: reduces transmission risk by 50 % (Wald 2001 - JAMA) \u2192 but protection is incomplete as lesions or asymptomatic excretion may be present in areas not covered by the condom (perineum + pubis + buttock + periscrotal skin) \u2192 suppressive treatment with valaciclovir: additional 48 % reduction in transmission (Wald 2005 - NEJM PARTNERS trial) \u2192 combination condom + valaciclovir \u2192 estimated >90 % reduction in transmission by modeling \u2192 abstinence during active episodes (symptoms + visible lesions) + counseling on asymptomatic shedding \u2192 asymptomatic patient may transmit unknowingly \u2192 Tronstein 2011 - JAMA: asymptomatic transmission in the majority of cases \u2192 patient education essential \u2192 HSV vaccine: Simplirix (GSK - adjuvanted gD-2 vaccine) : HERPEVAC Trial (Stanberry 2002 - NEJM): efficacy 73 % in doubly seronegative women (HSV-1- and HSV-2-) \u2192 no protection in HSV-1+ men or women \u2192 partial and short-lived efficacy \u2192 not marketed \u2192 2nd and 3rd generation vaccines in trials (DNA + recombinant proteins + mRNA) \u2192 no vaccine available in Canada in 2026 + management of serodiscordant couple: identify source partner \u2192 type-specific serology of both partners \u2192 if seronegative receiving partner \u2192 counseling + suppressive treatment of source partner + condom + avoid intercourse during outbreaks \u2192 discuss voluntary reporting (no legal requirement to report genital herpes in Canada); HSV-2 and HIV - major bidirectional interaction: HSV-2 \u2192 increases the risk of HIV acquisition by 2-3\u00d7 (Wald 2009 - Current Opinion in Infectious Diseases) \u2192 mechanism: genital erosions and ulcerations \u2192 HIV entry doors + reactivation of HIV replication at HSV foci of inflammation \u2192 HIV patient + HSV-2 \u2192 increased HIV viral load in genital secretions during HSV episodes \u2192 HSV-2 suppressive therapy in HIV+ patients: reduces HSV shedding + slightly lowers HIV viral load + Celum 2010 - NEJM (HPTN 039): aciclovir 400 mg \u00d7 2\/d in HSV-2\/HIV-positive patients \u2192 reduced HIV acquisition by 7 % (not significant) \u2192 aciclovir alone is insufficient to prevent HIV acquisition \u2192 HIV PrEP remains the strategy of choice + Barnabas 2016 - NEJM: valaciclovir + HIV positive + HSV-2 \u2192 reduction of HSV episodes + modest lowering of HIV viral load \u2192 but no effect on HIV transmission; Mollaret meningitis (recurrent HSV-2 meningitis): recurrent episodes of lymphocytic aseptic meningitis + fever + meningismus + headache \u2192 duration 3-5d per episode + several episodes over years \u2192 pathognomonic: Mollaret cells (large endothelial cells in CSF - historical observation not pathognomonic in reality) \u2192 diagnosis: HSV-2 PCR on CSF during an acute episode \u2192 treatment: aciclovir IV or oral \u00d7 5-7d per episode + valaciclovir prophylaxis 500-1,000 mg\/d if frequent episodes \u2192 favorable prognosis \u2192 ocular herpes - herpetic keratitis: HSV-1 as main cause \u2192 dendritic keratitis (fern-leaf epithelial ulcer) \u2192 treatment: ophthalmic aciclovir 3 % ointment \u00d7 5\/d \u00d7 10-14d + or ganciclovir ophthalmic gel 0.15 % \u00d7 5\/d + or trifluridine eye drops (Viroptic) \u2192 CONTRAINDICATION of ocular topical corticoids in the absence of antiviral (aggravation of corneal herpes) \u2192 Wilhelmus 2008 - Cochrane: trifluridine + IDU + aciclovir \u2192 comparable efficiencies for epithelial keratitis \u2192 stromal ocular herpes (stromal keratitis - immune lesion) \u2192 corticoids + oral antiviral \u2192 ophthalmic opinion + suppressive therapy: aciclovir 400 mg \u00d7 2\/d \u2192 prevention of recurrences + HEDS Trial (Herpetic Eye Disease Study - Wilhelmus 1994 - Archives of Ophthalmology): oral aciclovir \u2192 41 % reduction in ocular recurrences \u2192 recommended if frequent recurrences <\/td>\n <td>Fundamental data on prevention and special situations: Wald 2001 - JAMA: condom \u2192 transmission reduction 50 % + EVA 28 % of HSV-2 seropositive female samples \u2192 educational role + Wald 2005 - NEJM (PARTNERS trial): valaciclovir 500 mg\/d + serodiscordant couple \u2192 -48 % HSV-2 transmission \u2192 rigorous demonstration of preventive role of suppressive therapy + Stanberry 2002 - NEJM (HERPEVAC): gD-2 vaccine \u2192 73 % efficacy doubly seronegative women \u2192 not marketed \u2192 2nd-generation vaccine expected + Wald 2009 - Current Opinion in Infectious Diseases: HSV-2 \u2192 increased risk of HIV acquisition \u00d7 2-3 \u2192 bidirectional interaction + Celum 2010 - NEJM (HPTN 039): aciclovir + HSV-2\/HIV- \u2192 reduced HIV acquisition 7 % (not significant) \u2192 HIV PrEP remains the primary strategy + Tronstein 2011 - JAMA: EVA \u2192 mostly asymptomatic transmission \u2192 mandatory counseling + Wilhelmus 2008 - Cochrane: comparable ocular treatments \u2192 HEDS Trial Wilhelmus 1994 - Archives of Ophthalmology: oral aciclovir \u2192 reduced ocular recurrences 41 % + CDC 2021 STI + STI Canada 2022 ASPC + ACOG 2020 + SOGC 2008: recommendations for prevention and management of herpes during pregnancy<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>In case of suspected herpes encephalitis, start IV acyclovir immediately without waiting for PCR results.<\/strong> Herpes simplex encephalitis is the most common cause of fatal viral encephalitis. Every hour of delay in acyclovir treatment increases the risk of irreversible neurological sequelae and death. HSV PCR on CSF (sensitivity 96-98 %) is the gold standard test, but it should never delay treatment. If clinical suspicion is high (fever + behavioral changes + seizures + temporal lobe involvement on MRI), IV acyclovir 10 mg\/kg \u00d7 3\/day should be started as soon as lumbar puncture is performed, even before results are available.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations Requiring a 911 Call or Urgent Medical Attention<\/div>\n <p><strong>Fever + intense headaches + behavioral or memory disturbances + olfactory-gustatory hallucinations + confusion + seizures + MRI showing abnormal temporal signal<\/strong> Herpes encephalitis \u2192 Call 911 \u2192 Emergency hospitalization \u2192 Lumbar puncture + CSF PCR + Start IV acyclovir 10 mg\/kg \u00d7 3\/day WITHOUT waiting for results \u2192 Every hour of delay worsens the neurological prognosis.<\/p>\n <p><strong>Newborn with fever + irritability + skin vesicles + seizures + jaundice + hemodynamic instability whose mother had a primary herpes infection late in pregnancy or active lesions at delivery<\/strong> neonatal herpes \u2192 pediatric emergencies \u2192 acyclovir IV 60 mg\/kg\/day \u00d7 3 doses \u2192 HSV PCR blood + CSF + skin swab + funduscopy \u2192 NICU if available.<\/p>\n <p><strong>Immunocompromised patient (HIV + transplant + chemotherapy) with persistent or spreading cutaneous or mucosal herpes lesions despite oral acyclovir for >14 days<\/strong> \u2192 Possible acyclovir resistance \u2192 Lesional PCR + culture + viral antibiogram \u2192 Infectious disease consultation \u2192 IV foscarnet if TK resistance confirmed \u2192 do not increase acyclovir alone.<\/p>\n <p><strong>Eye pain + photophobia + corneal ulcer visible with a slit lamp or decreased visual acuity + history of ocular herpes.<\/strong> Recurrent herpetic keratitis \u2192 urgent ophthalmological consultation \u2192 acyclovir ophthalmic ointment or ganciclovir gel \u2192 never use ocular corticosteroids alone without antivirals (possible worsening of herpetic keratitis).<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron physicians prescribe PCR HSV on lesion or genital samples for the diagnosis of herpes simplex, initiate episodic or suppressive antiviral treatment as appropriate, prescribe type-specific serology for validated indications (serodiscordant couple + STI workup + pregnancy), refer to the emergency department in cases of suspected herpes encephalitis or neonatal herpes, and provide transmission prevention counseling. Consultations are available at several service points in Quebec and via telemedicine. To make an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The content of this page is for informational purposes only and does not substitute for the advice of a physician or infectious disease specialist. Herpes encephalitis and neonatal herpes are medical emergencies requiring immediate IV treatment without diagnostic delay.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Herp\u00e8s PCR (HSV-1 et HSV-2) : diagnostic, interpr\u00e9tation et traitement | Clinique Omicron Infectiologie & Dermatologie & Neurologie & M\u00e9decine de famille Herp\u00e8s PCR (HSV-1 et HSV-2) Les virus de l’herp\u00e8s simplex de type 1 (HSV-1) et de type 2 (HSV-2) sont des virus \u00e0 ADN double brin de la famille des Herpesviridae, caract\u00e9ris\u00e9s par… <a href=\"https:\/\/cliniqueomicron.ca\/en\/herpes-pcr-hsv-1-et-2\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Herpes PCR (HSV-1 and HSV-2): Diagnosis, Interpretation, and Treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Herp\u00e8s PCR (HSV-1 et HSV-2) : | Brossard | Clinique Omicron","_metasync_otto_description":"La PCR HSV est le test de r\u00e9f\u00e9rence pour diagnostiquer l'herp\u00e8s simplex (HSV-1 et HSV-2). Herp\u00e8s g\u00e9nital, labial, enc\u00e9phalite, m\u00e9ningite, traitement antivira...","_metasync_otto_keywords":"","_metasync_otto_og_title":"Herp\u00e8s PCR (HSV-1 et HSV-2) : | Brossard | Clinique Omicron","_metasync_otto_og_description":"La PCR HSV est le test de r\u00e9f\u00e9rence pour diagnostiquer l'herp\u00e8s simplex (HSV-1 et HSV-2). Herp\u00e8s g\u00e9nital, labial, enc\u00e9phalite, m\u00e9ningite, traitement antivira...","_metasync_otto_twitter_title":"Herp\u00e8s PCR (HSV-1 et HSV-2) : | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"La PCR HSV est le test de r\u00e9f\u00e9rence pour diagnostiquer l'herp\u00e8s simplex (HSV-1 et HSV-2). Herp\u00e8s g\u00e9nital, labial, enc\u00e9phalite, m\u00e9ningite, traitement antivira...","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":"Herp\u00e8s PCR (HSV-1 et HSV-2) : diagnostic, interpr\u00e9tation et traitement | Clinique Omicron","_aioseo_description":"La PCR HSV est le test de r\u00e9f\u00e9rence pour diagnostiquer l'herp\u00e8s simplex (HSV-1 et HSV-2). 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\n\t\t\t\t\t\n\n\n\n\nHerpes PCR (HSV-1 and HSV-2): Diagnosis, Interpretation, and Treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"HSV PCR is the gold standard test for diagnosing herpes simplex (HSV-1 and HSV-2). Genital herpes, cold sores, encephalitis, meningitis, antiviral treatment, and management in Quebec.\">\n<meta name=\"keywords\" content=\"PCR herp\u00e8s HSV, herp\u00e8s simplex diagnostic, HSV-1 HSV-2 traitement, herp\u00e8s g\u00e9nital PCR, enc\u00e9phalite herp\u00e9tique PCR LCR, aciclovir valaciclovir herp\u00e8s, herp\u00e8s r\u00e9current suppressif, herp\u00e8s Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap*{font-family:'Poppins',sans-serif;box-sizing:border-box}\n.co-wrap{max-width:1100px;margin:0 auto;padding:30px 0 60px}\n.co-label{font-family:'Cinzel',serif;font-size:14px;font-weight:bold;letter-spacing:1px;text-transform:uppercase;color:#4D6577;margin-bottom:14px;display:block}\n.co-wrap h1{font-size:32px;font-weight:500;color:#323C52;margin:0 0 22px;line-height:1.2}\n.co-intro{font-size:16px;line-height:1.75;color:#4D6577;margin-bottom:36px;padding-bottom:32px;border-bottom:1px solid rgba(77,101,119,.2)}\n.co-wrap h2{font-size:20px;font-weight:600;color:#323C52;margin:32px 0 12px}\n.co-wrap p{font-size:15px;color:#4D6577;line-height:1.7;margin-bottom:14px}\n.co-list{list-style:none;padding:0;margin:12px 0 24px}\n.co-list li{font-size:15px;color:#4D6577;padding:10px 14px 10px 38px;margin-bottom:8px;border-radius:6px;position:relative;background:rgba(77,101,119,.06);border-left:3px solid #4D6577}\n.co-list li::before{content:\"\u2713\";position:absolute;left:12px;font-weight:700;color:#4D6577}\n.co-table{width:100%;border-collapse:collapse;margin:14px 0 22px;font-size:14px;border-radius:8px;overflow:hidden;table-layout:fixed}\n.co-table thead tr{background:#323C52;color:#fff}\n.co-table thead th{padding:11px 16px;text-align:left;font-weight:600;font-size:13px}\n.co-table tbody tr:nth-child(even){background:rgba(77,101,119,.06)}\n.co-table tbody tr:nth-child(odd){background:#fff}\n.co-table td{padding:10px 16px;color:#4D6577;border-bottom:1px solid rgba(77,101,119,.12);font-size:14px;vertical-align:top}\n.co-table td:first-child{font-weight:600;color:#323C52}\n.co-infobox{display:flex;gap:12px;background:rgba(77,101,119,.06);border-radius:8px;border-left:4px solid #4D6577;padding:14px 18px;margin:18px 0 28px;font-size:14px;color:#4D6577;line-height:1.65}\n.co-infobox .ico{font-size:18px;flex-shrink:0}\n.co-urgence{background:#fff8f8;border-left:5px solid #c0392b;border-radius:6px;padding:20px 26px;margin:24px 0 32px}\n.co-urgence .co-urgence-titre{font-size:13px;font-weight:700;color:#c0392b;letter-spacing:1.5px;text-transform:uppercase;margin-bottom:10px}\n.co-urgence p{color:#5a2020;font-size:14px;margin:0 0 10px;line-height:1.7}\n.co-urgence p:last-child{margin-bottom:0}\n.co-disclaimer{font-size:13px;color:#8a9aaa;font-style:italic;border-top:1px solid rgba(77,101,119,.15);padding-top:24px;margin-top:40px;line-height:1.6}\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Infectious Diseases & Dermatology & Neurology & Family Medicine<\/span>\n <h1>Herpes PCR (HSV-1 and HSV-2)<\/h1>\n\n <div class=\"co-intro\">\n Herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2) are double-stranded DNA viruses of the Herpesviridae family, characterized by their ability to establish a lifelong latent infection in sensory ganglia after primary infection, with periodic symptomatic or asymptomatic reactivations. PCR (polymerase chain reaction) has become the reference test for the diagnosis of all forms of HSV infection - definitively supplanting viral culture, Tzanck cytology and serology in most clinical contexts - due to its far superior sensitivity (90-100 %), near-absolute specificity (99-100 %), rapidity (results in 2-6 hours for multiplex panels) and ability to differentiate HSV-1 from HSV-2. HSV PCR on cerebrospinal fluid (CSF) is indispensable in the diagnosis of herpes encephalitis - the most frequent cause of fatal sporadic viral encephalitis in developed countries - where one hour's delay in IV aciclovir can definitively compromise the neurological prognosis. PCR on genital, urethral, cervical or anal swabs is the method of choice for diagnosing genital herpes, replacing Vero cell culture, whose sensitivity fell to 30-50 % in the healing phase. Type-specific serology (gG-based serology) has a distinct place in partner screening and management, but should not be used as a replacement for PCR for the diagnosis of an active clinical episode.\n <\/div>\n\n <h2>Virology, epidemiology, and pathophysiology<\/h2>\n <ul class=\"co-list\">\n <li><strong>Viral biology and mechanisms of latency and reactivation:<\/strong> structure and biology : HSV-1 and HSV-2 = enveloped viruses with 152 kb linear double-stranded DNA \u2192 family Herpesviridae (subfamily Alphaherpesvirinae) \u2192 11 envelope glycoproteins (gB + gC + gD + gE + gG + gH + gI + gJ + gK + gL + gM) \u2192 gD = main fusion protein and target of neutralizing antibodies \u2192 gG = glycoprotein type-specificity \u2192 gG-1 vs gG-2 \u2192 basis for type-specific serological tests \u2192 replication cycle : attachment via gB\/gC to heparan sulfates + binding of gD to entry receptors (nectin-1 + nectin-2 + HVEM + 3-O-sulfate HS) \u2192 envelope fusion \u2192 internalization of nucleocapsid \u2192 transport to nucleus \u2192 viral DNA replication \u2192 budding release + retrograde axonal transport to sensory ganglia \u2192 latency; latency mechanisms in sensory ganglia: retrograde axonal transport of virion along axons \u2192 trigeminal ganglion (HSV-1) or sacral ganglion S2-S4 (HSV-2) \u2192 circularization of viral DNA \u2192 formation of episomes in neuronal nuclei \u2192 limited transcription of LATs (Latency-Associated Transcripts) \u2192 non-coding RNAs \u2192 inhibit neuronal apoptosis \u2192 maintain latency \u2192 reactivation mechanisms: triggering stimuli: psychological stress + immunosuppression + UV (herpes labialis) + fever + microtrauma (sexual intercourse \u2192 genital herpes) + menstruation + trigeminal ganglion surgery \u2192 anterograde axonal transport \u2192 replication in skin or mucosal epithelia \u2192 symptomatic or asymptomatic viral shedding \u2192 Spruance 1977 - Lancet: pathophysiological model of the HSV latency-reactivation cycle \u2192 Bloom 2010 - Journal of Neurovirology: molecular mechanisms of HSV latency + role of LATs; global and Canadian epidemiology: HSV-1 seroprevalence: 67 % of world population (Looker 2015 - PLOS ONE: WHO meta-analysis \u2192 3.7 billion people under 50 years of age HSV-1 carriers) \u2192 genital HSV-1: 30-50 % of genital primary infections in high-income countries \u2192 increase in young adults (decrease in oral exposure in childhood) \u2192 HSV-2 seroprevalence: 11 % worldwide (Looker 2015 - PLOS ONE) \u2192 491 million carriers aged 15-49 \u2192 Canada: HSV-2 seroprevalence \u2248 14-16 % adults \u2192 HSV-1 seroprevalence \u2248 60-67 % adults \u2192 asymptomatic viral shedding (AVE): key mechanism of transmission \u2192 Tronstein 2011 - JAMA: 9 % of days \u2192 HSV-2 excreted asymptomatically \u2192 76 % of excretion is asymptomatic \u2192 up to 5 daily micro-short (<6h) episodes \u2192 responsible for the majority of transmissions because the source partner is asymptomatic \u2192 Schiffer 2010 - PLOS Medicine: modeling asymptomatic excretion \u2192 fountain model (fountain model) \u2192 multiple daily reactivations of short duration \u2192 biological differences HSV-1 vs HSV-2: HSV-2 \u2192 frequency of genital recurrences 5.1 recurrences\/year vs genital HSV-1 1.3 recurrences\/year (Langenberg 1999 - Annals of Internal Medicine) \u2192 HSV-2 \u2192 more frequent asymptomatic excretion \u2192 HSV-1 \u2192 more frequent in encephalitis + recurrent herpes labialis \u2192 different neurotropism + different antiviral resistances (TK-mutations for aciclovir - more frequent under immunosuppression)<\/li>\n <li><strong>Clinical manifestations by type and location:<\/strong> orofacial herpes (HSV-1 predominant): primary infection (herpetic gingivostomatitis): children 1-5 years + young adults \u2192 vesicles + painful erosions on gingiva + oral mucosa + palate + lips + cervical adenopathies + fever + dysphagia + duration: 7-14 days + 10-15 % of symptomatic primary infections \u2192 recurrent herpes labialis (cold sore): vesicles clustered at labial mucocutaneous junction \u2192 5 phases: prodrome (1-2d) + vesicular (2-3d) + pustular + ulcerative + healing \u2192 total duration: 8-10 days + recurrences: 1-6\/year on average \u2192 triggers: UV + stress + fever + menstruation + local trauma \u2192 ocular herpes: dendritic keratitis (fern-leaf corneal ulcer) + conjunctivitis + uveitis \u2192 HSV-1 = leading cause of infectious corneal blindness in developed countries (Wilhelmus 2008 - Cochrane) \u2192 herpetic panariasis (herpetic whitlow): finger \u00b1 in caregivers or nail-drinkers; genital herpes (HSV-2 predominant but HSV-1 increasing): genital primary infection: often asymptomatic (60-80 %) or not very typical \u2192 if symptomatic: vesicles + painful erosions on penis + vulva + vagina + cervix + perineal + anorectal region + aseptic meningitis (15-30 % of HSV-2 primary infections) \u2192 urinary retention syndrome + 20-40 days resolution \u2192 prolonged viral excretion + recurrences : HSV-2 genital \u2192 5-7 recurrences\/year on average in the first few years \u2192 HSV-1 genital \u2192 1-3 recurrences\/year + prodromes (burning + tingling) 12-24h before \u2192 prevalence of atypical manifestations (fissure + erythematous papule + pain without visible lesion) \u2192 frequent underdiagnosis; severe forms and complications: herpetic encephalitis: HSV-1 involved in 90 % of cases + life-threatening neurological emergency \u2192 fever + behavioral disorders + olfacto-gustatory hallucinations + headaches + disorientation \u2192 temporal localization (temporal gyrus + insula + cingulate) \u2192 Whitley 1982 - NEJM: IV aciclovir vs vidarabine in herpetic encephalitis \u2192 mortality reduced by 70 % \u2192 28 % (aciclovir) vs 54 % (vidarabine) \u2192 time to treatment = major prognostic factor \u2192 if treatment within first 4 days: mortality 1 month = AIDS criterion) <\/ul>\n\n <h2>Diagnostic by PCR, serology, and treatment<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Domain<\/th><th>Data, modalities, and criteria<\/th><th>Key studies and recommendations<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>PCR HSV \u2014 methods, sample collection, and diagnostic performance<br><small style=\"font-weight:400;color:#7a8fa0;\">Real-time PCR \u2014 multiplex \u2014 LCR \u2014 genital sample \u2014 swabbing \u2014 HSV-1\/HSV-2 differentiation \u2014 false negatives \u2014 sensitivity\/specificity<\/small><\/td>\n <td>HSV PCR methods available: quantitative or qualitative real-time PCR (qPCR): reference method \u2192 amplification of a conserved region of the HSV genome (glycoprotein B genes or DNA polymerase - UL30) \u2192 TaqMan or SYBR Green probes \u2192 results in 2-4h \u2192 sensitivity: 95-100 % \u2192 specificity: 99-100 % \u2192 HSV-1\/HSV-2 differentiation by type-specific probes \u2192 viral load quantification possible (useful in encephalitis and monitoring of the immunocompromised) \u2192 multiplex PCR on CSF (example: BioFire FilmArray Meningitis\/Encephalitis Panel): simultaneous detection of 14 agents (HSV-1 + HSV-2 + CMV + HHV-6 + EBV + VZV + enterovirus + parechovirus + meningeal bacteria) \u2192 results in 1h \u2192 very useful in emergencies \u2192 but: sensitivity slightly lower than conventional PCR for some rare agents \u2192 high cost \u2192 viral culture (historical method): Vero cells or human diploid cells \u2192 EPC (cytopathogenic effect) visible in 2-7d \u2192 sensitivity: 70-85 % in vesicular phase \u2192 30-50 % in healed ulcer phase \u2192 abandoned in practice in favor of PCR \u2192 useful if antiviral resistance suspected (viral antibiogram) \u2192 Tzanck cytology: multinucleated giant cells (Cowdry type A intranuclear inclusion) \u2192 sensitivity: 50-70 % \u2192 very unspecific (does not differentiate HSV from VZV) \u2192 only in limited resources \u2192 direct immunofluorescence (DIF): fluorescent monoclonal antibodies + sensitivity: 70-85 % + gradual abandonment in favor of PCR; types of samples and preanalytical conditions: lesion sampling (mucocutaneous herpes) : dacron or nylon swab (no cotton - PCR inhibitors) \u2192 rub the base of the lesion vigorously (ruptured blister or active ulcer) \u2192 place in Universal Transport Medium (UTM) or PBS \u2192 store at +4\u00b0C \u2192 analyze within 48-72h \u2192 sensitivity decreases sharply if lesion is healing \u2192 frequent false negatives if : crusty lesion + delay between sampling and analysis + poor technique (insufficient superficial sampling) + insufficient volume \u2192 CSF sampling (meningitis + herpetic encephalitis): lumbar puncture \u2192 CSF in a sterile tube \u2192 HSV PCR on CSF: reference method \u2192 sensitivity: 96-98 % + specificity: 99 % \u2192 Aurelius 1993 - Lancet: PCR on CSF \u2192 diagnostic revolution in herpetic encephalitis \u2192 replaces brain biopsy as gold standard \u2192 do not delay aciclovir while waiting for PCR \u2192 result may be falsely negative if: sampling <72h after onset of symptoms + rare but documented early false negative \u2192 repeat LP at 48-72h if strong clinical suspicion and first negative result \u2192 genital sampling: urethral swab (male) + cervical or vaginal swab (female) + swab of visible lesions \u2192 PCR on desquamated cells \u2192 do not use lubricating gel (PCR inhibitor) + rectal or anal swab if anal herpes suspected \u2192 PCR on oral or pharyngeal lesions \u2192 direct swabbing; comparative sensitivity of methods according to lesion stage: vesicular phase: PCR = 100 % + culture = 85 % + Tzanck = 70 % \u2192 ulcerative phase: PCR = 95 % + culture = 60 % \u2192 scabby phase: PCR = 70 % + culture = 30 % \u2192 healed lesion: PCR = 40 % (residual DNA) + culture = 0 % \u2192 PCR is 3-5\u00d7 more sensitive than culture on lesions in regression phase \u2192 saliva sample \/ genital secretion without visible lesion: EVA (asymptomatic viral excretion) \u2192 PCR detects EVA \u2192 does not immediately predict contagiousness as quantities are small \u2192 epidemiological value + useful in serodiscordant couple workup + Wald 2001 - JAMA: asymptomatic HSV-2 excretion \u2192 detected in 28 % of specimens in HSV-2 seropositive women without symptoms \u2192 antiviral resistance workup: culture + antibiogram (IC50 aciclovir) \u2192 mutations in the TK gene (UL23) or DNA polymerase (UL30) \u2192 indication: clinical resistance (persistent lesions on aciclovir after 14-21d in the immunocompromised) \u2192 alternative treatment: foscarnet + cidofovir<\/td>\n <td>Fundamental data on diagnostic performance: Aurelius 1993 - Lancet: CSF PCR in herpetic encephalitis \u2192 sensitivity 96 % + specificity 99 % \u2192 diagnostic revolution \u2192 abandons brain biopsy as gold standard \u2192 Corey 1992 - Sexually Transmitted Diseases: PCR vs culture for diagnosis of genital herpes \u2192 PCR 3-5\u00d7 more sensitive on lesions in regression phase \u2192 Wald 1995 - Annals of Internal Medicine: lesion PCR = reference method for genital herpes \u2192 sensitivity 98 % in active phase \u2192 Wald 2001 - JAMA: asymptomatic HSV-2 shedding \u2192 28 % of PCR-positive specimens in symptomless HIV-positive women \u2192 serodiscordant couple workup \u2192 Tronstein 2011 - JAMA (prospective cohort): 9 % of HSV-2 days excreted + 76 % asymptomatic excretion \u2192 PCR is the essential tool for VAS measurement + IDSA 2015: PCR = test of choice for all HSV syndromes \u2192 replaces culture + CDC 2021 STI Guidelines: PCR on genital lesion or swab \u2192 reference test for genital herpes \u2192 type-specific (gG) serology reserved for asymptomatic screening + STI national guidelines Canada 2022 (PHAC): HSV PCR = test of choice in Canada<\/td>\n <\/tr>\n <tr>\n <td>HSV Type-Specific Serology (gG-based) \u2014 Role and Limitations<br><small style=\"font-weight:400;color:#7a8fa0;\">IgG HSV-1 \u2014 IgG HSV-2 \u2014 reactivity index \u2014 serological window \u2014 false positives \u2014 asymptomatic screening \u2014 serodiscordant couple<\/small><\/td>\n <td>Type-specific gG-based serology - principles: detects IgG against the glycoprotein G of HSV-1 (gG-1) and HSV-2 (gG-2) \u2192 the two antigens are sufficiently different to allow reliable distinction between serotypes \u2192 methods: ELISA (HerpeSelect 2 Focus Diagnostics + Captia Herpes Select + Trinity Biotech) \u2192 immunoblot (Kalon HSV-2) \u2192 results expressed as index of reactivity (IR): for HerpeSelect ELISA \u2192 IR \u22651,10 = positive \u2192 IR 1,10-3,49 = gray area \u2192 IR \u22653,50 = strong positive \u2192 problem of false positives in the gray area (IR 1,10-3,49) \u2192 confirmations recommended by Western blot or immunoblot (Johnston 2016 - Sexually Transmitted Infections: false positive in 50-80 % of IRs between 1.10 and 3.49 if low prevalence) \u2192 HSV-2 serology does not provide information on site of infection or active nature \u2192 serological window: anti-HSV IgG appear 2-12 weeks after primary infection \u2192 a negative result within the first 12 weeks does not exclude infection \u2192 do not use serology to diagnose an acute episode + current role of type-specific serology: asymptomatic screening in high-risk individuals (MSM + UDIV + multiple partners + history of STI) \u2192 assessment of serodiscordant couple: identify source partner + adapt prevention measures \u2192 pregnant woman with HSV-2 seropositive partner: screening to assess risk of periconceptional acquisition \u2192 patients with atypical picture whose diagnosis of genital herpes is suspicious but without active lesion \u2192 decision on suppressive therapy \u2192 USPSTF 2023: routine screening for HSV-2 by serology is not recommended in the asymptomatic general population without risk factors \u2192 serology is recommended in the clinical contexts listed above \u2192 HSV IgM: not recommended \u2192 does not reliably distinguish primary infection and reactivation \u2192 often false positive by cross-reactivity + not type-specific \u2192 to be avoided; interpretation of common serological profiles: HSV-1 IgG + \/ HSV-2 IgG - : HSV-1 seropositivity only \u2192 oral infection in childhood in most cases \u2192 an episode of genital herpes in this context \u2192 genital HSV-1 primary infection possible + HSV-2 IgG + : HSV-2 infection (most often genital) \u2192 suppressive therapy to be considered + preventive measures \u2192 both positive : double seropositivity \u2192 very frequent (50-60 % of sexually active adults in certain populations) + HSV-1 IgG - \/ HSV-2 IgG - : uninfected \u2192 susceptible \u2192 preventive counseling + HSV-2 IgG in the gray area (IR 1.10-3.49) \u2192 confirm by Western immunoblot before concluding<\/td>\n <td>Fundamental data on serology: Johnston 2016 - Sexually Transmitted Infections: HerpeSelect ELISA in IR 1.10-3.49 \u2192 false positives 50-80 % if low prevalence \u2192 confirmation by immunoblot recommended \u2192 Looker 2015 - PLOS ONE (WHO meta-analysis): worldwide HSV-1 seroprevalence: 67 % + HSV-2: 11 % \u2192 3.7 billion and 491 million carriers respectively \u2192 Wald 2005 - NEJM: suppressive treatment with valaciclovir \u2192 reduction of HSV-2 transmission to serodiscordant partners by 48 % \u2192 demonstration that serology + suppression are a prevention strategy + Tronstein 2011 - JAMA: HSV-2 VAS \u2192 9 % days + 76 % asymptomatic \u2192 serology identifies asymptomatic carriers \u2192 preventive measures \u2192 USPSTF 2023: no routine HSV-2 screening by serology in general population \u2192 but in high-risk settings + Langenberg 1999 - Annals of Internal Medicine: HSV-2 genital recurrences 5.1\/year vs HSV-1 genital 1.3\/year \u2192 basis for suppressive therapy decision according to type \u2192 CDC 2021 STI Guidelines + STI Canada 2022 (PHAC): serology algorithm in STI \u2192 validated contexts of use<\/td>\n <\/tr>\n <tr>\n <td>Antiviral Treatment \u2014 Acyclovir, Valacyclovir, Famciclovir, and Special Situations<br><small style=\"font-weight:400;color:#7a8fa0;\">Acyclovir \u2014 Valacyclovir \u2014 Famciclovir \u2014 Encephalitis \u2014 Neonatal \u2014 Genital \u2014 Suppressive \u2014 Pregnancy \u2014 Immunocompromised \u2014 Resistance \u2014 Foscarnet<\/small><\/td>\n <td>Mechanism of action of anti-HSV antivirals: aciclovir (aciclovir = ACV + valaciclovir = aciclovir prodrug \u00d7 3-5 best oral bioavailability + famciclovir = penciclovir prodrug) : viral TK (thymidine kinase) phosphorylates aciclovir to aciclovir monophosphate \u2192 cellular kinases add 2nd and 3rd phosphates \u2192 aciclovir triphosphate \u2192 guanosine triphosphate (GTP) competitor \u2192 incorporation into growing viral DNA by viral DNA polymerase (UL30) \u2192 DNA chain termination (absence of the 3'-OH group) \u2192 viral DNA polymerase is 10-30\u00d7 more sensitive to inhibition by aciclovir triphosphate than cellular DNA polymerase \u2192 very good therapeutic index \u2192 no toxicity on uninfected cells + resistance : TK gene mutation (UL23) \u2192 non-functional TK \u2192 no phosphorylation \u2192 resistance \u2192 or DNA polymerase mutation (UL30) \u2192 less frequent \u2192 treatment of resistance : foscarnet (direct inhibitor of viral DNA polymerase - no need for TK phosphorylation) + or cidofovir (nephrotoxic); treatment of herpetic encephalitis - absolute emergency: aciclovir IV 10 mg\/kg \u00d7 3\/d \u00d7 14-21 days (in immunocompetent adults) \u2192 adjustment according to renal function (longer interval if CKD) \u2192 Whitley 1986 - NEJM : IV aciclovir vs vidarabine \u2192 mortality 28 % vs 54 % \u2192 aciclovir = standard of care since 1986 \u2192 Raschilas 2002 - Annals of Neurology: prognostic factors in herpetic encephalitis \u2192 time to treatment + age + Glasgow score on admission \u2192 treatment before D4 = major protective factor \u2192 if strong clinical suspicion + inflammatory CSF \u2192 start IV aciclovir WITHOUT waiting for PCR result (early treatment takes priority over confirmation) \u2192 assess response at D7 by control CSF PCR \u2192 duration 21 days if severe or immunocompromised \u2192 oral relay (valaciclovir 2 g \u00d7 3\/d \u00d7 3 months in some postencephalitis protocols); treatment of genital herpes: primary infection: aciclovir 400 mg \u00d7 3\/d \u00d7 7-10d OR valaciclovir 1 g \u00d7 2\/d \u00d7 7-10d OR famciclovir 250 mg \u00d7 3\/d \u00d7 7-10d \u2192 Mertz 1984 - NEJM: aciclovir in primary genital infection \u2192 reduction in duration of symptoms from 5 to 8 days + reduction in duration of viral excretion \u2192 standard of care since the 1980s \u2192 symptomatic recurrence (episodic treatment): valaciclovir 500 mg \u00d7 2\/d \u00d7 3-5d OR aciclovir 800 mg \u00d7 3\/d \u00d7 2d (short regimen) OR famciclovir 1,000 mg \u00d7 2\/d \u00d7 1d (single dose) \u2192 to be initiated within 24 h of prodrome or appearance of lesions \u2192 continuous suppressive therapy: valaciclovir 500 mg\/d \u00d7 12 months (or indefinite) \u2192 indicated if: \u22656 recurrences\/year + or reduction in transmission to HIV-negative partner + or anxiety related to recurrences + or pregnancy \u2192 Reitano 1998 - Journal of Infectious Diseases: valaciclovir 500 mg\/d \u2192 reduction in recurrences by 80 % + reduction in VAS \u2192 Wald 2005 - NEJM (PARTNERS study): valaciclovir 500 mg\/d in serodiscordant couple \u2192 reduced transmission by 48 % + reduced recurrences by 79 % \u2192 dual role (suppressive + transmission preventive) \u2192 Strauss 1984 - NEJM: first trial suppressive aciclovir in genital \u2192 reduction in recurrences + feasibility; recurrent herpes labialis (topical + oral aciclovir): topical aciclovir (Zovirax cream): reduces duration from \u00bd to 1 day \u2192 modest efficacy + Spruance 2003 - Antimicrobial Agents and Chemotherapy: valaciclovir 2 g \u00d7 2 taken 12h apart \u2192 single dose \u2192 reduction in lesion duration by 1.5 days + abortive effect of the episode in 40 % of cases \u2192 taken as soon as prodrome \u2192 famciclovir 1,500 mg single dose (Spruance 2006 - JAMA) \u2192 penciclovir cream (Denavir): Spruance 1997 - JAMA \u2192 reduced duration; neonatal herpes (Kimberlin 2001 - NEJM CASG 103): aciclovir IV 60 mg\/kg\/d divided into 3 doses \u00d7 14-21 days \u2192 depending on form \u2192 disseminated or CNS form: 21 days \u2192 after IV: suppressive oral aciclovir 300 mg\/m\u00b2\/dose \u00d7 3\/d \u00d7 6 months \u2192 significant improvement in survival + neurological development; pregnancy and herpes \u2192 prevention of neonatal transmission: woman with primary HSV infection in late pregnancy (3rd trimester): aciclovir 400 mg \u00d7 3\/d from 36 SA \u2192 reduction of viral excretion at the time of delivery \u2192 or Caesarean section if active lesions in labor + woman with recurrence of genital HSV herpes in late pregnancy: aciclovir 400 mg \u00d7 3\/d from 36 SA \u2192 ACOG 2020 + SOGC 2008 \u2192 recommendation to reduce the risk of neonatal transmission + woman with active lesions at the time of labor \u2192 cesarean section recommended \u2192 no contraindication to breastfeeding if no lesions in the breast; immunocompromised (HIV + transplant patients + chemotherapy): high-dose IV or oral aciclovir \u2192 valaciclovir 1 g \u00d7 2\/d \u2192 antiviral prophylaxis indicated if CD4 <200 or profound immunosuppression \u2192 Gnann 2012 - NEJM: aciclovir IV + immunosuppressed with disseminated herpes \u2192 reduced mortality + Kimberlin 1996 - Journal of Infectious Diseases: resistance to aciclovir in immunosuppressed patients \u2192 foscarnet 40-60 mg\/kg \u00d7 3\/d IV \u2192 cidofovir 5 mg\/kg IV qwk \u00d7 2 with hydration and probenecid<\/td>\n <td>Fundamental data on treatment: Whitley 1982 - NEJM: aciclovir IV vs vidarabine in herpetic encephalitis \u2192 mortality 28 % vs 54 % \u2192 aciclovir = absolute standard + Whitley 1986 - NEJM: confirmation of superiority \u2192 therapeutic revolution \u2192 Raschilas 2002 - Annals of Neurology (n=93 encephalitis): treatment delay <4d \u2192 major prognostic factor \u2192 treatment without waiting for PCR if strong suspicion + Mertz 1984 - NEJM: aciclovir in genital primary infection \u2192 reduction in duration from 5-8 days \u2192 founder + Reitano 1998 - JID: valaciclovir 500 mg\/d suppressive \u2192 -80 % recurrences + Wald 2005 - NEJM (PARTNERS trial): valaciclovir 500 mg\/d + serodiscordant couple \u2192 -48 % transmission \u2192 demonstration of preventive role + Spruance 2003 - AAC: valaciclovir 2 g \u00d7 2 doses \u2192 abortion 40 % labial episode \u2192 Kimberlin 2001 - NEJM (CASG 103): aciclovir IV 60 mg\/kg\/d neonatal \u2192 reduced disseminated mortality + better neurological development + 6-month suppression \u2192 ACOG 2020 + SOGC 2008: suppressive aciclovir from 36 SA if history of genital herpes + CDC 2021 STI Guidelines + STI Canada 2022 ASPC: recommendations for episodic + suppressive + pregnancy prophylaxis treatment<\/td>\n <\/tr>\n <tr>\n <td>Prevention, partner screening, and special situations<br><small style=\"font-weight:400;color:#7a8fa0;\">Condom \u2014 HSV PrEP \u2014 Transmission \u2014 Serodiscordant Couple \u2014 HIV + HSV \u2014 Mollaret's Meningitis \u2014 Ocular Herpes \u2014 Informed Consent<\/small><\/td>\n <td>Prevention of HSV transmission: condom: reduces transmission risk by 50 % (Wald 2001 - JAMA) \u2192 but protection is incomplete as lesions or asymptomatic excretion may be present in areas not covered by the condom (perineum + pubis + buttock + periscrotal skin) \u2192 suppressive treatment with valaciclovir: additional 48 % reduction in transmission (Wald 2005 - NEJM PARTNERS trial) \u2192 combination condom + valaciclovir \u2192 estimated >90 % reduction in transmission by modeling \u2192 abstinence during active episodes (symptoms + visible lesions) + counseling on asymptomatic shedding \u2192 asymptomatic patient may transmit unknowingly \u2192 Tronstein 2011 - JAMA: asymptomatic transmission in the majority of cases \u2192 patient education essential \u2192 HSV vaccine: Simplirix (GSK - adjuvanted gD-2 vaccine) : HERPEVAC Trial (Stanberry 2002 - NEJM): efficacy 73 % in doubly seronegative women (HSV-1- and HSV-2-) \u2192 no protection in HSV-1+ men or women \u2192 partial and short-lived efficacy \u2192 not marketed \u2192 2nd and 3rd generation vaccines in trials (DNA + recombinant proteins + mRNA) \u2192 no vaccine available in Canada in 2026 + management of serodiscordant couple: identify source partner \u2192 type-specific serology of both partners \u2192 if seronegative receiving partner \u2192 counseling + suppressive treatment of source partner + condom + avoid intercourse during outbreaks \u2192 discuss voluntary reporting (no legal requirement to report genital herpes in Canada); HSV-2 and HIV - major bidirectional interaction: HSV-2 \u2192 increases the risk of HIV acquisition by 2-3\u00d7 (Wald 2009 - Current Opinion in Infectious Diseases) \u2192 mechanism: genital erosions and ulcerations \u2192 HIV entry doors + reactivation of HIV replication at HSV foci of inflammation \u2192 HIV patient + HSV-2 \u2192 increased HIV viral load in genital secretions during HSV episodes \u2192 HSV-2 suppressive therapy in HIV+ patients: reduces HSV shedding + slightly lowers HIV viral load + Celum 2010 - NEJM (HPTN 039): aciclovir 400 mg \u00d7 2\/d in HSV-2\/HIV-positive patients \u2192 reduced HIV acquisition by 7 % (not significant) \u2192 aciclovir alone is insufficient to prevent HIV acquisition \u2192 HIV PrEP remains the strategy of choice + Barnabas 2016 - NEJM: valaciclovir + HIV positive + HSV-2 \u2192 reduction of HSV episodes + modest lowering of HIV viral load \u2192 but no effect on HIV transmission; Mollaret meningitis (recurrent HSV-2 meningitis): recurrent episodes of lymphocytic aseptic meningitis + fever + meningismus + headache \u2192 duration 3-5d per episode + several episodes over years \u2192 pathognomonic: Mollaret cells (large endothelial cells in CSF - historical observation not pathognomonic in reality) \u2192 diagnosis: HSV-2 PCR on CSF during an acute episode \u2192 treatment: aciclovir IV or oral \u00d7 5-7d per episode + valaciclovir prophylaxis 500-1,000 mg\/d if frequent episodes \u2192 favorable prognosis \u2192 ocular herpes - herpetic keratitis: HSV-1 as main cause \u2192 dendritic keratitis (fern-leaf epithelial ulcer) \u2192 treatment: ophthalmic aciclovir 3 % ointment \u00d7 5\/d \u00d7 10-14d + or ganciclovir ophthalmic gel 0.15 % \u00d7 5\/d + or trifluridine eye drops (Viroptic) \u2192 CONTRAINDICATION of ocular topical corticoids in the absence of antiviral (aggravation of corneal herpes) \u2192 Wilhelmus 2008 - Cochrane: trifluridine + IDU + aciclovir \u2192 comparable efficiencies for epithelial keratitis \u2192 stromal ocular herpes (stromal keratitis - immune lesion) \u2192 corticoids + oral antiviral \u2192 ophthalmic opinion + suppressive therapy: aciclovir 400 mg \u00d7 2\/d \u2192 prevention of recurrences + HEDS Trial (Herpetic Eye Disease Study - Wilhelmus 1994 - Archives of Ophthalmology): oral aciclovir \u2192 41 % reduction in ocular recurrences \u2192 recommended if frequent recurrences <\/td>\n <td>Fundamental data on prevention and special situations: Wald 2001 - JAMA: condom \u2192 transmission reduction 50 % + EVA 28 % of HSV-2 seropositive female samples \u2192 educational role + Wald 2005 - NEJM (PARTNERS trial): valaciclovir 500 mg\/d + serodiscordant couple \u2192 -48 % HSV-2 transmission \u2192 rigorous demonstration of preventive role of suppressive therapy + Stanberry 2002 - NEJM (HERPEVAC): gD-2 vaccine \u2192 73 % efficacy doubly seronegative women \u2192 not marketed \u2192 2nd-generation vaccine expected + Wald 2009 - Current Opinion in Infectious Diseases: HSV-2 \u2192 increased risk of HIV acquisition \u00d7 2-3 \u2192 bidirectional interaction + Celum 2010 - NEJM (HPTN 039): aciclovir + HSV-2\/HIV- \u2192 reduced HIV acquisition 7 % (not significant) \u2192 HIV PrEP remains the primary strategy + Tronstein 2011 - JAMA: EVA \u2192 mostly asymptomatic transmission \u2192 mandatory counseling + Wilhelmus 2008 - Cochrane: comparable ocular treatments \u2192 HEDS Trial Wilhelmus 1994 - Archives of Ophthalmology: oral aciclovir \u2192 reduced ocular recurrences 41 % + CDC 2021 STI + STI Canada 2022 ASPC + ACOG 2020 + SOGC 2008: recommendations for prevention and management of herpes during pregnancy<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong>In case of suspected herpes encephalitis, start IV acyclovir immediately without waiting for PCR results.<\/strong> Herpes simplex encephalitis is the most common cause of fatal viral encephalitis. Every hour of delay in acyclovir treatment increases the risk of irreversible neurological sequelae and death. HSV PCR on CSF (sensitivity 96-98 %) is the gold standard test, but it should never delay treatment. If clinical suspicion is high (fever + behavioral changes + seizures + temporal lobe involvement on MRI), IV acyclovir 10 mg\/kg \u00d7 3\/day should be started as soon as lumbar puncture is performed, even before results are available.<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations Requiring a 911 Call or Urgent Medical Attention<\/div>\n <p><strong>Fever + intense headaches + behavioral or memory disturbances + olfactory-gustatory hallucinations + confusion + seizures + MRI showing abnormal temporal signal<\/strong> Herpes encephalitis \u2192 Call 911 \u2192 Emergency hospitalization \u2192 Lumbar puncture + CSF PCR + Start IV acyclovir 10 mg\/kg \u00d7 3\/day WITHOUT waiting for results \u2192 Every hour of delay worsens the neurological prognosis.<\/p>\n <p><strong>Newborn with fever + irritability + skin vesicles + seizures + jaundice + hemodynamic instability whose mother had a primary herpes infection late in pregnancy or active lesions at delivery<\/strong> neonatal herpes \u2192 pediatric emergencies \u2192 acyclovir IV 60 mg\/kg\/day \u00d7 3 doses \u2192 HSV PCR blood + CSF + skin swab + funduscopy \u2192 NICU if available.<\/p>\n <p><strong>Immunocompromised patient (HIV + transplant + chemotherapy) with persistent or spreading cutaneous or mucosal herpes lesions despite oral acyclovir for >14 days<\/strong> \u2192 Possible acyclovir resistance \u2192 Lesional PCR + culture + viral antibiogram \u2192 Infectious disease consultation \u2192 IV foscarnet if TK resistance confirmed \u2192 do not increase acyclovir alone.<\/p>\n <p><strong>Eye pain + photophobia + corneal ulcer visible with a slit lamp or decreased visual acuity + history of ocular herpes.<\/strong> Recurrent herpetic keratitis \u2192 urgent ophthalmological consultation \u2192 acyclovir ophthalmic ointment or ganciclovir gel \u2192 never use ocular corticosteroids alone without antivirals (possible worsening of herpetic keratitis).<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Clinique Omicron physicians prescribe PCR HSV on lesion or genital samples for the diagnosis of herpes simplex, initiate episodic or suppressive antiviral treatment as appropriate, prescribe type-specific serology for validated indications (serodiscordant couple + STI workup + pregnancy), refer to the emergency department in cases of suspected herpes encephalitis or neonatal herpes, and provide transmission prevention counseling. Consultations are available at several service points in Quebec and via telemedicine. To make an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">The content of this page is for informational purposes only and does not substitute for the advice of a physician or infectious disease specialist. Herpes encephalitis and neonatal herpes are medical emergencies requiring immediate IV treatment without diagnostic delay.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Herp\u00e8s PCR (HSV-1 et HSV-2) : diagnostic, interpr\u00e9tation et traitement | Clinique Omicron Infectiologie & Dermatologie & Neurologie & M\u00e9decine de famille Herp\u00e8s PCR (HSV-1 et HSV-2) Les virus de l’herp\u00e8s simplex de type 1 (HSV-1) et de type 2 (HSV-2) sont des virus \u00e0 ADN double brin de la famille des Herpesviridae, caract\u00e9ris\u00e9s par… <a href=\"https:\/\/cliniqueomicron.ca\/en\/herpes-pcr-hsv-1-et-2\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Herpes PCR (HSV-1 and HSV-2): Diagnosis, Interpretation, and Treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Herp\u00e8s PCR (HSV-1 et HSV-2) : | Brossard | Clinique Omicron","_metasync_otto_description":"La PCR HSV est le test de r\u00e9f\u00e9rence pour diagnostiquer l'herp\u00e8s simplex (HSV-1 et HSV-2). 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