In New Zealand, herpes Simplex Infection is managed by infectious diseases. 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.
The key symptoms of 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..
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.
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.
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.
Find specialists →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).
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.
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.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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