How prevalent is herpes simplex?

HSV infections are remarkably prevalent — making herpes one of the most common human infections globally. HSV-1: approximately 3.7 billion people under 50 are infected worldwide (66.6%) — predominantly acquired in childhood through oral contact. HSV-2: approximately 491 million people aged 15-49 are infected (13.2%) — acquired primarily through sexual contact. Africa has the highest rates of both HSV-1 and HSV-2. In practice, most people with herpes do not know they are infected.

What is the difference between HSV-1 and HSV-2?

HSV-1 and HSV-2 are closely related but traditionally associated with different body sites. HSV-1 (herpes labialis): cold sores/fever blisters on lips — the classic orolabial herpes, acquired in childhood through oral contact. HSV-2 (herpes genitalis): genital ulcers — sexually transmitted. However, these distinctions have blurred: HSV-1 now causes approximately 50% of new genital herpes infections in HICs (through oral sex); HSV-2 can cause orolabial herpes (less commonly). Both cause identical disease clinically at either site.

What are the symptoms?

Primary infection (first episode): may be severe, with multiple painful ulcers, systemic symptoms (fever, lymphadenopathy, myalgia) lasting 2-3 weeks. Many primary infections are asymptomatic or minimally symptomatic. Recurrent episodes: milder, briefer (5-10 days), preceded by prodromal tingling/itching. HSV-1 orolabial: cold sores on lips/perioral skin. HSV-2 genital: painful ulcers on genitalia, buttocks, thighs. Importantly: most HSV transmission occurs during asymptomatic shedding — when no lesions are visible.

How does herpes affect HIV risk?

HSV-2 infection approximately doubles or triples the risk of acquiring HIV infection, through two mechanisms: (1) genital ulcers and micro-abrasions provide a portal of entry for HIV; (2) HSV-induced genital inflammation recruits CD4+ T-cells and macrophages (the target cells for HIV) to the genital mucosa. Controlling HSV-2 infection is therefore an HIV prevention strategy. Aciclovir suppressive therapy reduces HSV-2 shedding and genital inflammation — but trials have shown only modest impact on HIV acquisition risk, suggesting other mechanisms are also important.

How is herpes treated?

No cure exists — antivirals suppress HSV replication but do not eliminate latent infection. Aciclovir, valaciclovir (prodrug — much better bioavailability) and famciclovir are the three approved antivirals. Episodic therapy: at the first sign of an outbreak (prodromal symptoms), starting antivirals reduces duration and severity. Suppressive therapy: daily low-dose antiviral (valaciclovir 500mg once daily) reduces recurrence frequency by 70-80% and reduces transmission to sexual partners by approximately 50%. First episode: treat with 7-10 day course; primary genital herpes may require 10-day course given severity.

Can herpes be prevented?

Consistent condom use reduces (but does not eliminate) HSV-2 transmission risk — HSV can be shed from skin not covered by condoms. Suppressive antiviral therapy (valaciclovir 500mg daily) in the infected partner reduces transmission to an uninfected partner by approximately 50%. Avoiding sexual contact during outbreaks reduces (but does not eliminate) transmission risk. No approved vaccine exists — but mRNA-based HSV-2 vaccines and therapeutic vaccines are in clinical trials.

How does GMJ News cover herpes simplex?

GMJ News covers WHO HSV burden data, HSV-1 and HSV-2 epidemiology, the HSV-HIV link, neonatal herpes management, suppressive therapy evidence, and vaccine development. Herpes simplex — the most prevalent viral STI globally — is directly relevant to PHIG's STI and HIV prevention programmes and the Georgian Medical Journal.

Home › Topics › Herpes Simplex Virus

Herpes Simplex Virus

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Herpes simplex virus (HSV) infections are among the most prevalent viral infections in humanity: HSV-1 infects approximately 3.7 billion people globally (66.6% of those under 50) and HSV-2 approximately 491 million (13.2% of those aged 15-49) — making herpes the most prevalent viral sexually transmitted infection and one of the most common infections of any kind (WHO 2023). Both viruses establish lifelong latent infection in sensory ganglia with periodic reactivation, and both significantly amplify HIV acquisition and transmission risk (approximately 2-3 fold). No vaccine is yet approved, though candidates are in development.

Key messages

3.7 billion HSV-1 + 491 million HSV-2 infected globally

HSV-1 infects 3.7 billion people under 50 (66.6%) and HSV-2 infects 491 million aged 15-49 (13.2%) — making herpes the most prevalent viral STI and one of the most prevalent human infections of any kind (WHO 2023).

Both HSV-1 and HSV-2 cause genital herpes

HSV-1, once predominantly causing orolabial herpes (cold sores), now causes approximately 50% of genital herpes in HICs — primarily through oral-genital contact. Both viruses establish lifelong latent infection in sensory ganglia with periodic reactivation.

HIV amplification — 2-3 fold

HSV-2 infection dramatically increases HIV acquisition risk (approximately 2-3 fold) by disrupting the genital mucosal barrier and recruiting HIV target cells (CD4+ T lymphocytes). Suppressive antiviral therapy for HSV-2 reduces HIV risk.

Neonatal herpes — rare but dangerous

Neonatal HSV infection — from maternal genital herpes during delivery — causes devastating disease (disseminated disease, HSV encephalitis). Incidence approximately 10 per 100,000 births; high mortality/morbidity without IV aciclovir.

Antivirals suppress but do not cure

Aciclovir, valaciclovir and famciclovir suppress HSV replication, reducing outbreak frequency and severity and viral shedding. Suppressive therapy (daily antiviral) reduces transmission to sexual partners. No cure exists — latent infection in ganglia is not eliminated by any current therapy.

No approved vaccine

Despite decades of research, no HSV vaccine is approved. Multiple candidates in development — including mRNA vaccines, therapeutic vaccines and subunit vaccines.

Key statistics

3.7B

people under 50 with HSV-1 infection globally (66.6%)

WHO 2023

491M

people aged 15-49 with HSV-2 infection globally (13.2%)

WHO 2023

2-3x

increased HIV acquisition risk from HSV-2

WHO

~10/100K

live births with neonatal herpes (approximately)

WHO

50%

of genital herpes in HICs now caused by HSV-1

WHO

approved HSV vaccines

WHO 2024

HSV-1 and HSV-2 global seroprevalence by WHO region (%) — WHO 2023

Source: WHO 2023. Africa has highest HSV-1 and HSV-2 seroprevalence.

Glossary of key terms

Herpes simplex virus types
WHOHSV-1 and HSV-2 are closely related alpha-herpesviruses. HSV-1: predominantly establishes latency in trigeminal ganglion (orolabial herpes), but increasingly causes genital herpes. HSV-2: predominantly establishes latency in sacral ganglia (genital herpes). Both types cause equivalent genital disease clinically.

Latency and reactivation
WHOAfter primary infection, HSV establishes latency in sensory ganglia — persisting for life as episomal circular DNA in neurons, immune to antiviral drugs. Periodic reactivation (triggered by fever, stress, UV light, immunosuppression, menstruation) causes recurrent outbreaks or asymptomatic shedding (viral shedding without visible lesions — the major source of transmission to sexual partners).

Asymptomatic shedding
WHOHSV can be shed from mucosal surfaces without any symptoms — the primary mechanism of transmission to sexual partners who do not know their partner has herpes. Suppressive antiviral therapy (valaciclovir 500mg daily) reduces asymptomatic shedding by approximately 73% and transmission by approximately 50%.

Neonatal herpes
WHO/ACOGHSV infection of the neonate — acquired perinatally (most common — during delivery through infected birth canal), postnatally (from kissing) or rarely intrauterinely. Three forms: localised (skin/eyes/mouth — best prognosis); CNS (encephalitis — high morbidity); disseminated (involving multiple organs including liver, adrenals, brain — highest mortality). IV aciclovir (60mg/kg/day × 14-21 days) dramatically reduces mortality.

HSV encephalitis
WHOThe most common sporadic viral encephalitis — caused predominantly by HSV-1. Presents with fever, headache, behavioural change (frontal/temporal lobe involvement — personality change, hallucinations), seizures and altered consciousness. MRI: temporal lobe signal change (DWI/FLAIR). Diagnosis: CSF HSV PCR (gold standard). Treatment: IV aciclovir (10mg/kg 8-hourly × 14-21 days) — must be started empirically without waiting for PCR result.

Aciclovir/Valaciclovir
WHO EMLAciclovir (and its prodrug valaciclovir) — the foundation of HSV treatment. Inhibits viral DNA polymerase specifically (after phosphorylation by viral thymidine kinase). Episodic therapy (at outbreak onset) reduces outbreak duration. Suppressive therapy (daily) reduces recurrence frequency by 70-80% and reduces transmission. Aciclovir resistance (uncommon in immunocompetent; important in HIV+) treated with foscarnet.