Herpes simplex virus 2 is an enveloped, double‑stranded DNA virus in the Herpesviridae family. Its genome is enclosed within an icosahedral capsid surrounded by a proteinaceous tegument and a lipid envelope studded with glycoproteins. HSV‑2 belongs to the alpha herpesvirus subfamily and primarily infects the genital mucosa. It can establish lifelong infection.
Biology and Pathogenesis
Herpes simplex virus 2 has a four‑layered structure with a double‑stranded DNA core, icosahedral capsid, tegument and glycoprotein‑bearing envelope. Its short replicative cycle reflects its classification as an alpha herpesvirus. Initial replication occurs in genital epithelial cells where virus multiplication produces clusters of vesicles. From there, viral particles ascend sensory nerve endings and travel retrograde to the sacral dorsal root ganglia. Latent genomes persist in neuronal nuclei and can remain dormant for years. Reactivation triggers anterograde transport of viral particles back to peripheral skin, producing recurrent lesions. Transmission requires direct contact with mucosal surfaces or abraded skin, which is why HSV‑2 infection is usually spread by genital contact. The virus can infect the oral mucosa but recurrences there are uncommon compared with genital sites. Host defence relies on mucosal immunity and cell‑mediated responses, yet the virus evades clearance by establishing latency. Primary infection often involves fever and malaise along with painful vesicles on the external genitalia or perianal skin. As vesicles rupture, they form shallow ulcers that heal over several weeks. Viral particles shed from lesions and from asymptomatic mucosa contribute to transmission. After the initial episode, periodic reactivation produces milder lesions or subclinical shedding. The frequency of recurrences varies widely among individuals. The virus can also ascend peripheral nerves to the central nervous system; in rare cases it causes meningitis or encephalitis. Neonates exposed to HSV‑2 at birth may develop disseminated disease, skin‑eye‑mouth infection or central nervous system involvement.
Clinical Highlights
Primary genital herpes is characterized by clusters of painful vesicles on genital or perigenital skin accompanied by dysuria and inguinal lymphadenopathy. These lesions often recur when latent virus reactivates. Recurrent episodes are generally less severe and shorter in duration than the initial outbreak. Asymptomatic shedding means people can transmit HSV‑2 even when no lesions are visible, contributing to its high prevalence. Neonatal herpes arises when a baby is exposed to HSV‑2 during delivery; disseminated infection may affect the liver, lungs and central nervous system and carries a high risk of mortality if untreated. HSV‑2 is also a risk factor for acquiring and transmitting human immunodeficiency virus because genital lesions disrupt mucosal barriers. HSV‑2 is a DNA virus that establishes latency in sensory ganglia and reactivates to cause recurrent genital lesions. Transmission typically occurs through sexual contact or perinatal exposure. Effective antiviral therapy suppresses symptoms but does not eliminate latent infection, so preventative measures and education remain essential. Related Terms: Herpes Simplex Virus 1, Varicella‑Zoster Virus, Epstein–Barr Virus, Cytomegalovirus, Human Herpesvirus 6