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Herpes simplex virus type 2 (HSV-2) is an enveloped, double-stranded DNA virus of the family *Herpesviridae*, subfamily *Alphaherpesvirinae*, primarily responsible for genital herpes in humans[3][5]. The virus has a ∼152 kb linear DNA genome surrounded by anicosahedral capsid, a proteinaceous tegument, and a lipid envelope embedded with distinct glycoproteins (notably gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL, gM, gN)[2]. The viral glycoproteins mediate host cell attachment, entry, and cell fusion, while the internal proteins direct genome transport and viral replication[2][5]. HSV-2 establishes lifelong latency in neurons and is reactivated periodically, resulting in recurrent disease. Treatment is primarily with nucleoside analogs (e.g., acyclovir), but drug resistance and latent infection remain therapeutic challenges[3]. While the virus as a whole serves as a therapeutic target for antivirals and vaccines, individual virally encoded proteins—such as DNA polymerase, thymidine kinase, and envelope glycoproteins (gB, gD, gH/gL)—are the actual molecular targets for drug design and mechanistic studies[2][7].
Inhibition of viral DNA polymerase (nucleoside analogs, e.g., acyclovir) - Inhibition of viral helicase-primase complex (e.g., pritelivir) - Inhibition of viral entry or membrane fusion (experimental fusion/attachment inhibitors targeting viral glycoproteins)
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