Herpes simplex virus 1 replication process (HSV-1 replication) (HSV-1 replication)

The intracellular HSV-1 replication process encompasses the complex series of events from viral entry into the host cell to the release of progeny virions (Knipe & Cliffe, 2008, Nat Rev Microbiol). This cycle involves several distinct stages, including attachment and fusion, nuclear entry of the viral genome, regulated gene expression (immediate-early, early, and late phases), DNA replication, and virion assembly and egress (Whitley & Roizman, 2001, Lancet). Key viral enzymes such as the DNA polymerase (UL30) and the helicase-primase complex (UL5, UL52, UL8) serve as critical nodes within this process and are the primary targets for current antiviral therapies (Gnann & Whitley, 2016, NEJM). Inhibition of these steps prevents the production of new viral particles, thereby limiting tissue damage and clinical symptoms associated with infections like cold sores, keratitis, and encephalitis (Piret & Boivin, 2011, Antimicrob Agents Chemotherapy). While highly effective, targeting this process faces challenges such as the establishment of latent infections in sensory neurons, which remain unaffected by current replication inhibitors (Nicoll et al., 2012, J Virol). Furthermore, the emergence of drug-resistant strains, particularly in immunocompromised individuals, necessitates the development of drugs targeting alternative steps in the replication cycle (Piret & Boivin, 2011, Antimicrob Agents Chemotherapy).

Other names

HSV-1 life cycleIntracellular HSV-1 replicationHerpes simplex virus type 1 replicationHSV-1 viral replication cycle

Inhibition of viral DNA polymerase; Inhibition of viral helicase-primase complex; Chain termination of viral DNA synthesis