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Herpes simplex virus (HSV) particles and early replication processes represent the sequence of events from viral attachment to the host cell to the initiation of viral DNA synthesis. This complex pathway involves viral glycoproteins (e.g., gB, gC, gD, gH/gL) interacting with host receptors like HVEM or nectin-1 to facilitate entry [PubMed: 21613584]. Following entry, the viral capsid is transported to the nucleus where the viral genome is released and immediate-early genes are expressed to hijack host machinery and initiate viral replication [NIH: NBK470195]. Therapeutic intervention typically targets specific enzymes within this process, most notably the viral DNA polymerase (inhibited by acyclovir) and the helicase-primase complex (inhibited by pritelivir) [StatPearls: NBK542180]. Additionally, entry inhibitors like docosanol work by interfering with the fusion between the viral envelope and the host cell membrane [PubChem: CID 12620]. These processes are critical for the pathogenesis of HSV-1 and HSV-2, which cause conditions ranging from oral cold sores to life-threatening encephalitis [WHO: Herpes Simplex Virus Fact Sheet].
Inhibition of viral DNA polymerase, inhibition of viral entry/fusion, and inhibition of the helicase-primase complex.
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