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Host receptors and entry factors used by varicella-zoster virus (VZV) comprise a diverse group of cellular proteins essential for viral attachment, membrane fusion, and entry. The primary receptor for VZV is the Insulin-like growth factor 2 receptor (IGF2R), also known as the cation-independent mannose 6-phosphate receptor (CI-MPR), which interacts with viral glycoprotein E (gE) to facilitate endocytosis [1][2]. Myelin-associated glycoprotein (MAG) has been identified as a functional receptor for glycoprotein B (gB), playing a significant role in the infection of the nervous system [3]. Additionally, Insulin-degrading enzyme (IDE) acts as a coreceptor for gE, although its requirement is cell-type specific [4]. Integrins, specifically the alpha-V subunit, have also been implicated in the entry process through interactions with the gH/gL complex [5]. Initial viral tethering to the host cell surface is typically mediated by Heparan sulfate proteoglycans (HSPGs) [6]. While current therapies like acyclovir target viral DNA replication, these host factors are being investigated as potential targets for novel entry inhibitors to prevent both primary infection and shingles reactivation [7].
Inhibition of viral DNA polymerase (Acyclovir, Valacyclovir, Famciclovir, Foscarnet, Cidofovir); Inhibition of viral helicase-primase complex (Amenamevir)
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