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Varicella-zoster virus (VZV) entry factors consist of a coordinated group of viral glycoproteins and host cell receptors that facilitate the infection of human cells. The core viral fusion machinery includes glycoproteins gB and the gH/gL complex, while gE is essential for skin pathogenesis and efficient cell-to-cell spread (Zerboni et al., 2014, Nature Reviews Microbiology). On the host side, insulin-degrading enzyme (IDE) has been identified as a major receptor that interacts with gB to mediate viral entry (Li et al., 2006, Nature). Additionally, mannose 6-phosphate receptors (MPRs) play a role in the intracellular trafficking and egress of the virus (Chen et al., 2004, Cell). In the nervous system, myelin-associated glycoprotein (MAG) serves as a receptor, contributing to the virus's characteristic neurotropism (Suenaga et al., 2010, PNAS). While current clinical treatments like acyclovir target viral DNA polymerase, these entry factors are primary targets for vaccines and the development of novel entry inhibitors designed to prevent primary infection (chickenpox) and reactivation (shingles).
Inhibition of viral attachment and membrane fusion by blocking interactions between viral glycoproteins (gB, gH/gL, gE) and host cell receptors (IDE, MPR, MAG).
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