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Varicella-zoster virus (VZV), also known as human alphaherpesvirus 3, is a highly contagious pathogen responsible for varicella (chickenpox) and herpes zoster (shingles). The virus particle, or virion, is enveloped and displays several essential surface glycoproteins, including gE, gB, gH, and gL, which mediate viral attachment, fusion, and cell-to-cell spread (UniProt: P09333; PubMed: PMID 28733318). Glycoprotein E (gE) is the most abundant and immunogenic surface protein, making it a primary target for recombinant vaccines and neutralizing antibodies. Therapeutic strategies targeting these surface components include live-attenuated vaccines that provide broad immune stimulation and recombinant subunit vaccines that specifically target gE to prevent reactivation (CDC: Shingles Vaccination, 2023). Additionally, passive immunization with VZV-specific immune globulins can neutralize circulating virions to prevent or attenuate disease in high-risk individuals. Understanding the structure and function of these glycoproteins is crucial for developing effective preventatives and treatments for VZV-related complications like postherpetic neuralgia.
Vaccines induce active immunity by stimulating the production of VZV-specific antibodies and T-cells that recognize surface glycoproteins, while immune globulins provide passive immunity by neutralizing virions and preventing cell entry (StatPearls: Varicella Zoster Virus, 2023; PubMed: PMID 28733318).
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