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Coxsackievirus B (CVB) antigens consist of the structural and non-structural proteins produced by the six serotypes of Coxsackievirus B (B1–B6), which are members of the Enterovirus genus. The structural proteins, VP1 through VP4, assemble to form the icosahedral capsid that protects the viral RNA and mediates entry into host cells by binding to receptors such as the Coxsackievirus and Adenovirus Receptor (CAR) (StatPearls, 2023). Non-structural proteins, including the 3C protease and 3D RNA-dependent RNA polymerase, are essential for processing the viral polyprotein and replicating the viral genome (UniProt, P03300). CVB is a primary etiological agent for several serious conditions, most notably acute and chronic myocarditis, and it is strongly implicated in the pathogenesis of Type 1 Diabetes through the infection of pancreatic islet cells (PubMed, PMID: 33433434). Therapeutic interventions targeting these antigens include capsid-binding small molecules like pleconaril, which prevent viral uncoating, and investigational vaccines like PRV-101 designed to elicit protective neutralizing antibodies (Sanofi/Provention Bio). Despite their potential, drug development faces challenges such as the rapid mutation of viral antigens leading to resistance and the risk of exacerbating autoimmune responses through cross-reactive epitopes.
Capsid binding to prevent viral uncoating; inhibition of viral 3C protease to prevent polyprotein processing; inhibition of viral RNA-dependent RNA polymerase; induction of neutralizing antibodies via vaccination.
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