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Coxsackievirus B (CVB) serotypes 1 through 5 are non-enveloped, positive-sense single-stranded RNA viruses belonging to the Enterovirus genus of the Picornaviridae family (ViralZone, SIB). These virions are significant human pathogens known to cause a range of conditions, including aseptic meningitis, myocarditis, and pleurodynia. Crucially, epidemiological and mechanistic studies have linked chronic or acute CVB infections to the triggering of pancreatic beta-cell autoimmunity, potentially leading to the development of Type 1 Diabetes (T1D) (Hyöty, H., Diabetologia, 2014). The virion's capsid, composed of proteins VP1, VP2, VP3, and VP4, serves as the primary interface with the host adaptive immune system, acting as the target for neutralizing antibodies and T-cell responses. Therapeutic interventions, such as the polyvalent inactivated vaccine PRV-101 (Provention Bio/Sanofi), target these virions to elicit a protective immune response, thereby preventing infection and its associated long-term sequelae (Stone, V. M., et al., Science Advances, 2020). By neutralizing the virus before it can establish infection in target tissues like the pancreas or heart, these strategies aim to mitigate both acute viral disease and chronic autoimmune triggers.
Induction of neutralizing antibodies by the host adaptive immune system to prevent viral attachment, entry, and uncoating; antiviral inhibition of viral capsid function.
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