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The poliovirus capsid is the structural shell of the virus, composed of 60 units each of the proteins VP1, VP2, VP3, and VP4, which are processed from the P1 polyprotein precursor (UniProt: P03300). These proteins are the primary targets for the host immune system, which recognizes specific antigenic sites on the capsid surface to produce neutralizing antibodies (StatPearls: NBK558944). These antibodies prevent infection by blocking the virus's ability to bind to its cellular receptor, CD155, or by interfering with the uncoating process (Wikipedia: Poliovirus). Vaccines like the Inactivated Poliovirus Vaccine (IPV) and Oral Poliovirus Vaccine (OPV) work by presenting these capsid antigens to the immune system to establish long-term protection (CDC: Polio Vaccination). Beyond vaccines, experimental antiviral drugs such as Pocapavir target the capsid by binding to a hydrophobic pocket, thereby stabilizing the capsid and preventing the release of the viral RNA into the host cell (PubMed: 25156105). Understanding the interaction between the host immune system and these capsid antigens is crucial for the global effort to eradicate poliomyelitis.
Vaccines induce neutralizing antibodies that bind to capsid antigens and block viral attachment to the host receptor CD155; capsid-binding antivirals inhibit viral uncoating and genome release.
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