Poliovirus type 3 Sabin strain capsid (PV3 Sabin capsid)

The Poliovirus type 3 Sabin strain capsid is the icosahedral protein shell of the attenuated serotype 3 poliovirus, which is a key component of the Oral Poliovirus Vaccine (OPV). It is composed of 60 copies each of four structural proteins—VP1, VP2, VP3, and VP4—which protect the positive-sense single-stranded RNA genome (UniProt, P03301). The capsid's primary biological function is to mediate host cell recognition and entry by binding to the Poliovirus Receptor (CD155) (Mendelsohn et al., 1989). In the context of public health, this capsid is the target of vaccine-induced immunity, where neutralizing antibodies recognize specific epitopes on the capsid surface to prevent infection. However, the Sabin 3 strain is uniquely characterized by its genetic instability, often requiring only a few mutations in the capsid and non-coding regions to revert to a neurovirulent phenotype (Kew et al., 2005). This instability poses a significant challenge for global polio eradication efforts due to the risk of vaccine-associated paralytic poliomyelitis (VAPP) and the circulation of vaccine-derived polioviruses (cVDPVs). Therapeutic interventions targeting the capsid include small-molecule inhibitors like Pocapavir, which occupy a hydrophobic pocket in VP1 to block viral uncoating (Collett et al., 2017). Monitoring the capsid's sequence is essential for detecting the emergence of neurovirulent variants in the environment and in clinical cases.

Other names

Sabin 3 capsidPoliovirus type 3 structural proteinPV3 VP1-VP4 complexPoliovirus type 3 Sabin strain structural proteins

Vaccines containing the capsid proteins induce the production of neutralizing antibodies that block viral attachment to the host receptor CD155 (Mendelsohn et al., 1989). Antiviral capsid inhibitors like Pocapavir bind to a hydrophobic pocket within the VP1 protein, stabilizing the capsid and preventing the conformational changes required for viral uncoating and genome release (Collett et al., 2017).