Coxsackievirus B capsid protein

Coxsackievirus B capsid proteins (VP1–VP4) are the four structural proteins comprising the icosahedral shell of Coxsackievirus B virions (serotypes 1–5), which belong to the Enterovirus genus, Picornaviridae family[1][3]. The major capsid proteins mediate attachment to host cell receptors—primarily Coxsackievirus and adenovirus receptor (CAR)—initiating viral entry[3]. Key antigenic sites and receptor-binding regions are found in VP1 and VP2, with structural features such as the “canyon” playing critical roles in host specificity[3]. Capsid proteins also interact with the viral RNA and can manipulate host cell cycle (e.g., VP1 induces G1 arrest via heat shock protein pathways), promote apoptosis, or contribute to immune evasion[1][3][5]. Variability, especially in VP1/VP2, affects viral infectivity, pathogenicity, and capsid stability, and can influence antiviral drug sensitivity[2]. Coxsackievirus B is a known cause of myocarditis, meningitis, pancreatitis, and is implicated in type 1 diabetes pathology[3]. While investigational compounds like pleconaril can bind similar enteroviral capsids, no capsid-specific antivirals are currently approved for Coxsackievirus B.

Other names

Coxsackievirus B viral capsid proteinCVB capsid proteinEnterovirus B capsid proteinCVB VP1, VP2, VP3, VP4

Inhibition of viral uncoating by binding to capsid “pocket factor” site; prevention of receptor attachment or capsid destabilization.