Human rhinovirus capsid protein

The human rhinovirus capsid protein (commonly called “coat protein” in generic references, but more precisely a complex of four proteins: VP1, VP2, VP3, and VP4) forms the outer shell of the human rhinovirus, a non-enveloped, single-stranded positive-sense RNA virus in the Picornaviridae family[1][6][7]. The capsid is icosahedral, assembled from 60 copies of these four distinct proteins, which together encapsulate and protect the viral RNA and mediate the first steps of infection, including receptor recognition and attachment to host cells, primarily through VP1[1][6][7]. The major groups of rhinoviruses differ in the cell-surface receptors they use for host entry: most bind intercellular adhesion molecule 1 (ICAM-1), while fewer use members of the low-density lipoprotein receptor (LDLR) family—variation that localizes to certain structural regions of the capsid proteins[1][2][7]. Surface-exposed loops of VP1, VP2, and VP3 are the main antigenic determinants, responsible for the large number of HRV serotypes, while VP4 is small and internal, lining the capsid’s inner surface[1][6]. The hydrophobic “pocket” in VP1 is a target for capsid-binding antiviral compounds, which can stabilize the capsid and block uncoating or receptor attachment; these antiviral mechanisms are the basis for experimental and repurposed drug therapies[5][8]. Clinical development of drugs and vaccines is complicated by the high degree of antigenic heterogeneity among HRV strains, making sequence-specific approaches challenging[1]. Note: The phrase “human rhinovirus coat protein” is not a standard canonical target name, as it groups multiple viral proteins; the structured data above best maps to the collective “Human rhinovirus capsid protein,” and relevant drug targeting typically focuses on specific components (mainly VP1)[1][5][8].

Other names

Rhinovirus coat proteinHRV capsid proteinViral protein 1 (VP1)Viral protein 2 (VP2)Viral protein 3 (VP3)Viral protein 4 (VP4)

Capsid stabilization (preventing uncoating), Inhibition of receptor binding, Blocking viral entry