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Human rhinoviruses are small, non-enveloped viruses with a single-stranded positive-sense RNA genome of about 7,200–7,500 nucleotides, belonging to the genus Enterovirus within the family Picornaviridae[1][2][3][7][8]. The viral capsid consists of four structural proteins (VP1, VP2, VP3, VP4) arranged as an icosahedron, encapsidating the RNA genome[1][3][5][7]. Rhinoviruses are divided antigenically and genetically into three main species: HRV-A, HRV-B, and HRV-C, each with numerous serotypes and extensive antigenic diversity[2][7][8]. They are the primary cause of the common cold and can exacerbate asthma and other chronic respiratory disorders[1][8]. Entry into host cells is mediated by the major group using intercellular adhesion molecule-1 (ICAM-1), minor group using low-density lipoprotein receptor (LDLR), and HRV-C using cadherin-related family member 3 (CDHR3)[2][5][7]. Due to the existence of more than 160 genotypes and considerable structural diversity, development of universal therapeutics or vaccines has proven challenging. Experimental antivirals have targeted the viral capsid to block attachment or uncoating, and viral protease 3C to inhibit viral replication, but there are no widely approved HRV-specific drugs[4][5].\n\nNote: Rhinovirus is a pathogenic virus, not a single molecular target. For drug targeting, one would consider its capsid proteins (e.g., VP1), its proteases (e.g., 3Cpro), or receptors it uses for entry (e.g., ICAM-1, LDLR, CDHR3) as true drug targets[4][5][7].
(For antiviral agents:) Inhibition of viral attachment or uncoating, inhibition of viral 3C protease (essential for viral polyprotein processing)
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