Human rhinovirus replication cycle (HRV replication cycle)

The Human rhinovirus (HRV) replication cycle encompasses the multi-step process by which the virus infects host respiratory epithelial cells and replicates its genetic material (Jacobs et al., 2013). The cycle begins with the attachment of the viral capsid to host cell receptors, such as Intercellular Adhesion Molecule 1 (ICAM-1) or the Low-Density Lipoprotein Receptor (LDLR), followed by receptor-mediated endocytosis (Fuchs & Blaas, 2010). Upon entry, the viral capsid undergoes uncoating to release its positive-sense single-stranded RNA genome into the cytoplasm, where it is translated into a single large polyprotein. This polyprotein is subsequently processed into functional structural and non-structural proteins by the action of viral proteases 2A and 3C (Blaas & Fuchs, 2016). The viral RNA-dependent RNA polymerase (3Dpol) then replicates the genome, and new virions are assembled and released through cell lysis, leading to the clinical symptoms of the common cold or exacerbations of underlying respiratory conditions like asthma. Therapeutic strategies targeting this cycle include capsid binders (e.g., pleconaril) that inhibit uncoating and protease inhibitors (e.g., rupintrivir) that block protein maturation (Patick, 2006). Despite extensive research, the high genetic diversity of over 160 HRV serotypes and the rapid development of resistance remain significant challenges for the clinical approval of specific antiviral therapies.

Other names

Rhinovirus infection/replication cycleHRV life cycleRhinovirus replicationHRV infection pathway

Capsid binding to prevent viral uncoating; Inhibition of 3C protease to prevent polyprotein cleavage; Inhibition of RNA-dependent RNA polymerase