Abstract
Currently, complete or partial genome sequences of more than 150 human rhinovirus (HRV) isolates are known. Twelve species A use members of the low-density lipoprotein receptor family for cell entry, whereas the remaining HRV-A and all HRV-B bind ICAM-1. HRV-Cs exploit an unknown receptor. At least all A and B type viruses depend on receptor-mediated endocytosis for infection. In HeLa cells, they are internalized mainly by a clathrin- and dynamin-dependent mechanism. Upon uptake into acidic compartments, the icosahedral HRV capsid expands by ~4% and holes open at the 2-fold axes, close to the pseudo-3-fold axes and at the base of the star-shaped dome protruding at the vertices. RNA-protein interactions are broken and new ones are established, the small internal myristoylated capsid protein VP4 is expelled, and amphipathic N-terminal sequences of VP1 become exposed. The now hydrophobic subviral particle attaches to the inner surface of endosomes and transfers its genomic (+) ssRNA into the cytosol. The RNA leaves the virus starting with the poly(A) tail at its 3′-end and passes through a membrane pore contiguous with one of the holes in the capsid wall. Alternatively, the endosome is disrupted and the RNA freely diffuses into the cytoplasm.
Highlights
Human rhinoviruses (HRVs) are icosahedral (30 nm in diameter) and nonenveloped with a (+) ssRNA genome of ∼7100 bases
Many more rhinoviruses were identified in clinical specimens [3,4,5]. Independent from this classification, HRV-A and HRV-B are divided into two groups based upon the receptors exploited for host cell attachment; the minor receptor group, including the so far identified 12 HRV-A, bind low-density lipoprotein receptor (LDLR), very-LDLR (VLDLR), and LDLR-related protein 1 (LRP1) [6,7,8,9], while the remaining HRVA and HRV-B use intercellular adhesion molecule 1 (ICAM-1) for cell entry [10]
Some major group HRVs (HRV8, 54, and 89) can use heparan sulfate proteoglycans (HSPG) as an additional receptor [7, 11, 12] either as wild type or after adaptation to grow in cells lacking ICAM-1
Summary
Human rhinoviruses (HRVs) are icosahedral (30 nm in diameter) and nonenveloped with a (+) ssRNA genome of ∼7100 bases. HRV-C infections, in addition to symptoms of the common cold, cause pharyngitis, croup, otitis media, bronchiolitis, or pneumonia. This species must have circulated in the population for at least 10 years, but probably much longer, as they escaped detection because of being refractive to propagation in tissue culture [15]. Other means of disease prevention are believed to be more effective [30] These include antiviral agents inhibiting either uncoating (by binding into a hydrophobic pocket within the capsid) or replication (by targeting virally encoded enzymes, such as the proteases). None of the initially promising compounds has reached clinical application
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