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. 1. Introduction Human rhinoviruses (HRVs) are icosahedral (30？nm in diameter) and nonenveloped with a (+) ssRNA genome of ~7100 bases. Belonging to the family Picornaviridae, genus Enterovirus, they are composed of 60 copies each of four capsid proteins, VP1 to VP4. In 1987, HRVs from clinical samples were serotyped into 100 strains [1]. Recently, complete genome sequences of all known HRVs were determined. Phylogenetic analyses grouped them into 3 species; 74 HRV-A, 25 HRV-B, and 6 HRV-C [2]. Since then, many more rhinoviruses (mostly of type C) were identified in clinical specimens [3–5]. 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) [6–9], while the remaining HRVA and HRV-B (constituting the majority, that is, the major group) use intercellular adhesion molecule 1 (ICAM-1) for cell entry [10]. Some major group HRVs (HRV8, 54, and 89) can also use heparan sulfate proteoglycans (HSPG) as an additional receptor [7, 11, 12] either as wild type (wt) or after adaptation to grow in cells lacking ICAM-1. This is achieved by numerous cycles alternating between
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