The Structure and Replication of Rhinoviruses

Productive Entry Pathways of Human Rhinoviruses

“…Upon arrival of the viral genome in the cytosol the RNA is translated into a polyprotein that is autocatalytically and cotranslationally cleaved by the viral proteinases 2A pro , 3C pro , and its precursor 3CD pro , into structural proteins VP1, VP0, VP3, and the nonstructural proteins required for virus replication [34]. These include the RNA-dependent RNA polymerase 3D pol as well as the precursor proteins (3CD, 2AB) that induce the formation of membrane vesicles derived from intracellular membrane-bounded compartments acting as scaffold for the RNA polymerase.…”

Human rhinoviruses: The cold wars resume

“…Picornaviruses recognize a variety of receptors (Rossmann, 1994;Khan et al, 2008;Uncapher et al, Minor group HRV strains are underlined, major group are shown in bold. M (only found in HRV A; propensity for monkey cells) and H strains (located in both species; grew in human cell cultures) (Gwaltney and Jordan, 1964;Stott et al, 1969;Rosenbaum et al, 1971;Tyrrell and Parsons, 1960;Tyrrell and Bynoe, 1961;Ketler et al, 1962;Taylor-Robinson and Tyrrell, 1962;Cooney and Kenny, 1977;Bloom et al, 1963) are indicated with superscripts and generally correlate with receptor usage (Macnaughton, 1982). Assignment of some strains to this sub-classification may also have been influenced by the viral load in the inoculum (Douglas et al, 1966a;Hamre, 1967).…”

Rhinoviruses

“…HRVs that preferred growth using monkey cells were called "M" strains and those (the majority) that grew only in human cell cultures, "H" strains [ 56 , 176 -180 ]. These two groups correlate with receptor usage [ 131 ] (Table 29.1 ) and possibly with the titer of the inoculum employed [ 181 ]. In 1962 it was proposed to abandon this terminology in favor of a sequential numbering system [ 177 ].…”

“…Genomic RNA (plus strand) is the template for complementary minus strand synthesis which in turn is the template for new genomic plus strands that become incorporated into virions [ 131 ]. Virions are synthesized from 4 to 7 h after infection and reach maximum release levels at 10-18 h [ 131 ]. HRV replication in epithelial cells may shut off host cell transcriptional activity via direct cleavage of transcription factors and nuclear pore complex components.…”

“…Single-stranded infectious RNA forms after RIs start to accumulate [ 130 ]. Genomic RNA (plus strand) is the template for complementary minus strand synthesis which in turn is the template for new genomic plus strands that become incorporated into virions [ 131 ]. Virions are synthesized from 4 to 7 h after infection and reach maximum release levels at 10-18 h [ 131 ].…”