Picornaviruses

Abstract

The name picornavirus is derived from pico for small and ribonucleic acid (RNA), denoting the chemical nature of the genome. Virions are nonenveloped icosahedral particles approximately 30 nm in diameter. The capsid is constructed from 60 copies of each of four structural proteins, which account for 70% of the particle mass and enclose the single‐strand genome of 7500–8500 nucleotides. The positive‐strand genome acts directly as a messenger RNA to template a single polyprotein product. This is subsequently processed by virally encoded proteases into mature active proteins. Several intermediate products have distinct functions to the final fully processed proteins. Replication of the genome is initiated by an uridylated peptide and proceeds via a negative‐strand intermediate template. Picornaviruses are among the smallest pathogens of vertebrates and are responsible for many important diseases in humans and animals. Key Concepts There are effective vaccines against polio, hepatitis A and foot‐and‐mouth disease viruses. In addition, movement control and slaughter is used to control foot‐and‐mouth disease. There are no licensed drugs for picornavirus infections. Genome sequence comparisons have replaced biological and biophysical comparisons as the bases for classification within the family. Picornavirus particles comprise 60 copies each of four structural proteins, which form a quasi‐T1 icosohedral capsid encasing the single‐strand RNA genome. The picornavirus RNA genome functions as a messenger RNA to template the synthesis of a single polyprotein, which is posttranslationally processed by viral proteases. Picornaviruses bind to cell‐specific surface receptors, and this interaction is an important factor in determining host and tissue specificity of each virus. Picornaviruses cannot gain entry to cells by membrane fusion, as is the case for enveloped viruses, and require special mechanisms to breach cellular membranes and safely deliver the genome into the host cell. Genome replication occurs in association with virus‐modified cellular membranes. Viral RNA templates complementary negative‐strand molecules, which in turn template multiple positive‐strand copies. The synthesis of all RNA molecules is initiated by an uridylated peptide primer. The mechanisms of transmission of infection play key roles in the epidemiology of picornavirus infections. Picornaviruses are responsible for a wide range of clinical diseases resulting from multiple factors such as receptor specificity, tissue‐specific susceptibility, virulence and the mechanisms of transmission.

Do We Know Rhinoviruses and Their Clinical Impact?

“…Viral RNA genome is released into the cytoplasm of the infected cell, where the host-cell translation machinery directly translates positive-sense RNA (33,34). Translation is initiated by a cap-independent mechanism (35), resulting in a single large polyprotein which is further proteolytically processed into ten proteins and several functional intermediates. The replication of the genome takes place on virusinduced membrane structures (36).…”

“…The replication of the genome takes place on virusinduced membrane structures (36). The process is carried out by a virus specific RNA-dependent RNA polymerase via semi-conservative mechanism (35). Mature rhinovirus virions exit the host cells without destroying the cell.…”