Hijacking Host Functions for Translation and RNA Replication by Enteroviruses
Sonia Maciejewski and Bert L. Semler
from: Enteroviruses: Omics, Molecular Biology, and Control (Edited by: William T. Jackson and Carolyn B. Coyne). Caister Academic Press, U.K. (2018) Pages: 23-50.
Abstract
The Enterovirus genus includes the species poliovirus, coxsackievirus, rhinovirus, and enterovirus. These viruses can cause severe diseases in certain individuals, including poliomyelitis, myocarditis, and meningitis. Rhinovirus is responsible for one of the most prevalent human diseases in the world, the common cold. Although diseases caused by these infections can be severe, no antiviral against enteroviruses is currently available. To develop broad-spectrum antivirals, the molecular components and mechanistic steps of the viral replication cycle must be identified. Due to the small genomic RNA (≈7.5 kb) of enteroviruses, host proteins are utilized to mediate viral replication. Although some of these cellular proteins have been identified and their roles in picornavirus replication have been characterized, it is necessary to identify and elucidate the replication functions of additional cellular proteins to develop new potential targets for antiviral therapeutics. Enteroviruses are known to modify cellular proteins to stimulate their levels of gene expression and RNA synthesis, but there are some cases where unaltered host proteins can aid in viral replication. Enteroviruses can also evade the antiviral response by altering host proteins involved in the immune and stress response to ensure efficient viral replication. How enteroviruses modify and utilize these host proteins will be discussed in this chapter read more ...
