Switch from Cap- to Factorless IRES-Dependent 0 and +1 Frame Translation during Cellular Stress and Dicistrovirus Infection

Wang, Qing S.; Jan, Eric

Viruses are exquisitely dependent on host translational machinery, however, the strategies by how this is achieved are diverse [7, 47] . For some RNA viruses such as picornaviruses, specific steps in cap-dependent translation are compromised thus increasing the available pool of ribosomes and initiations factors for viral IRES translation. In contrast, DNA viruses like human cytomegalovirus (HCMV), host translation is not impaired and virus replication relies on stimulation of cap-dependent translation machinery and increases in initiation factors concentration [48, 49] . Other viruses target host mRNA metabolism. For example, vesicular stomatitis virus inhibits the nuclear export of cellular mRNAs [50] , and severe acute respiratory virus (SARS) suppresses host translation by inactivating 40S ribosomes and selectively promoting host but not viral RNA degradation [51, 52] . In the case of herpes virus infection, host translation is inhibited in part through degradation of host mRNAs, whereas the accelerated viral mRNA turnover helps regulate different population of viral mRNAs expression. [53] [54] [55] . Alternatively, it has been proposed that replicating viral RNA genomes can outcompete for host factors and ribosomes for viral protein synthesis.