Journal
CURRENT OPINION IN IMMUNOLOGY
Volume 79, Issue -, Pages -Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2022.102254
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Funding
- Marie Sklodowska-Curie Actions (MSCA) Innovative Training Networks (ITN): H2020-MCSA-ITN-2019 [813343]
- Dutch Research Council [OCENW.KLEIN.344]
- Marie Curie Actions (MSCA) [813343] Funding Source: Marie Curie Actions (MSCA)
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When viruses enter host cells, they face a strong immune defense. The integrated stress response (ISR) is a well-known antiviral pathway, where eukaryotic initiation factor 2 (eIF2) becomes phosphorylated, inhibiting eIF2B and causing global translational arrest. Some viruses have developed antagonistic mechanisms against ISR, including a recently discovered class of viral antagonists that target eIF2B, allowing continued translation initiation even at high levels of phosphorylated eIF2.
Viruses, when entering their host cells, are met by a fierce intracellular immune defense. One prominent antiviral pathway is the integrated stress response (ISR). Upon activation of the ISR - typically though not exclusively upon detection of dsRNA - translation-initiation factor eukaryotic initiation factor 2 (eIF2) becomes phosphorylated to act as an inhibitor of guanine nucleotide-exchange factor eIF2B. Thus, with the production of ternary complex blocked, a global translational arrest ensues. Successful virus replication hinges on effective countermeasures. Here, we review ISR antagonists and antagonistic mechanisms employed by picorna-and coronaviruses. Special attention will be given to a recently discovered class of viral antagonists that inhibit the ISR by targeting eIF2B, thereby allowing unabated translation initiation even at exceedingly high levels of phosphorylated eIF2.
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