Special Issue "Viruses and the OAS-RNase L Pathway"
A special issue of Viruses (ISSN 1999-4915).
Deadline for manuscript submissions: closed (30 September 2019) | Viewed by 13104
Interests: coronavirus pathogenesis; murine coronavirus; human respiratory coronaviruses; MERS-CoV; SARS-CoV-2; common CoVs; viral antagonism of innate immunity; OAS/RNase L; endogenous dsRNA induced pathogenesis; Zika virus
OAS-RNase L is a potent interferon-regulated antiviral pathway that severely limits the pathogenesis of many different types of viruses. Upon sensing viral (non-self) dsRNA, OASs produce 2’,5’-oligoadenylates (2-5A) that bind to and cause the activation of RNase L. RNase L then cleaves both the host and viral single-stranded RNA, thereby limiting protein production, virus replication and spread, and causing apoptosis. Recent and exciting advances emphasize the importance of OAS-RNase L in antiviral innate immunity. Some of these studies reveal how viruses evolved many strategies to antagonize OAS-RNase L, including sequestering dsRNA from OAS, degrading 2-5A by viral- or host-encoded enzymes or directly inhibiting RNase L. Other studies extend beyond the antiviral state into cellular responses to host (self) dsRNA induced by genetic or epigenetic events. This unique and first-of-its-kind issue on OAS-RNase L will contribute to our understanding of how this remarkable innate immune pathway impacts human health in the context of viral and genetic diseases and cancer.
Prof. Dr. Susan Weiss
Prof. Dr. Robert H. Silverman
Manuscript Submission Information
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- Ribonuclease L
- oligoadenylate synthetase
- viral antagonists
- endogenous dsRNA
- antiviral pathways