AI Article Synopsis
- ASFV resists the host's antiviral response by inhibiting interferon secretion and interferon-stimulated gene activity, complicating its replication process.
- The OAS1 gene emerges as a crucial factor that can inhibit ASFV replication through a mechanism that depends on RNaseL and can activate the JAK-STAT pathway, enhancing innate immune responses.
- OAS1 also interacts with the ASFV P72 protein, promoting its degradation via ubiquitination, which in turn helps to suppress ASFV infection.
Article Abstract
African swine fever virus (ASFV) completes the replication process by resisting host antiviral response inhibiting interferon (IFN) secretion and interferon-stimulated genes (ISGs) function. 2', 5'-Oligoadenylate synthetase gene 1 (OAS1) has been reported to inhibit the replication of various RNA and some DNA viruses. However, the regulatory mechanisms involved in the ASFV-induced IFN-related pathway still need to be fully elucidated. Here, we found that OAS1, as a critical host factor, inhibits ASFV replication in an RNaseL-dependent manner. Furthermore, overexpression of OAS1 can promote the activation of the JAK-STAT pathway promoting innate immune responses. In addition, OAS1 plays a new function, which could interact with ASFV P72 protein to suppress ASFV infection. Mechanistically, OAS1 enhances the proteasomal degradation of P72 by promoting TRIM21-mediated ubiquitination. Meanwhile, P72 inhibits the production of avSG and affects the interaction between OAS1 and DDX6. Our findings demonstrated OAS1 as an important target against ASFV replication and revealed the mechanisms and intrinsic regulatory relationships during ASFV infection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10617512 | PMC |
| http://dx.doi.org/10.1128/jvi.01217-23 | DOI Listing |
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