ArticleJournal of virology2026
SADS-CoV NS3 induces apoptosis by blocking the formation of Bcl-xL-BAK complex.
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Swine acute diarrhea syndrome coronavirus (SADS-CoV) is an emerging porcine coronavirus with characteristics of bat origin, posing a potential threat to animal welfare and public health. Recent studies have shown that apoptosis induced by SADS-CoV contributes to virus replication. However, the virus proteins involved in SADS-CoV-induced apoptosis and their potential molecular mechanisms remain largely unknown. This study found that the SADS-CoV accessory protein NS3 interacted with the BH3 domain of Bcl-xL in the mitochondria. This interaction disrupted the Bcl-xL-BAK complex, leading to increased activation of BAK and subsequent induction of mitochondrion-mediated apoptosis. Furthermore, knockout of Bcl-xL reduced the NS3-induced apoptosis and increased the replication of SADS-CoV. Additionally, deletion of the NS3 gene decreased SADS-CoV-induced apoptosis and diminished the viral pathogenicity in murine models, indicating that NS3 is a critical determinant of SADS-CoV pathogenicity. In conclusion, our findings firstly reveal the mechanism by which SADS-CoV NS3 regulates apoptosis to enhance the viral replication and pathogenicity.
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