AI Article Synopsis
- Senecavirus A (SVA) is a picornavirus linked to vesicular disease that has developed mechanisms to avoid the host's immune system, though its infection process is not fully understood.
- The study highlights that SERPINB1 enhances SVA replication by regulating innate immunity and the autophagy pathway through the degradation of IκB kinase epsilon (IKBKE).
- Findings suggest SERPINB1 could serve as a potential therapeutic target for controlling SVA infections by modulating viral replication and immune responses.
Article Abstract
Senecavirus A (SVA) is an emerging picornavirus associated with vesicular disease, which wide spreads around the world. It has evolved multiple strategies to evade host immune surveillance. The mechanism and pathogenesis of the virus infection remain unclear. In this study, we show that SERPINB1, a member of the SERPINB family, promotes SVA replication, and regulates both innate immunity and the autophagy pathway. SERPINB1 catalyzes K48-linked polyubiquitination of IκB kinase epsilon (IKBKE) and degrades IKBKE through the proteasome pathway. Inhibition of IKBKE expression by SERPINB1 induces autophagy to decrease type I interferon signaling, and ultimately promotes SVA proliferation. These results provide importantly the theoretical basis of SVA replication and pathogenesis. SERPINB1 could be a potential therapeutic target for the control of viral infection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10617579 | PMC |
| http://dx.doi.org/10.1128/jvi.01045-23 | DOI Listing |
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