AI Article Synopsis
- Inflammasomes are key in fighting infections, and the study focuses on how HSV-1, a contagious virus, uniquely interacts with the host's immune response.
- The researchers discovered that a gene called TET3 is critical for HSV-1 infection, as it helps activate a specific inflammasome in the nucleus by binding to caspase-1.
- Blocking TET3’s interactions can hinder the virus’s ability to spread, suggesting potential new treatments for HSV-1 infections in the future.
Article Abstract
Inflammasomes play important roles in resisting infections caused by various pathogens. HSV-1 is a highly contagious virus among humans. The process by which HSV-1 particles bud from the nucleus is unique to herpes viruses, but the specific mechanism is still unclear. Here, we screened genes involved in HSV-1 replication. We found that TET3 plays an essential role in HSV-1 infection. TET3 recognizes the UL proteins of HSV-1 and, upon activation, can directly bind to caspase-1 to activate an ASC-independent inflammasome in the nucleus. The subsequent cleavage of GSDMD in the nucleus is crucial for the budding of HSV-1 particles from the nucleus. Inhibiting the perforation ability of GSDMD on the nuclear membrane can significantly reduce the maturation and spread of HSV-1. Our results may provide a new approach for the treatment of HSV-1 in the future.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11527991 | PMC |
| http://dx.doi.org/10.1038/s41423-024-01221-2 | DOI Listing |
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