{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T14:15:14Z","timestamp":1780064114884,"version":"3.54.0"},"reference-count":44,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T00:00:00Z","timestamp":1751500800000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T00:00:00Z","timestamp":1751328000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>One of the unknowns related to severe acute respiratory syndrome coronavirus 2 (SARS\u2010CoV\u20102) infection is the mechanism underlying the inflammatory response induced by the virus. Poly(A) polymerase gamma (PAPOLG) was previously shown to be upregulated during SARS\u2010CoV\u20102 infection. The present study explored how PAPOLG affects the inflammatory reaction triggered by SARS\u2010CoV\u20102. PAPOLG was knocked down or overexpressed in THP\u20101 macrophages. Target pathways were identified using RNA sequencing and bioinformatics analysis. The levels of PAPOLG, transcriptional regulator nuclear factor kappa\u2010light\u2010chain\u2010enhancer of activated B cells (NF\u2010\u03baB), and cytokines TNF\u2010\u03b1 and IL\u20106 were measured, along with an assessment of NF\u2010\u03baB mRNA stability. PAPOLG was significantly upregulated in SARS\u2010CoV\u20102\u2010infected THP\u20101 macrophages. Genes subjected to alternative polyadenylation were enriched in immune pathways, and NF\u2010\u03baB emerged as a key regulator. Knockdown of PAPOLG promoted NF\u2010\u03baB mRNA degradation, while decreasing the levels of tumor necrosis factor\u2010alpha (TNF\u2010\u03b1) and interleukin\u20106 (IL6). Conversely, overexpression of PAPOLG stabilized NF\u2010\u03baB mRNA and enhanced TNF\u2010\u03b1 and IL\u20106 expression. PAPOLG contributes to the inflammatory response in SARS\u2010CoV\u20102\u2010infected macrophages by stabilizing NF\u2010\u03baB mRNA. Thus, PAPOLG may be targeted to control COVID\u201019\u2010related inflammation.<\/jats:p>","DOI":"10.1002\/jmv.70478","type":"journal-article","created":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T09:56:46Z","timestamp":1751536606000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["SARS\u2010CoV\u20102\u2010Induced PAPOLG Contributes to Inflammation Response by Stabilizing NF\u2010\u03baB mRNA"],"prefix":"10.1002","volume":"97","author":[{"given":"Yanyan","family":"Liao","sequence":"first","affiliation":[{"name":"Biosafety III Laboratory, Life Science Institute Guangxi Medical University Nanning Guangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4260-692X","authenticated-orcid":false,"given":"Qiuli","family":"Chen","sequence":"additional","affiliation":[{"name":"Guangxi Key Laboratory of AIDS Prevention and Treatment, School of Public Health Guangxi 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