期刊
SCIENCE
卷 337, 期 6091, 页码 199-204出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1222213
关键词
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资金
- Wellcome Trust [088789, 073126]
- U.K. Medical Research Council [G0700815]
- NIH
- National Institute of Allergy and Infectious Diseases (NIAID), NIH
- Science Foundation Ireland [08/IN.1/B1889]
- Defense Threat Reduction Agency [HDTRA-1-08-C-0023]
- Luxembourg Centre for Systems Biomedicine
- University of Luxembourg
- U.K. Biotechnology and Biological Sciences Research Council
- Cambridge Infectious Disease Consortium
- NIH-Oxford-Cambridge Research Scholars program
- Biotechnology and Biological Sciences Research Council [BBS/E/D/20241864] Funding Source: researchfish
- Medical Research Council [MR/J002232/1, G0700815, G9800943] Funding Source: researchfish
- BBSRC [BBS/E/D/20241864] Funding Source: UKRI
- MRC [G9800943, G0700815, MR/J002232/1] Funding Source: UKRI
Influenza A virus (IAV) infection leads to variable and imperfectly understood pathogenicity. We report that segment 3 of the virus contains a second open reading frame (X-ORF), accessed via ribosomal frameshifting. The frameshift product, termed PA-X, comprises the endonuclease domain of the viral PA protein with a C-terminal domain encoded by the X-ORF and functions to repress cellular gene expression. PA-X also modulates IAV virulence in a mouse infection model, acting to decrease pathogenicity. Loss of PA-X expression leads to changes in the kinetics of the global host response, which notably includes increases in inflammatory, apoptotic, and T lymphocyte-signaling pathways. Thus, we have identified a previously unknown IAV protein that modulates the host response to infection, a finding with important implications for understanding IAV pathogenesis.
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