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Influenza virus infection causes global RNAPII termination defects
N. Zhao, V. Sebastiano, N. Moshkina, N. Mena, J. Hultquist, D. Jimenez-Morales, Y. Ma, A. Rialdi, R. Albrecht, R. Fenouil, MT. Sánchez-Aparicio, J. Ayllon, S. Ravisankar, B. Haddad, JSY. Ho, D. Low, J. Jin, V. Yurchenko, RK. Prinjha, A....
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S.
Grantová podpora
R01 AI113186
NIAID NIH HHS - United States
S10 OD018522
NIH HHS - United States
U19 AI106754
NIAID NIH HHS - United States
NLK
ProQuest Central
od 2004-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2004-01-01 do Před 1 rokem
- MeSH
- chřipka lidská genetika MeSH
- lidé MeSH
- RNA-polymerasa II genetika MeSH
- terminátorové oblasti (genetika) genetika MeSH
- virulence MeSH
- virus chřipky A patogenita fyziologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
Viral infection perturbs host cells and can be used to uncover regulatory mechanisms controlling cellular responses and susceptibility to infections. Using cell biological, biochemical, and genetic tools, we reveal that influenza A virus (IAV) infection induces global transcriptional defects at the 3' ends of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. Deregulated RNAPII leads to expression of aberrant RNAs (3' extensions and host-gene fusions) that ultimately cause global transcriptional downregulation of physiological transcripts, an effect influencing antiviral response and virulence. This phenomenon occurs with multiple strains of IAV, is dependent on influenza NS1 protein, and can be modulated by SUMOylation of an intrinsically disordered region (IDR) of NS1 expressed by the 1918 pandemic IAV strain. Our data identify a strategy used by IAV to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins can affect the outcome of an infection.
Cancer Cell Biology Programme Centro Nacional de Investigaciones Oncológicas CNIO Madrid Spain
Department of Medicine Clinical Immunology Icahn School of Medicine at Mount Sinai New York NY USA
Department of Medicine Northwestern University Feinberg School of Medicine Chicago IL USA
Institute of Molecular and Cell Biology Singapore Singapore
Laboratory of Immune Cell Epigenetics and Signaling The Rockefeller University New York NY USA
Life Science Research Centre Faculty of Science University of Ostrava Ostrava Czech Republic
Citace poskytuje Crossref.org
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- $a Zhao, Nan $u Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
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