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oai:riubu.ubu.es:10259/109192025-10-04T00:05:26Zcom_10259_4862com_10259_5086com_10259_2604col_10259_4863

00925njm 22002777a 4500 dc Zhao, Nan author Sebastiano, Vittorio author Moshkina, Natasha author Mena, Nacho author Hultquist, Judd author Jimenez-Morales, David author Ma, Yixuan author Rialdi, Alex author Albrecht, Randy author Fenouil, Romain author Sánchez-Aparicio, M. T. author Ayllón Barasoain, Juan author Ravisankar, Sweta author Haddad, Bahareh author Ho, Sook-Yiun author Low, Diana author Jin, Jian author Yurchenko, Vyacheslav author Prinjha, Rab K. author Tarakhovsky, Alexander author Squatrito, Massimo author Pinto, Dalila author Kimaada, Allette author Byun, Minji author Smith, Melissa Laird author Sebra, Robert author Guccione, Ernesto author Tumpey, Terrence author Krogan, Nevan author Greenbaum, Benjamin author van Bakel, Harm author García Sastre, Adolfo author Marazzi, Ivan author 2018-09 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. 1545-9993 https://hdl.handle.net/10259/10919 10.1038/s41594-018-0124-7 1545-9985 Influenza virus infection causes global RNAPII termination defects