Influenza virus infection causes global RNAPII termination defects

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...

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Detalles Bibliográficos
Autores: Zhao, Nan, Sebastiano, Vittorio, Moshkina, Natasha, Mena, Nacho, Hultquist, Judd, Jimenez-Morales, David, Ma, Yixuan, Rialdi, Alex, Albrecht, Randy, Fenouil, Romain, Sánchez-Aparicio, M. T., Ayllón Barasoain, Juan, Ravisankar, Sweta, Haddad, Bahareh, Ho, Sook-Yiun, Low, Diana, Jin, Jian, Yurchenko, Vyacheslav, Prinjha, Rab K., Tarakhovsky, Alexander, Squatrito, Massimo, Pinto, Dalila, Kimaada, Allette, Byun, Minji, Smith, Melissa Laird, Sebra, Robert, Guccione, Ernesto, Tumpey, Terrence, Krogan, Nevan, Greenbaum, Benjamin, van Bakel, Harm, García Sastre, Adolfo, Marazzi, Ivan
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2018
País:España
Institución:Universidad de Burgos (UBU)
Repositorio:Repositorio Institucional de la Universidad de Burgos (RIUBU)
OAI Identifier:oai:riubu.ubu.es:10259/10919
Acceso en línea:https://hdl.handle.net/10259/10919
Access Level:acceso abierto
Palabra clave:Virus
Poli ADP ribosa polimerasa
NAD-ADP-ribosyltransferase
Descripción
Sumario: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.

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