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innate immunity

  • OASL Triggered by Novel Goose Astrovirus via ORF2 Restricts Its Replication
    Virus-Cell Interactions
    OASL Triggered by Novel Goose Astrovirus via ORF2 Restricts Its Replication

    Astroviruses cause gastroenteritis and encephalitis in human, and nephritis, hepatitis, and gout disease in poultry. However, the host immune response activated by astrovirus is mostly unknown. Here, we found that a novel goose astrovirus, GAstV-GD, and its ORF2 protein could efficiently induce a high level of OASL in vitro and in vivo, which could feed back to restrict the replication of GAstV-GD, revealing novel...

    Dan Ren, Tuofan Li, Xinyu Zhang, Xiaohui Yao, Wei Gao, Quan Xie, Jianjun Zhang, Hongxia Shao, Zhimin Wan, Aijian Qin, Jianqiang Ye
  • Open Access
    Loss of the Nuclear Protein RTF2 Enhances Influenza Virus Replication
    Cellular Response to Infection | Spotlight
    Loss of the Nuclear Protein RTF2 Enhances Influenza Virus Replication

    Viral infection triggers the secretion of type I interferons, which in turn induce the expression of hundreds of antiviral genes. However, the roles of these induced genes in controlling viral infections remain largely unknown, limiting our ability to develop host-based antiviral therapeutics against pathogenic viruses, such as influenza virus. Here, we performed a loss-of-function genetic CRISPR screen in cells prestimulated with type...

    Bing Shao Chia, Bo Li, Ang Cui, Thomas Eisenhaure, Raktima Raychowdhury, David Lieb, Nir Hacohen
  • Reovirus σ3 Protein Limits Interferon Expression and Cell Death Induction
    Cellular Response to Infection
    Reovirus σ3 Protein Limits Interferon Expression and Cell Death Induction

    We use mammalian reovirus as a model to study how virus infection modulates innate immune signaling and cell death induction. Here, we sought to determine how viral factors regulate these processes. Our work highlights a previously unknown role for the reovirus outer capsid protein σ3 in limiting the induction of a necrotic form of cell death called necroptosis. Induction of cell death by necroptosis requires production of interferon....

    Katherine E. Roebke, Yingying Guo, John S. L. Parker, Pranav Danthi
  • Retinoic Acid Inducible Gene I and Protein Kinase R, but Not Stress Granules, Mediate the Proinflammatory Response to Yellow Fever Virus
    Virus-Cell Interactions
    Retinoic Acid Inducible Gene I and Protein Kinase R, but Not Stress Granules, Mediate the Proinflammatory Response to Yellow Fever Virus

    Yellow fever is a mosquito-borne acute hemorrhagic disease caused by yellow fever virus (YFV). The mechanisms responsible for its pathogenesis remain largely unknown, although increased inflammation has been linked to worsened outcome. YFV targets the liver, where it primarily infects hepatocytes. We found that two RNA-sensing proteins, RIG-I and PKR, participate in the induction of proinflammatory mediators in human hepatocytes...

    Guillaume Beauclair, Felix Streicher, Maxime Chazal, Daniela Bruni, Sarah Lesage, Ségolène Gracias, Salomé Bourgeau, Laura Sinigaglia, Takashi Fujita, Eliane F. Meurs, Frédéric Tangy, Nolwenn Jouvenet
  • IRF1 Promotes the Innate Immune Response to Viral Infection by Enhancing the Activation of IRF3
    Pathogenesis and Immunity
    IRF1 Promotes the Innate Immune Response to Viral Infection by Enhancing the Activation of IRF3

    The activation of innate immunity is essential for host cells to restrict the spread of invading viruses and other pathogens. IRF3 plays a critical role in the innate immune response to RNA viral infection. However, whether IRF1 plays a role in innate immunity is unclear. In this study, we demonstrated that IRF1 promotes the innate immune response to viral infection. IRF1 is induced by viral infection. Notably, IRF1 targets and augments...

    Jingjing Wang, Huiyi Li, Binbin Xue, Rilin Deng, Xiang Huang, Yan Xu, Shengwen Chen, Renyun Tian, Xintao Wang, Zhen Xun, Ming Sang, Haizhen Zhu
  • Open Access
    Respiratory Syncytial Virus Sequesters NF-κB Subunit p65 to Cytoplasmic Inclusion Bodies To Inhibit Innate Immune Signaling
    Virus-Cell Interactions | Spotlight
    Respiratory Syncytial Virus Sequesters NF-κB Subunit p65 to Cytoplasmic Inclusion Bodies To Inhibit Innate Immune Signaling

    Many viruses replicate almost entirely in the cytoplasm of infected cells; however, how these pathogens are able to compartmentalize their life cycle to provide favorable conditions for replication and to avoid the litany of antiviral detection mechanisms in the cytoplasm remains relatively uncharacterized. In this manuscript, we show that bovine respiratory syncytial virus (bRSV), which infects cattle, does this by generating inclusion...

    Fatoumatta Jobe, Jennifer Simpson, Philippa Hawes, Efrain Guzman, Dalan Bailey
  • Free
    Type I and Type III Interferons Restrict SARS-CoV-2 Infection of Human Airway Epithelial Cultures
    Cellular Response to Infection
    Type I and Type III Interferons Restrict SARS-CoV-2 Infection of Human Airway Epithelial Cultures

    The current pandemic of respiratory illness, COVID-19, is caused by a recently emerged coronavirus named SARS-CoV-2. This virus infects airway and lung cells causing fever, dry cough, and shortness of breath. Severe cases of COVID-19 can result in lung damage, low blood oxygen levels, and even death. As there are currently no vaccines approved for use in humans, studies of the mechanisms of SARS-CoV-2 infection are urgently needed. Our...

    Abigail Vanderheiden, Philipp Ralfs, Tatiana Chirkova, Amit A. Upadhyay, Matthew G. Zimmerman, Shamika Bedoya, Hadj Aoued, Gregory M. Tharp, Kathryn L. Pellegrini, Candela Manfredi, Eric Sorscher, Bernardo Mainou, Jenna L. Lobby, Jacob E. Kohlmeier, Anice C. Lowen, Pei-Yong Shi, Vineet D. Menachery, Larry J. Anderson, Arash Grakoui, Steven E. Bosinger, Mehul S. Suthar
  • Open Access
    Interferon-Induced Protein 44 and Interferon-Induced Protein 44-Like Restrict Replication of Respiratory Syncytial Virus
    Pathogenesis and Immunity
    Interferon-Induced Protein 44 and Interferon-Induced Protein 44-Like Restrict Replication of Respiratory Syncytial Virus

    RSV infects all children under 2 years of age, but only a subset of children get severe disease. We hypothesize that susceptibility to severe RSV necessitating hospitalization in children without predefined risk factors is, in part, mediated at the antiviral gene level. However, there is a large array of antiviral genes, particularly in the ISG family, the mechanism of which is poorly understood. Having previously identified IFI44 and...

    D. C. Busse, D. Habgood-Coote, S. Clare, C. Brandt, I. Bassano, M. Kaforou, J. Herberg, M. Levin, J.-F. Eléouët, P. Kellam, J. S. Tregoning
  • The Measles Virus V Protein Binding Site to STAT2 Overlaps That of IRF9
    Structure and Assembly
    The Measles Virus V Protein Binding Site to STAT2 Overlaps That of IRF9

    To evade host immunity, many pathogenic viruses inactivate host Janus kinase signal transducer and activator of transcription (STAT) signaling pathways using diverse strategies. Measles virus utilizes P and V proteins to counteract this signaling pathway. Data derived largely from cell-based assays have indicated several amino acid residues of P and V proteins as important. However, biophysical properties of V protein or its direct...

    Yuma Nagano, Aoi Sugiyama, Madoka Kimoto, Takuya Wakahara, Yasuyo Noguchi, Xinxin Jiang, Shinya Saijo, Nobutaka Shimizu, Nana Yabuno, Min Yao, Paul R. Gooley, Gregory W. Moseley, Takashi Tadokoro, Katsumi Maenaka, Toyoyuki Ose
  • Open Access
    Innate Intracellular Antiviral Responses Restrict the Amplification of Defective Virus Genomes of Parainfluenza Virus 5
    Virus-Cell Interactions
    Innate Intracellular Antiviral Responses Restrict the Amplification of Defective Virus Genomes of Parainfluenza Virus 5

    Copyback defective virus genomes (DVGs) are powerful inducers of innate immune responses both in vitro and in vivo. They impact the outcome of natural infections, may help drive virus‐host coevolution, and promote virus persistence. Due to their potent interfering and immunostimulatory properties, DVGs may also be used therapeutically as antivirals and vaccine adjuvants. However, little is known of the host cell...

    Elizabeth B. Wignall-Fleming, Andri Vasou, Dan Young, John A. L. Short, David J. Hughes, Steve Goodbourn, Richard E. Randall

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