Aberrant innate immune response in lethal infection of macaques with the 1918 influenza virus

By D. Kobasa, S. Jones, K. Shinya, J. Kash, J. Copps, H. Ebihara, Yasuko Hatta, J. -. Kim, P. Halfmann, M. Hatta and 7 more. Nature, 2007

958 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/3550f58d1c2aa3714bdc197d158bd283f44a8c78

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Citations in the corpus

Effector T cells control lung inflammation during acute influenza virus infection by producing IL-10 (2009, background): “In certain instances (for example, infection with the highly pathogenic avian H5N1 or 1918 pandemic influenza virus strains), this counter-regulation fails, as infection results in a massive inflammatory cell infiltration into the infected lungs and excessive proinflammatory cytokine productio”
Influenza A viruses: new research developments (2011, background): “However, despite the 1918 pandemic H1N1 virus lacking an HA multibasic cleavage site, infection with this virus in animal models results in high levels of viral replication and induction of pro-inflammatory cytokines, leading to severe diseas”
Wild Mouse Gut Microbiota Promotes Host Fitness and Improves Disease Resistance (2017, positive): “The type of hyperactivation and cytokine response seen in LabR and Lab is consistent with descriptions of cytokine storms associated with a lethal IAV infection (Kash et al., 2006; Kobasa et al., 2007; Tisoncik et al., 2012).”
NLRP3 (NALP3/CIAS1/Cryopyrin) mediates key innate and healing responses to influenza A virus via the regulation of caspase-1 (2009, positive): “Recent analysis indicates that a very rapid onset, proinflammatory cytokine 566 Immunity 30, 566–575, April 17, 2009 ª2009 Elsevier Inc. ‘‘storm’’ is a major contributor to the lethality induced by these highly pathogenic viruses in humans, mice, and macaques (de Jong et al., 2006; Hampton, 2007; Ko”
IFITM3 restricts the morbidity and mortality associated with influenza (2012, neutral): “We note this pathology is similar to that produced by infection of mice and primates with 1918 H1N1 virus [9] [10] [11] .”
Into the Eye of the Cytokine Storm (2012, background): “For example, strong upregulation of IL-6, IL-8, CCL2, and CCL5 cytokine and chemokine gene expression in the lungs was mirrored by elevated levels of IL-8, CCL2, and CCL5 in the sera of infected animals (78).”
Distinct RIG-I and MDA5 Signaling by RNA Viruses in Innate Immunity (2007, background): “provide evidence that infection with the 1918 pandemic strain of influenza A virus triggers the persistent expression of an overlapping pool of immune-related genes (17,21).”
Endothelial cells are central orchestrators of cytokine amplification during influenza virus infection (2011, background): “Pathogenic Influenza Virus Challenge in Mice Early dysregulated innate immune responses in the lung have been associated with morbidity and mortality during infection with highly pathogenic strains of influenza virus (Cillóniz et al., 2009; Kobasa et al., 2007).”
Excessive Neutrophils and Neutrophil Extracellular Traps Contribute to Acute Lung Injury of Influenza Pneumonitis (2011, neutral): “7–9 Although ARDS is a prevailing complication in influenza-associated deaths, the etiology for progression into ARDS is poorly understood.”
Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis (2012, background): “Dysregulated cytokine and chemokine production, excessive immune cell influx, and damage to the lungs are hypothesized underlie influenza pathology (Hennet et al., 1992; Kash et al., 2004; Kash et al., 2006; Kobasa et al., 2007; Perrone et al., 2008; Tumpey et al., 2005).”
H5N1 and 1918 Pandemic Influenza Virus Infection Results in Early and Excessive Infiltration of Macrophages and Neutrophils in the Lungs of Mice (2008, background): “virus and H5N1 viruses in humans [9,25,26] as well as in animal models [11,12,18].”