Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a mechanism for the unusual severity of human disease?

By C. Cheung, L. Poon, A. Lau, W. Luk, Y. Lau, K. Shortridge, S. Gordon, Yi Guan, J. Peiris. The Lancet, 2002

978 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b117a3e911db105e6de3e515df568fe2f8e6430a

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Citations in the corpus

Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia (2006, background): “Laboratory experiments suggest that virus-induced cytokine dysregulation may contribute to disease severity [6] [7] [8] [9] .”
Insights into the Interaction between Influenza Virus and Pneumococcus (2006, result): “Similar findings for humans with highly pathogenic H5N1 avian influenza viruses provide further support for this concept (8, 21).”
Influenza: lessons from past pandemics, warnings from current incidents (2005, background): “Interestingly, infection with viruses containing the NS gene from the 1997 Hong Kong H5N1 virus led to increased transcription of proinflammatory cytokine genes (such as TNF-α and IFN-β) in human primary monocyte-derived macrophages in vitro compared with infection with other types of viruse”
COVID-19: what has been learned and to be learned about the novel coronavirus disease (2020, background): “• Use of steroids: As described above, steroids are immunosuppressant commonly used as an adjunctive therapy for infectious diseases to reduce the severity of inflammatory damage [104] .”
Re-emergence of fatal human influenza A subtype H5N1 disease (2004, positive): “4 TNF ␣ and interferons are early-phase cytokines that act locally to trigger a cascade of other cytokines including IP-10, interleukin 1, and interleukin 6. IP-10 is a macrophage chemoattractant and its presence might explain the prominent macrophage inflammatory infiltrate in the lung ( figure 1) ”
Avian Influenza Virus (H5N1): a Threat to Human Health (2007, background): “However, the replication competence of HPAI H5N1 viruses was comparable to that of human H1N1 viruses in primary human respiratory epithelial cells and macrophages (25, 32).”
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”
Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications (2010, background): “The parenchyma injury is associated with overexpression of cytokines and inflammatory mediators and with upregulation of adhesion molecules in vascular beds (40, 310, 320).”
The multifunctional NS1 protein of influenza A viruses. (2008, background): “The viruses responsible for the outbreak were potent inducers of pro-inflammatory cytokines, especially TNF-a (Cheung et al., 2002), and the viral infection was characterized by hypercytokinaemia and reactive haemophagocytic syndrome (To et al.”
Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury (2008, methodology): “Since H5N1 subtype influenza A viruses are more potent inducers of cytokines in macrophages than H1N1 subtype influenza (Cheung et al., 2002), we used H1N1 as a control.”
H5N1 and 1918 Pandemic Influenza Virus Infection Results in Early and Excessive Infiltration of Macrophages and Neutrophils in the Lungs of Mice (2008, background): “Macrophages and neutrophils can secrete chemokines and cytokines that can act in an autocrine fashion which in turn can promote the increased migration of those cells and other leukocytes into the lung tissue [30].”
Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome (2004, background): “In contrast to H5N1 infection [15] , plasma TNF-a was not elevated in our patients.”
Coronavirus as a possible cause of severe acute respiratory syndrome (2003, background): “It is pertinent that severe human disease associated with the avian influenza subtype H5N1, another virus that has crossed from animals to human beings, has also been postulated to have an immunopathological component. 14 In common with H5N1 disease, patients with severe SARS are adults, have lympho”