2020
DOI: 10.3390/v12040376
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Host–Virus Interaction: How Host Cells Defend against Influenza A Virus Infection

Abstract: Influenza A viruses (IAVs) are highly contagious pathogens infecting human and numerous animals. The viruses cause millions of infection cases and thousands of deaths every year, thus making IAVs a continual threat to global health. Upon IAV infection, host innate immune system is triggered and activated to restrict virus replication and clear pathogens. Subsequently, host adaptive immunity is involved in specific virus clearance. On the other hand, to achieve a successful infection, IAVs also apply multiple s… Show more

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Cited by 21 publications
(12 citation statements)
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“…The body's natural defense mechanism of inflammation which promotes cell repair and healing [107] was mimicked in our wdNHBE model, with the increased expression of proinflammatory cytokines and chemokines such as TNF, IL1B, IL6, CXCL8 and CXCL10. This suggests that wdNHBE cells recognize IAV and poly(I:C) through binding to pattern recognition receptors (PRRs) such as the Toll-like receptors (TLR3, TLR7, and TLR8), retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein-5 (MDA-5), triggering innate immune response signaling cascades as occurs in vivo [22,54,55,[108][109][110][111][112][113][114]. Antiviral, pro-and anti-inflammatory cytokines and chemokines are then upregulated in the host [27,56,115].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…The body's natural defense mechanism of inflammation which promotes cell repair and healing [107] was mimicked in our wdNHBE model, with the increased expression of proinflammatory cytokines and chemokines such as TNF, IL1B, IL6, CXCL8 and CXCL10. This suggests that wdNHBE cells recognize IAV and poly(I:C) through binding to pattern recognition receptors (PRRs) such as the Toll-like receptors (TLR3, TLR7, and TLR8), retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein-5 (MDA-5), triggering innate immune response signaling cascades as occurs in vivo [22,54,55,[108][109][110][111][112][113][114]. Antiviral, pro-and anti-inflammatory cytokines and chemokines are then upregulated in the host [27,56,115].…”
Section: Discussionmentioning
confidence: 99%
“…They form AJCs, exhibit ion transport, mucus secretion and mucociliary clearance [ 25 , 48 , 49 , 50 , 51 ]. wdNHBE cells also produce host–pathogen responses when exposed to respiratory viruses, such as the production of antiviral, immune and pro- and anti-inflammatory molecules [ 52 , 53 ], as occurs in the host in vivo (reviewed in: [ 20 , 21 , 22 , 27 , 54 , 55 , 56 , 57 ]). The response of airway epithelial cells (from different donors, cell preparations, etc.)…”
Section: Introductionmentioning
confidence: 99%
“…In the past ten years, the large-scale outbreaks of SARS, MERs, H1N1, H7N9 and other viruses have brought serious harm to human life and health (Atkin-Smith G.K et al, 2018). The "cytokine storm" triggered by in uenza virus infection can cause lung in ammation and acute respiratory distress syndrome, which is an important reason for mortality (Zhang Y et al, 2020;Xiaoyong C et al, 2018). So far, the prevention and control of in uenza virus remains a worldwide problem.…”
Section: Introductionmentioning
confidence: 99%
“…SARS-CoV-2 infection was identi ed to activate the host innate immune system via the bindings of its spike glycoprotein (S-protein) to the angiotensin-converting enzyme 2 (ACE2) receptor and transmembrane protease serine 2 (TMPRSS2) [32,33], which engaged macrophages and monocytes to release cytokines and enhanced adaptive T and B cell immune response [34]. While in uenza infection is initiated by adhesion of hemagglutinin (HA) to sialic acids on the epithelial cells, followed with activation of innate immune signaling and further production of cytokines via host pathogen recognition receptors (PRPs) [35,36]. Further gene expression analyses have identi ed the expression pattern of cytokines, cytokine receptors, as well as transcription factors in COVID-19 patients, which quite differs from that of in uenza A infected patients [37,38].…”
Section: Discussionmentioning
confidence: 99%