Role of chicken toll-like receptor 3 in antiviral responses during H9N2 influenza virus infection

2008 ◽  
Author(s):  
Sze-mei Chan
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Toll Like Receptor ◽  
H9n2 Influenza Virus ◽  
Antiviral Responses

scholarly journals Polymerase Acidic Subunit of H9N2 Polymerase Complex Induces Cell Apoptosis by Binding to PDCD 7 in A549 Cells

2020 ◽  
Author(s):  
Shaohua Wang ◽  
Na Li ◽  
Shugang Jin ◽  
Ruihua Zhang ◽  
Tong Xu
Keyword(s):  
Cell Death ◽  
Influenza Virus ◽  
Cell Apoptosis ◽  
Influenza A ◽  
A549 Cells ◽  
Influenza Virus Infection ◽  
Economic Loss ◽  
Poultry Production ◽  
H9n2 Influenza Virus

Abstract Background: H9N2 influenza virus, a subtype of influenza A virus, can spread across different species and induce the respiratory infectious disease in humans, leading to a severe public health risk and a huge economic loss to poultry production. Increasing studies have shown that polymerase acidic (PA) subunit of RNA polymerase in ribonucleoproteins complex of H9N2 involves in crossing the host species barriers, the replication and airborne transmission of H9N2.Methods: Here, to further investigate the role of PA subunit during the infection of H9N2 influenza virus, we employed mass spectrometry (MS) to search the potential binding proteins of PA subunit of H9N2. Our MS results showed that programmed cell death protein 7 (PDCD7) is a binding target of PA subunit. Co-immunoprecipitation and pull-down assays further confirmed the interaction between PDCD7 and PA subunit. Overexpression of PA subunit in A549 lung cells greatly increased the levels of PDCD7 in the nuclear and induced cell death assayed by MTT assay.Results: Flow cytometry analysis and Western blot results showed that PA subunit overexpression significantly increased the expression of pro-apoptotic protein, bax and caspase 3, and induced cell apoptosis. However, knockout of PDCD7 effectively attenuated the effects of PA overexpression in cell apoptosis.Conclusions: In conclusion, the PA subunit of H9N2 bind with PDCD7 and regulated cell apoptosis, which provide new insights in the role of PA subunit during H9N2 influenza virus infection.

scholarly journals Cross-Reactive, Cell-Mediated Immunity and Protection of Chickens from Lethal H5N1 Influenza Virus Infection in Hong Kong Poultry Markets

2001 ◽  
Vol 75 (6) ◽  
pp. 2516-2525 ◽  
Author(s):  
Sang Heui Seo ◽  
Robert G. Webster
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Hong Kong ◽  
Virus Infection ◽  
Cellular Immunity ◽  
Influenza Virus Infection ◽  
Influenza Viruses ◽  
H5n1 Influenza Virus ◽  
H9n2 Influenza Virus ◽  
H5n1 Influenza

ABSTRACT In 1997, avian H5N1 influenza virus transmitted from chickens to humans resulted in 18 confirmed infections. Despite harboring lethal H5N1 influenza viruses, most chickens in the Hong Kong poultry markets showed no disease signs. At this time, H9N2 influenza viruses were cocirculating in the markets. We investigated the role of H9N2 influenza viruses in protecting chickens from lethal H5N1 influenza virus infections. Sera from chickens infected with an H9N2 influenza virus did not cross-react with an H5N1 influenza virus in neutralization or hemagglutination inhibition assays. Most chickens primed with an H9N2 influenza virus 3 to 70 days earlier survived the lethal challenge of an H5N1 influenza virus, but infected birds shed H5N1 influenza virus in their feces. Adoptive transfer of T lymphocytes or CD8+ T cells from inbred chickens (B2/B2) infected with an H9N2 influenza virus to naive inbred chickens (B2/B2) protected them from lethal H5N1 influenza virus. In vitro cytotoxicity assays showed that T lymphocytes or CD8+ T cells from chickens infected with an H9N2 influenza virus recognized target cells infected with either an H5N1 or H9N2 influenza virus in a dose-dependent manner. Our findings indicate that cross-reactive cellular immunity induced by H9N2 influenza viruses protected chickens from lethal infection with H5N1 influenza viruses in the Hong Kong markets in 1997 but permitted virus shedding in the feces. Our findings are the first to suggest that cross-reactive cellular immunity can change the outcome of avian influenza virus infection in birds in live markets and create a situation for the perpetuation of H5N1 influenza viruses.

scholarly journals Role of Host Immune Response and Viral Load in the Differential Outcome of Pandemic H1N1 (2009) Influenza Virus Infection in Indian Patients

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13099 ◽  
Author(s):  
Vidya A. Arankalle ◽  
Kavita S. Lole ◽  
Ravi P. Arya ◽  
Anuradha S. Tripathy ◽  
Ashwini Y. Ramdasi ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Viral Load ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Host Immune Response ◽  
Pandemic H1n1 ◽  
Differential Outcome ◽  
Pandemic H1n1 2009

Role of oxidants in influenza virus-induced gene expression

1998 ◽  
Vol 274 (1) ◽  
pp. L134-L142 ◽  
Author(s):  
Katharine Knobil ◽  
Augustine M. K. Choi ◽  
Gordon W. Weigand ◽  
David B. Jacoby
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Influenza Virus ◽  
Virus Infection ◽  
A549 Cells ◽  
Influenza Virus Infection ◽  
Pyrrolidine Dithiocarbamate ◽  
Oxygen Intermediates ◽  
Mrna Induction

Influenza virus-induced epithelial damage may be mediated, in part, by reactive oxygen intermediates (ROIs). In this study, we investigated the role of ROIs in the influenza virus-induced gene expression of antioxidant enzymes and in the activation of nuclear factor-κB (NF-κB), an oxidant-sensitive transcriptional factor. Influenza virus infection increased production of intracellular ROIs in A549 pulmonary epithelial cells. Induction of manganese superoxide dismutase (MnSOD) mRNA correlated with increased MnSOD protein and enzyme activity. Influenza virus infection also activated NF-κB binding as determined by an electrophoretic mobility shift assay. Pretreatment of A549 cells with N-acetyl-l-cysteine attenuated virus-induced NF-κB activation and interleukin (IL)-8 mRNA induction but did not block induction of MnSOD mRNA. In contrast, pyrrolidine dithiocarbamate blocked activation of NF-κB and induction of MnSOD and IL-8 mRNAs. Treatment with pyrrolidine dithiocarbamate also markedly decreased virus-induced cell death. Thus oxidants are involved in influenza virus-induced activation of NF-κB, in the expression of IL-8 and MnSOD, and in virus-induced cell death.

scholarly journals Role of Extracellular Vesicles in Influenza Virus Infection

2020 ◽  
Vol 10 ◽  
Author(s):  
Yuan Jiang ◽  
Xiaowen Cai ◽  
Jiwen Yao ◽  
Huanhuan Guo ◽  
Liangjun Yin ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Extracellular Vesicles ◽  
Influenza Virus Infection

Progranulin aggravates pulmonary immunopathology during influenza virus infection

Thorax ◽  
2018 ◽  
Vol 74 (3) ◽  
pp. 305-308 ◽  
Author(s):  
Qin Luo ◽  
Xingxing Yan ◽  
Hongmei Tu ◽  
Yibing Yin ◽  
Ju Cao
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Inflammatory Diseases ◽  
Influenza Virus Infection ◽  
Epithelial Barrier ◽  
Alveolar Epithelial ◽  
Cytokines And Chemokines ◽  
Deficient Mice ◽  
Experimental Influenza

Progranulin (PGRN) exerts multiple functions in various inflammatory diseases. However, the role of PGRN in the pathogenesis of virus infection is unknown. Here, we demonstrated that PGRN production was up-regulated in clinical and experimental influenza, which contributed to the deleterious inflammatory response after influenza virus infection in mice. PGRN-deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced influx of neutrophils and monocytes/macrophages, release of cytokines and chemokines, and permeability of the alveolar–epithelial barrier without affecting viral clearance. Our findings suggest that PGRN exacerbates pulmonary immunopathology during influenza virus infection.

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