scholarly journals Dysregulation of M segment gene expression contributes to influenza A virus host restriction

2019 ◽  
Vol 15 (8) ◽  
pp. e1007892 ◽  
Author(s):  
Brenda M. Calderon ◽  
Shamika Danzy ◽  
Gabrielle K. Delima ◽  
Nathan T. Jacobs ◽  
Ketaki Ganti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Influenza A Virus ◽  
Influenza A ◽  
Host Restriction

Amphotericin b effect on the sensitivity to influenza infection of WI-38 VA-13 cells with IFITM3 gene knockout

2021 ◽  
Vol 21 (3) ◽  
pp. 109-112
Author(s):  
Kira S. Koryabina ◽  
Mariya V. Sergeeva ◽  
Andrey B. Komissarov ◽  
Nataliya V. Eshchenko ◽  
Grigoriy A. Stepanov
Keyword(s):  
Amphotericin B ◽  
Influenza A Virus ◽  
Influenza A ◽  
Gene Knockout ◽  
Influenza Infection ◽  
Restriction Factors ◽  
Host Restriction ◽  
Host Restriction Factors ◽  
Infected Cells ◽  
The Difference

BACKGROUND: The application of CRISPR/Cas9 is one of the most rapidly developing areas in biotechnology. This method was used to obtain clones of а human origin cell line with knockout of one or more genes of the IFITM family, representing host restriction factors for influenza infection. Amphotericin B has previously been shown to promote influenza infection by blocking IFITM3 function. AIM: The aim of this study was to evaluate the effect of amphotericin B on the sensitivity of IFITM knockout cells to influenza A virus infection. MATERIALS AND METHODS: WI-38 VA-13 cells and mutant clones with IFITM3 knockout (F3 clone) or IFITM1, IFITM3 knockout (clone E12) were infected with influenza virus A/PR/8/34 (H1N1) in the presence or absence of amphotericin B. Forty-four hours after infection, the culture medium was taken to determine the infectious activity of the virus by titration in the MDCK cell culture, as well as the hemagglutinating activity of the virus. The infected cells were stained with fluorescently labeled antibodies against the viral NP protein, and the number of NP-positive cells was determined by flow cytometry. RESULTS: The addition of amphotericin B increased the hemagglutinating and infectious activity of the virus in WI-38 VA-13cells, while the difference was insignificant for clones with IFITM gene knockout. A similar dependency was obtained for the percent of infected cells. CONCLUSIONS: Mutant cells with a knockout of one or several genes of the IFITM family were equally susceptible to influenza infection regardless of the addition of amphotericin B, which confirms the crucial importance of a defect in the IFITM3 protein in increasing the permissiveness of cells to influenza A virus.

scholarly journals Early postnatal infection with neurotropic influenza A virus: effects on gene expression and behavior in mice

2008 ◽  
Vol 2 (S1) ◽  
Author(s):  
Linnéa Asp ◽  
Simret Beraki ◽  
Krister Kristensson ◽  
Sven OveÖgren ◽  
Håkan Karlsson
Keyword(s):  
Gene Expression ◽  
Influenza A Virus ◽  
Influenza A ◽  
And Behavior ◽  
Postnatal Infection

scholarly journals The NS1 Protein of Influenza A Virus Blocks RIG-I-Mediated Activation of the Noncanonical NF-κB Pathway and p52/RelB-Dependent Gene Expression in Lung Epithelial Cells

2012 ◽  
Vol 86 (18) ◽  
pp. 10211-10217 ◽  
Author(s):  
Andrea Rückle ◽  
Emanuel Haasbach ◽  
Ilkka Julkunen ◽  
Oliver Planz ◽  
Christina Ehrhardt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Influenza A Virus ◽  
Influenza A ◽  
Target Gene ◽  
Lung Epithelial Cells ◽  
Ns1 Protein ◽  
Antiviral Immune Response ◽  
Lung Epithelial ◽  
Infected Cells

Influenza A virus (IAV) infection of epithelial cells activates NF-κB transcription factors via the canonical NF-κB signaling pathway, which modulates both the antiviral immune response and viral replication. Since almost nothing is known so far about a function of noncanonical NF-κB signaling after IAV infection, we tested infected cells for activation of p52 and RelB. We show that the viral NS1 protein strongly inhibits RIG-I-mediated noncanonical NF-κB activation and expression of the noncanonical target gene CCL19.

scholarly journals TNF-α and IFN-α enhance influenza-A-virus-induced chemokine gene expression in human A549 lung epithelial cells

Virology ◽  
2006 ◽  
Vol 345 (1) ◽  
pp. 96-104 ◽  
Author(s):  
Ville Veckman ◽  
Pamela Österlund ◽  
Riku Fagerlund ◽  
Krister Melén ◽  
Sampsa Matikainen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Influenza A Virus ◽  
Influenza A ◽  
Lung Epithelial Cells ◽  
Chemokine Gene ◽  
Tnf Α ◽  
Lung Epithelial ◽  
Human A549 ◽  
A549 Lung ◽  
Chemokine Gene Expression

scholarly journals Influenza Virus A/Anhui/1/2013 (H7N9) Replicates Efficiently in the Upper and Lower Respiratory Tracts of Cynomolgus Macaques

mBio ◽  
2014 ◽  
Vol 5 (4) ◽  
Author(s):  
Emmie de Wit ◽  
Angela L. Rasmussen ◽  
Friederike Feldmann ◽  
Trenton Bushmaker ◽  
Cynthia Martellaro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Influenza Virus ◽  
Respiratory Tract ◽  
Influenza A Virus ◽  
Influenza A ◽  
Clinical Aspects ◽  
Polymorphonuclear Cells ◽  
H7n9 Virus ◽  
Cynomolgus Macaques ◽  
H7n9 Infection

ABSTRACT In March 2013, three fatal human cases of infection with influenza A virus (H7N9) were reported in China. Since then, human cases have been accumulating. Given the public health importance of this virus, we performed a pathogenicity study of the H7N9 virus in the cynomolgus macaque model, focusing on clinical aspects of disease, radiographic, histological, and gene expression profile changes in the upper and lower respiratory tracts, and changes in systemic cytokine and chemokine profiles during infection. Cynomolgus macaques developed transient, mild to severe disease with radiographic evidence of pulmonary infiltration. Virus replicated in the upper as well as lower respiratory tract, with sustained replication in the upper respiratory tract until the end of the experiment at 6 days after inoculation. Virus shedding occurred mainly via the throat. Histopathological changes in the lungs were similar to those observed in humans, albeit less severe, with diffuse alveolar damage, infiltration of polymorphonuclear cells, formation of hyaline membranes, pneumocyte hyperplasia, and fibroproliferative changes. Analysis of gene expression profiles in lung lesions identified pathways involved in tissue damage during H7N9 infection as well as leads for development of therapeutics targeting host responses rather than virus replication. Overall, H7N9 infection was not as severe in cynomolgus macaques as in humans, supporting the possible role of underlying medical complications in disease severity as discussed for human H7N9 infection (H. N. Gao et al., N. Engl. J. Med. 368:2277–2285, 2013, doi:10.1056/NEJMoa1305584). IMPORTANCE Influenza A virus H7N9 emerged early in 2013, and human cases have continued to emerge since then. Although H7N9 virus-induced disease in humans is often very severe and even lethal, the majority of reported H7N9 cases occurred in older people and people with underlying medical conditions. To better understand the pathogenicity of this virus, healthy cynomolgus macaques were inoculated with influenza A virus H7N9. Cynomolgus macaques were used as a model because the receptor distribution for H7N9 virus in macaques was recently shown to be more similar to that in humans than that of other frequently used animal models. From comparison with previous studies, we conclude that the emerging H7N9 influenza virus was more pathogenic in cynomolgus macaques than seasonal influenza A viruses and most isolates of the pandemic H1N1 virus but less pathogenic than the 1918 Spanish influenza virus or highly pathogenic avian influenza (HPAI) H5N1 virus.

scholarly journals Glycyrrhizin Exerts Antioxidative Effects in H5N1 Influenza A Virus-Infected Cells and Inhibits Virus Replication and Pro-Inflammatory Gene Expression

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e19705 ◽  
Author(s):  
Martin Michaelis ◽  
Janina Geiler ◽  
Patrizia Naczk ◽  
Patchima Sithisarn ◽  
Anke Leutz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
H5n1 Influenza ◽  
Antioxidative Effects ◽  
Infected Cells
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