scholarly journals An NS-segment exonic splicing enhancer regulates influenza A virus replication in mammalian cells

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Xiaofeng Huang ◽  
Min Zheng ◽  
Pui Wang ◽  
Bobo Wing-Yee Mok ◽  
Siwen Liu ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Mammalian Cells ◽  
Influenza A ◽  
Exonic Splicing Enhancer ◽  
Splicing Enhancer

scholarly journals Viral and Host Factors Required for Avian H5N1 Influenza A Virus Replication in Mammalian Cells

Viruses ◽  
2013 ◽  
Vol 5 (6) ◽  
pp. 1431-1446 ◽  
Author(s):  
Hong Zhang ◽  
Benjamin Hale ◽  
Ke Xu ◽  
Bing Sun
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Mammalian Cells ◽  
Influenza A ◽  
Host Factors ◽  
H5n1 Influenza

scholarly journals Dicer is involved in protection against influenza A virus infection

2007 ◽  
Vol 88 (10) ◽  
pp. 2627-2635 ◽  
Author(s):  
Alexey A. Matskevich ◽  
Karin Moelling
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Mammalian Cells ◽  
Influenza A ◽  
Virus Production ◽  
Vero Cells ◽  
Antiviral Response ◽  
Protein Levels ◽  
Infected Cells ◽  
Influenza A Virus Infection

In mammals the interferon (IFN) system is a central innate antiviral defence mechanism, while the involvement of RNA interference (RNAi) in antiviral response against RNA viruses is uncertain. Here, we tested whether RNAi is involved in the antiviral response in mammalian cells. To investigate the role of RNAi in influenza A virus-infected cells in the absence of IFN, we used Vero cells that lack IFN-α and IFN-β genes. Our results demonstrate that knockdown of a key RNAi component, Dicer, led to a modest increase of virus production and accelerated apoptosis of influenza A virus-infected cells. These effects were much weaker in the presence of IFN. The results also show that in both Vero cells and the IFN-producing alveolar epithelial A549 cell line influenza A virus targets Dicer at mRNA and protein levels. Thus, RNAi is involved in antiviral response, and Dicer is important for protection against influenza A virus infection.

MC1568 inhibits HDAC6/8 activity and influenza A virus replication in lung epithelial cells: role of Hsp90 acetylation

2016 ◽  
Vol 8 (17) ◽  
pp. 2017-2031 ◽  
Author(s):  
Simona Panella ◽  
Maria Elena Marcocci ◽  
Ignacio Celestino ◽  
Sergio Valente ◽  
Clemens Zwergel ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

CRISPR-Cas9 mediated knockout of AnxA6 gene enhances influenza A virus replication in low-permissive HEK293FT cell line

Gene ◽  
2021 ◽  
pp. 146024
Author(s):  
Andrey Komissarov ◽  
Mariia Sergeeva ◽  
Evgenii Zhuravlev ◽  
Sergey Medvedev ◽  
Anastasia Malakhova ◽  
...  
Keyword(s):  
Cell Line ◽  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Hek293ft Cell

scholarly journals Sus scrofa miR-204 and miR-4331 Negatively Regulate Swine H1N1/2009 Influenza A Virus Replication by Targeting Viral HA and NS, Respectively

2017 ◽  
Vol 18 (4) ◽  
pp. 749 ◽  
Author(s):  
Shishuo Zhang ◽  
Ruifang Wang ◽  
Huijuan Su ◽  
Biaoxiong Wang ◽  
Suolang Sizhu ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Sus Scrofa ◽  
Influenza A

Santin inhibits influenza A virus replication through regulating MAPKs and NF-κB pathways

2018 ◽  
Vol 21 (12) ◽  
pp. 1205-1214 ◽  
Author(s):  
Ming Zhong ◽  
Hui-Qiang Wang ◽  
Hai-Yan Yan ◽  
Shuo Wu ◽  
Zheng-Yi Gu ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A

scholarly journals Cellular DDX21 RNA Helicase Inhibits Influenza A Virus Replication but Is Counteracted by the Viral NS1 Protein

2014 ◽  
Vol 15 (4) ◽  
pp. 484-493 ◽  
Author(s):  
Guifang Chen ◽  
Chien-Hung Liu ◽  
Ligang Zhou ◽  
Robert M. Krug
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Rna Helicase ◽  
Ns1 Protein

scholarly journals Novel Mode of ISG15-Mediated Protection against Influenza A Virus and Sendai Virus in Mice

2014 ◽  
Vol 89 (1) ◽  
pp. 337-349 ◽  
Author(s):  
David J. Morales ◽  
Kristen Monte ◽  
Lulu Sun ◽  
Jessica J. Struckhoff ◽  
Eugene Agapov ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Type I Interferon ◽  
Sendai Virus ◽  
Type I ◽  
Induced Genes

ABSTRACTISG15 is a diubiquitin-like modifier and one of the most rapidly induced genes upon type I interferon stimulation. Hundreds of host proteins and a number of viral proteins have been shown to be ISGylated, and understanding how these modifications affect the interferon response and virus replication has been of considerable interest. ISG15−/−mice exhibit increased susceptibility to viral infection, and in the case of influenza B virus and vaccinia virus, ISG15 conjugation has been shown to restrict virus replicationin vivo. A number of studies have also found that ISG15 is capable of antagonizing replication of some viruses in tissue culture. However, recent findings have demonstrated that ISG15 can protect mice from Chikungunya virus infection without affecting the virus burden. In order to better understand the function of ISG15in vivo, we characterized the pathogenesis of influenza A virus and Sendai virus in ISG15−/−mice. We found that ISG15 protects mice from virus induced lethality by a conjugation-dependent mechanism in both of these models. However, surprisingly, we found that ISG15 had minimal effect on virus replication and did not have an obvious role in the modulation of the acute immune response to infection. Instead, we observed an increase in the number of diseased small airways in mice lacking ISG15. This ability of ISG15 to protect mice in a conjugation-dependent, but nonantiviral, manner from respiratory virus infection represents a previously undescribed role for ISG15 and demonstrates the importance of further characterization of ISG15in vivo.IMPORTANCEIt has previously been demonstrated that ISG15−/−mice are more susceptible to a number of viral infections. Since ISG15 is one of the most strongly induced genes after type I interferon stimulation, analysis of ISG15 function has largely focused on its role as an antiviral molecule during acute infection. Although a number of studies have shown that ISG15 does have a small effect on virus replication in tissue culture, few studies have confirmed this mechanism of protectionin vivo. In these studies we have found that while ISG15−/−mice are more susceptible to influenza A virus and Sendai virus infections, ISGylation does not appear to mediate this protection through the direct inhibition of virus replication or the modulation of the acute immune response. Thus, in addition to showing a novel mode of ISG15 mediated protection from virus infection, this study demonstrates the importance of studying the role of ISG15in vivo.

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