The immune response to influenza A viruses

2008 ◽  
pp. 113-138
Author(s):  
Justine D. Mintern ◽  
Carole Guillonneau ◽  
Stephen J. Turner ◽  
Peter C. Doherty
Keyword(s):  
Immune Response ◽  
Influenza A ◽  
Influenza A Viruses

Contribution of innate immune cells to pathogenesis of severe influenza virus infection

2017 ◽  
Vol 131 (4) ◽  
pp. 269-283 ◽  
Author(s):  
Suzanne L. Cole ◽  
Ling-Pei Ho
Keyword(s):  
Immune Response ◽  
Influenza A ◽  
Influenza Virus Infection ◽  
Respiratory Illness ◽  
Airway Epithelial Cells ◽  
Innate Immune ◽  
Airway Epithelial ◽  
Cell Type ◽  
Influenza A Viruses ◽  
Effector Cells

Influenza A viruses (IAVs) cause respiratory illness of varying severity based on the virus strains, host predisposition and pre-existing immunity. Ultimately, outcome and recovery from infection rely on an effective immune response comprising both innate and adaptive components. The innate immune response provides the first line of defence and is crucial to the outcome of infection. Airway epithelial cells are the first cell type to encounter the virus in the lungs, providing antiviral and chemotactic molecules that shape the ensuing immune response by rapidly recruiting innate effector cells such as NK cells, monocytes and neutrophils. Each cell type has unique mechanisms to combat virus-infected cells and limit viral replication, however their actions may also lead to pathology. This review focuses how innate cells contribute to protection and pathology, and provides evidence for their involvement in immune pathology in IAV infections.

The Immune Response to Influenza A Viruses

2010 ◽  
pp. 173-197
Author(s):  
Justine D. Mintern ◽  
Carole Guillonneau ◽  
Stephen J. Turner ◽  
Peter C. Doherty
Keyword(s):  
Immune Response ◽  
Influenza A ◽  
Influenza A Viruses

scholarly journals Influenza Virus NS Vectors Expressing the Mycobacterium tuberculosis ESAT-6 Protein Induce CD4+ Th1 Immune Response and Protect Animals against Tuberculosis Challenge

2006 ◽  
Vol 13 (8) ◽  
pp. 898-904 ◽  
Author(s):  
Sabine Sereinig ◽  
Marina Stukova ◽  
Natalia Zabolotnyh ◽  
Boris Ferko ◽  
Christian Kittel ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Mycobacterium Tuberculosis ◽  
Influenza A ◽  
Mucosal Immunization ◽  
Influenza A Viruses ◽  
Reading Frame ◽  
Early Secretory Antigenic Target ◽  
Airborne Disease ◽  
Th1 Immune Response

ABSTRACT Infection with Mycobacterium tuberculosis remains a major cause of morbidity and mortality all over the world. Since the effectiveness of the only available tuberculosis vaccine, Mycobacterium bovis bacillus Calmette-Guérin (BCG), is suboptimal, there is a strong demand to develop new tuberculosis vaccines. As tuberculosis is an airborne disease, the intranasal route of vaccination might be preferable. Live influenza virus vaccines might be considered as potential vectors for mucosal immunization against various viral or bacterial pathogens, including M. tuberculosis. We generated several subtypes of attenuated recombinant influenza A viruses expressing the 6-kDa early secretory antigenic target protein (ESAT-6) of M. tuberculosis from the NS1 reading frame. We were able to demonstrate the potency of influenza virus NS vectors to induce an M. tuberculosis-specific Th1 immune response in mice. Moreover, intranasal immunization of mice and guinea pigs with such vectors induced protection against mycobacterial challenge, similar to that induced by BCG vaccination.

scholarly journals Deletion of Irf3 and Irf7 Genes in Mice Results in Altered Interferon Pathway Activation and Granulocyte-Dominated Inflammatory Responses to Influenza A Infection

2016 ◽  
Vol 9 (2) ◽  
pp. 145-161 ◽  
Author(s):  
Bastian Hatesuer ◽  
Hang Thi Thu Hoang ◽  
Peggy Riese ◽  
Stephanie Trittel ◽  
Ingo Gerhauser ◽  
...  
Keyword(s):  
Immune Response ◽  
Knockout Mice ◽  
Influenza A ◽  
Viral Infections ◽  
Inflammatory Responses ◽  
Adaptive Immune Response ◽  
Strong Increase ◽  
Type I ◽  
Influenza A Viruses ◽  
Double Knockout

The interferon (IFN) pathway plays an essential role in the innate immune response following viral infections and subsequent shaping of adaptive immunity. Infections with influenza A viruses (IAV) activate the IFN pathway after the recognition of pathogen-specific molecular patterns by respective pattern recognition receptors. The IFN regulatory factors IRF3 and IRF7 are key players in the regulation of type I and III IFN genes. In this study, we analyzed the role of IRF3 and IRF7 for the host response to IAV infections in Irf3-/-, Irf7-/-, and Irf3-/-Irf7-/- knockout mice. While the absence of IRF3 had only a moderate impact on IFN expression, deletion of IRF7 completely abolished IFNα production after infection. In contrast, lack of both IRF3 and IRF7 resulted in the absence of both IFNα and IFNβ after IAV infection. In addition, IAV infection of double knockout mice resulted in a strong increase of mortality associated with a massive influx of granulocytes in the lung and reduced activation of the adaptive immune response.

scholarly journals Host microRNA molecular signatures associated with human H1N1 and H3N2 influenza A viruses reveal an unanticipated antiviral activity for miR-146a

2013 ◽  
Vol 94 (5) ◽  
pp. 985-995 ◽  
Author(s):  
Olivier Terrier ◽  
Julien Textoris ◽  
Coralie Carron ◽  
Virginie Marcel ◽  
Jean-Christophe Bourdon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Innate Immune Response ◽  
Influenza A ◽  
Influenza Infection ◽  
Influenza Viruses ◽  
Innate Immune ◽  
Biological Processes ◽  
Human Influenza ◽  
Influenza A Viruses

While post-transcriptional regulation of gene expression by microRNAs (miRNAs) has been shown to be involved in influenza virus replication cycle, only a few studies have further investigated this aspect in a human cellular model infected with human influenza viruses. In this study, we performed miRNA global profiling in human lung epithelial cells (A549) infected by two different subtypes of human influenza A viruses (H1N1 and H3N2). We identified a common miRNA signature in response to infection by the two different strains, highlighting a pool of five miRNAs commonly deregulated, which are known to be involved in the innate immune response or apoptosis. Among the five miRNA hits, the only upregulated miRNA in response to influenza infection corresponded to miR-146a. Based on a previously published gene expression dataset, we extracted inversely correlated miR-146a target genes and determined their first-level interactants. This functional analysis revealed eight distinct biological processes strongly associated with these interactants: Toll-like receptor pathway, innate immune response, cytokine production and apoptosis. To better understand the biological significance of miR-146a upregulation, using a reporter assay and a specific anti-miR-146a inhibitor, we confirmed that infection increased the endogenous miR-146a promoter activity and that inhibition of miR-146a significantly increased viral propagation. Altogether, our results suggest a functional role of miR-146a in the outcome of influenza infection, at the crossroads of several biological processes.

scholarly journals NSP protein encoded in negative NS RNA strand of influenza A virus induces cellular immune response in infected animals

2019 ◽  
Vol 486 (3) ◽  
pp. 389-394
Author(s):  
O. P. Zhirnov ◽  
E. I. Isaeva
Keyword(s):  
Immune Response ◽  
Amino Acid ◽  
Influenza A Virus ◽  
Influenza A ◽  
Central Zone ◽  
Virus Genome ◽  
T Cell Epitopes ◽  
Influenza A Viruses ◽  
Protein Amino Acid ◽  
Cellular Immune

Infection of mice with influenza A viruses led to the formation of clones of lymphocytes that specifically recognizes viral domains in the central zone of the NSP protein (amino acid positions 83-119). Computer analysis of the primary structure of the NSP protein showed the presence of T-cell epitopes in the central part of the NSP molecule. The findings indicate that the viral NSP gene is expressed in the infected animals and support the concept of the bipolar strategy (ambisense strategy) of the influenza A virus genome.

TMPRSS2 is essential for pathogenicity of H7N9 and H1N1 influenza A viruses in mice

Pneumologie ◽  
2014 ◽  
Vol 68 (02) ◽  
Author(s):  
C Tarnow ◽  
G Engels ◽  
A Arendt ◽  
F Schwalm ◽  
H Sediri ◽  
...  
Keyword(s):  
Influenza A ◽  
H1n1 Influenza ◽  
Influenza A Viruses
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