Host Innate Immune Response to Influenza A Virus Infections

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 2684

Special Issue Editor


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Guest Editor
The Pirbright Institute, Ash Road, Pirbright, Woking, GU24 0NF, UK
Interests: Influenza A virus; innate immunity; influenza virus evolution; viral vector vaccine; CRISPR-Cas9

Special Issue Information

Dear colleagues,

The influenza A virus is an RNA virus that can infect humans and a wide range of animal hosts, such as birds, pigs, dogs and horses. Influenza infection can cause mild to severe disease. The innate immune system forms the first line of defence that prevents, controls, or eliminates host infection. However, aberrant innate immune responses, such as “cytokine storm”, can also contribute to the severity of virus infection. Moreover, the innate immune response might also affect the nature of the adaptive immune response. Therefore, research into the innate immune response to influenza A virus infection is not only vital to understanding the pathogenesis of influenza and to develop new intervention methods, but also critical to help facilitate vaccine development.

In this Special Issue of Pathogens, we invite you to contribute review or research articles about the avian or mammalian host innate immune response to different influenza A viruses.

Dr. Pengxiang Chang
Guest Editor

Manuscript Submission Information

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Keywords

  • influenza A virus
  • innate immunity
  • pathogenesis

Published Papers (1 paper)

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Research

12 pages, 2044 KiB  
Article
Replication of Influenza A Virus in Secondary Lymphatic Tissue Contributes to Innate Immune Activation
by Sarah-Kim Friedrich, Rosa Schmitz, Michael Bergerhausen, Judith Lang, Vikas Duhan, Cornelia Hardt, Matthias Tenbusch, Marco Prinz, Kenichi Asano, Hilal Bhat, Thamer A. Hamdan, Philipp Alexander Lang and Karl Sebastian Lang
Pathogens 2021, 10(5), 622; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10050622 - 19 May 2021
Cited by 1 | Viewed by 2260
Abstract
The replication of viruses in secondary lymphoid organs guarantees sufficient amounts of pattern-recognition receptor ligands and antigens to activate the innate and adaptive immune system. Viruses with broad cell tropism usually replicate in lymphoid organs; however, whether a virus with a narrow tropism [...] Read more.
The replication of viruses in secondary lymphoid organs guarantees sufficient amounts of pattern-recognition receptor ligands and antigens to activate the innate and adaptive immune system. Viruses with broad cell tropism usually replicate in lymphoid organs; however, whether a virus with a narrow tropism relies on replication in the secondary lymphoid organs to activate the immune system remains not well studied. In this study, we used the artificial intravenous route of infection to determine whether Influenza A virus (IAV) replication can occur in secondary lymphatic organs (SLO) and whether such replication correlates with innate immune activation. Indeed, we found that IAV replicates in secondary lymphatic tissue. IAV replication was dependent on the expression of Sialic acid residues in antigen-presenting cells and on the expression of the interferon-inhibitor UBP43 (Usp18). The replication of IAV correlated with innate immune activation, resulting in IAV eradication. The genetic deletion of Usp18 curbed IAV replication and limited innate immune activation. In conclusion, we found that IAV replicates in SLO, a mechanism which allows innate immune activation. Full article
(This article belongs to the Special Issue Host Innate Immune Response to Influenza A Virus Infections)
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