Viral Strategies to Regulate Host Immunity or Signal Pathways, 2nd Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 562

Special Issue Editor


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Guest Editor
Departments of Surgery and Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212, USA
Interests: viral immunity; RNA virus-host interaction; influenza; LCMV; sphingolipid network
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Special Issue Information

Dear Colleagues,

Viruses appear to have developed diverse strategies to regulate host immunity and cellular signal pathways in order to facilitate viral propagation. Highly pathogenic viruses effectively elude or suppress the host protective immune system and even utilize host machinery for robust viral replication or spread. Therefore, determining the mechanisms for pathogenic virus–host interactions and viral methodologies to escape the host immunity could help us understand how viruses cause diseases and ultimately help to design new therapeutics to cure the viral diseases.

This Special Issue will cover research on recent scientific discoveries about virus–host interaction, viral disruption of cellular signal pathways, viral utilization of host machinery, and viral tactics to escape or inhibit the host innate or adaptive immune responses. You are cordially invited to contribute unique research or review articles on the related research topics.

Prof. Dr. Bumsuk Hahm
Guest Editor

Manuscript Submission Information

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Keywords

  • virus–host interaction
  • viral immunity
  • viral pathogenesis
  • immune evasion
  • innate immunity
  • adaptive immunity
  • signal pathway

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Published Papers (1 paper)

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Research

14 pages, 4844 KB  
Article
Influenza A Virus Infection Induces Preferential Increases in Long-Chain Ceramides
by Savannah McKenna, Kwang Il Jung, Barbara Sumner, Jennifer J. Wolf, Lloyd W. Sumner and Bumsuk Hahm
Viruses 2026, 18(3), 339; https://doi.org/10.3390/v18030339 - 10 Mar 2026
Abstract
Influenza is a persistent public health concern worldwide. The elucidation of influenza A virus (IAV)–host interactions and the identification of host factors that regulate IAV infection would be beneficial for combating and treating the disease. Ceramides, comprising a host sphingolipid family, have been [...] Read more.
Influenza is a persistent public health concern worldwide. The elucidation of influenza A virus (IAV)–host interactions and the identification of host factors that regulate IAV infection would be beneficial for combating and treating the disease. Ceramides, comprising a host sphingolipid family, have been shown to regulate virus infections. However, the effect of IAV on individual ceramides remains unknown. This study aimed to investigate the changes in ceramide species during the infection of human lung epithelial A549 cells and human primary tracheal epithelial cells with IAV. We established a method utilizing UHPLC-MS analysis to measure individual ceramides (C14- to C26-ceramide). The results indicate that two main ceramide species, C16- and C24-ceramide, constitute approximately 80% of the ceramide population in human respiratory epithelial cells. Following IAV infection, these ceramides were found to undergo a shift in abundance, with a reduction in C16-ceramide and an increase in C24-ceramide, under various infection conditions. Primarily, IAV infection led to an increase in multiple long-chain ceramides. These findings could provide details for understanding how the ceramide system is disrupted during influenza virus infection and to further support the ongoing efforts to understand influenza–host interactions. Full article
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