Host Interaction and Immune Modulation of RNA Viruses

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: 22 December 2025 | Viewed by 3428

Special Issue Editors


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Guest Editor
Lady Davis Institute for Medical Research, Jewish General Hospital & Medicine Department, McGill University Montreal, Montreal, QC H2X 3X8, Canada
Interests: HIV-1; virus and host interaction; antivirus drugs screening and developments; viral immunology
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Department of Microbiology & Immunology, Center for Molecular Virology & Translational Neuroscience, Institute for Molecular Medicine & Infectious Disease, Drexel University College of Medicine, Philadelphia, PA, USA
Interests: emergent RNA viruses; coronaviruses; HIV-1; viral pathogenesis; innate immunity; neuroimmunology; animal models
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Special Issue Information

Dear Colleagues,

Continued global public health threats posed by RNA viruses underscore the critical need for a deeper understanding of their pathogenic processes and the urgent development of targeted therapeutic strategies. The intrusion of these viruses into host cells initiates a cascade of immune responses, primarily activating the innate immune system. During viral replication, pathogen-associated molecular patterns are released, which are then recognized by the host's pattern-recognition receptors, thereby initiating innate immune responses. As an integral part of the initial antiviral defense, the innate immune system is pivotal in recognizing pathogens and launching robust antiviral responses, which not only help to curtail viral replication and dissemination but also stimulate the adaptive immune response.

In this Special Issue, we focus on elucidating the primary mechanisms employed by emerging and re-emerging RNA viruses to circumvent the innate immune system, with a particular emphasis on pathogens posing substantial risks to public health. This Special Issue aims to offer an overview of the latest research on RNA virus-mediated infections, collating significant advancements in the regulation of the innate immune response against viruses and in the development of antiviral strategies that target the innate immune system. We encourage the submission of original research articles, review papers, case reports, communications, and study protocols within the scope of host interactions and immune modulations of RNA viruses.

Dr. Zhenlong Liu
Prof. Dr. Sonia Navas-Martin
Guest Editors

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Keywords

  • RNA viruses
  • viral immunology
  • antiviral therapy development

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Published Papers (2 papers)

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Research

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19 pages, 3184 KB  
Article
RNA Helicase DDX3 Interacts with the Capsid Protein of Hepatitis E Virus and Plays a Vital Role in the Viral Replication
by Shaoli Lin, Bhargava Teja Sallapalli, Peixi Chang, Jia He, Etienne Coyaud, Brian G. Pierce and Yan-Jin Zhang
Pathogens 2025, 14(2), 177; https://doi.org/10.3390/pathogens14020177 - 10 Feb 2025
Cited by 1 | Viewed by 1660
Abstract
DDX3 is an ATP-dependent RNA helicase that is involved in multiple cellular activities, including RNA metabolism and innate immunity. DDX3 is known to assist the replication of some viruses while restricting others through its direct interaction with viral proteins. However, the role of [...] Read more.
DDX3 is an ATP-dependent RNA helicase that is involved in multiple cellular activities, including RNA metabolism and innate immunity. DDX3 is known to assist the replication of some viruses while restricting others through its direct interaction with viral proteins. However, the role of DDX3 in the replication of the hepatitis E virus (HEV) is unknown. In this study, DDX3 was shown to interact with the HEV capsid protein and provide an important role in HEV replication. The DDX3 C-terminal domain was demonstrated to interact with the capsid protein. The depletion of DDX3 led to a significant reduction in HEV replication. Also, the ATPase motif of DDX3 was shown to be required in HEV replication as an ATPase-null mutant DDX3 failed to rescue the viral replication in the DDX3-depleted cells. These results demonstrate a pro-viral role of DDX3 in HEV replication, providing further insights on the virus–cell interactions. Full article
(This article belongs to the Special Issue Host Interaction and Immune Modulation of RNA Viruses)
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Review

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26 pages, 3915 KB  
Review
Dengue Virus and the Host Immune System: A Battle of Immune Modulation, Response and Evasion
by Anwesha Ghosh, Sudipta Mondal, Soumyodip Sadhukhan and Provash Chandra Sadhukhan
Pathogens 2025, 14(11), 1132; https://doi.org/10.3390/pathogens14111132 - 7 Nov 2025
Viewed by 1144
Abstract
Dengue virus (DENV) is a major global health concern, with pathogenesis driven by complex interactions between the virus, host genetics, and immune responses. Key determinants of disease severity include antibody-dependent enhancement (ADE), cross-reactive T cells, anti-NS1 antibodies, autoimmunity, and genetic predisposition, with the [...] Read more.
Dengue virus (DENV) is a major global health concern, with pathogenesis driven by complex interactions between the virus, host genetics, and immune responses. Key determinants of disease severity include antibody-dependent enhancement (ADE), cross-reactive T cells, anti-NS1 antibodies, autoimmunity, and genetic predisposition, with the NS1 protein and its antibodies strongly implicated in severe dengue. This review highlights recent advances in our understanding of how DENV impacts host immune responses at cellular, molecular, and genetic levels. We particularly focus on how the virus interacts with the host, alters immune responses, and escapes immune detection. These factors are crucial for disease progression and immune dysfunction. The host mounts both innate and adaptive immune responses involving interferon signalling, cytokine production, antigen presentation, and T-cell activation. However, DENV evades immunity by suppressing interferon pathways, disrupting antigen presentation, and leveraging antibody-dependent enhancement (ADE), leading to immune dysregulation, prolonged viremia, and severe dengue. Gaining insight into these host-pathogen interactions is essential for understanding dengue pathogenesis for designing safer and more effective therapeutics. Furthermore, integrating omics approaches with immune response models shows promise for identifying early, reliable markers that can predict disease severity and guide treatment. A deeper understanding of these processes will support the development of personalised treatment strategies and enhance preparedness for future dengue outbreaks. Full article
(This article belongs to the Special Issue Host Interaction and Immune Modulation of RNA Viruses)
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