Cellular Immune Response to Hepatitis Viruses

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 4843

Special Issue Editor


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Guest Editor
1. Inserm, UMR 1350 PaThLiv, Université Claude-Bernard Lyon 1, F-69003 Lyon, France
2. The Lyon Hepatology Institute, IHU EVEREST, F-69004 Lyon, France
Interests: development of new host-targeted therapeutic strategies against chronic HBV and HDV infection

Special Issue Information

Dear Colleagues,

The liver presents a delicate balance between immunological tolerance and the rapid elimination of invading pathogens. The alteration of this equilibrium can lead to hepatitis and the potential development of severe complications. In addition to the classical hepatitis A–E viruses (i.e., HAV, HBV, HCV, HDV, and HEV), a wide variety of emerging and re‑emerging agents, which include yellow fever (YFV), dengue (DENV), Zika (ZIKV), Crimean–Congo hemorrhagic fever (CCHFV), Rift Valley fever (RVFV), Lassa (LASV), and Ebola (EBOV), also target the liver and contribute to the global burden of viral hepatitis. Understanding how each of these viruses interacts, evades, and reshapes innate and adaptive immune responses is central for the design of novel prophylactic and therapeutic strategies.

This Special Issue, “Cellular Immune Response to Hepatitis Viruses”, will focus on the most recent developments related to viral sensing, immune evasion, immunopathology, immunomodulatory agents, and the use of preclinical models for the study of hepatotropic viruses.

We invite submissions of original research, short communications, and review articles on this highly dynamic field. We look forward to receiving your contributions.

Dr. Armando Andres Roca Suarez
Guest Editor

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Keywords

  • viral hepatitis
  • viral/host interactions
  • immune response
  • immune evasion
  • immunopathogenesis
  • immunomodulatory therapy
  • pre-clinical models

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Published Papers (2 papers)

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Review

20 pages, 1189 KB  
Review
Hepatitis D Virus Pathogenesis: A Sense of Complications
by Yann Haennel, Thomas F. Baumert and Joachim Lupberger
Viruses 2026, 18(3), 278; https://doi.org/10.3390/v18030278 - 24 Feb 2026
Viewed by 780
Abstract
Hepatitis D virus (HDV) is a satellite RNA virus of the hepatitis B virus (HBV) infecting an estimated 12 million people worldwide. Chronic HDV infection is causing the most severe form of chronic viral hepatitis, leading to a rapid progression of chronic inflammation [...] Read more.
Hepatitis D virus (HDV) is a satellite RNA virus of the hepatitis B virus (HBV) infecting an estimated 12 million people worldwide. Chronic HDV infection is causing the most severe form of chronic viral hepatitis, leading to a rapid progression of chronic inflammation to fibrosis, cirrhosis, liver decompensation and cancer. The detailed mechanisms responsible for HDV pathogenicity and its contribution to the development of hepatocellular carcinoma (HCC) are not clearly understood. This review aims to summarize the current knowledge of HDV-induced injuries, which gradually accumulate and increase the oncogenic pressure in the liver. Here, we provide a comprehensive yet concise overview of the following topics: (1) virus sensing and innate responses, (2) molecular basis of HDV pathogenesis, and (3) pathogenesis of chronic HDV infection in patients. We summarize the compelling evidence of the direct and indirect contributions of HDV to the development of HCC, which is driven by the rapid progression to liver cirrhosis. These results led to the classification of HDV as a group 1 carcinogenic agent in 2025 and emphasize the urgent need for improved antiviral and chemopreventive treatments. In addition, it highlights the necessity of routine HDV screening in patients with chronic hepatitis B and intensified HCC surveillance in patients with chronic hepatitis D. Full article
(This article belongs to the Special Issue Cellular Immune Response to Hepatitis Viruses)
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24 pages, 1310 KB  
Review
Interferon-α for Immune Modulation in Chronic Hepatitis B Toward Functional Cure
by Asha Ashuo, Jia Liu, Zhenghong Yuan and Jieliang Chen
Viruses 2025, 17(10), 1358; https://doi.org/10.3390/v17101358 - 10 Oct 2025
Viewed by 3707
Abstract
Chronic hepatitis B (CHB) remains a major global health challenge, largely due to the persistence of covalently closed circular DNA (cccDNA) and impaired host immunity. Interferon-α (IFN-α), a key antiviral cytokine, not only directly restricts HBV replication but also orchestrates innate and adaptive [...] Read more.
Chronic hepatitis B (CHB) remains a major global health challenge, largely due to the persistence of covalently closed circular DNA (cccDNA) and impaired host immunity. Interferon-α (IFN-α), a key antiviral cytokine, not only directly restricts HBV replication but also orchestrates innate and adaptive immune responses. This review summarizes current advances in IFN-α-mediated immune regulation, highlighting its effects across diverse immune cell populations. Evidence indicates that IFN-α can reprogram immune responses to promote viral clearance, although clinical efficacy is limited by modest response rates and adverse effects. Recent progress in cytokine engineering, subtype research, and rational combination strategies—including nucleo(s/t)ide analogs, RNA interference therapeutics, antisense oligonucleotides, therapeutic vaccines, and beyond—has expanded opportunities to improve treatment outcomes. While challenges remain, these advances lay the foundation for optimizing IFN-α–based interventions and highlight IFN-α as a key driver for innovative therapies aimed at achieving a functional cure of chronic hepatitis B. Full article
(This article belongs to the Special Issue Cellular Immune Response to Hepatitis Viruses)
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