Virological and Immunological Factors Underlying HBV Functional Cure and HBV Reactivation

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

Deadline for manuscript submissions: 15 December 2024 | Viewed by 127

Special Issue Editor


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Guest Editor
Department of Experimental Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
Interests: SARS-CoV-2; drug resistance; immune escape; HBV chronic infection; HBV reactivation; hepatocellular carcinoma; HIV; HDV
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Special Issue Information

Dear Colleagues,

The reactivation of hepatitis B virus (HBV), driven by immunosuppression, represents a virological and clinical challenge since, if not properly managed, it can lead to severe forms of hepatitis and result in death from acute liver failure. HBV reactivation is defined as an abrupt HBV reappearance in the serum of a person with a resolved infection, or a marked increase in serum HBV-DNA in a patient with chronic infection during immunosuppression. The risk of HBV reactivation is related to the persistence in the nuclei of hepatocytes of the circular covalently closed DNA (cccDNA). This mini-chromosome acts as a template to generate the RNAs necessary for viral replication, and its transcriptional activity is modulated by the immune system. The equilibrium between viral replication and immune control can explain why immunosuppression can enhance HBV replication in chronically infected patients and reactivate “quiescent” HBV in individuals with a resolved infection. HBV reactivation is most commonly reported in patients receiving cancer chemotherapy for hematological malignancies and among those undergoing hematopoietic stem cell transplantation. Nevertheless, this event can occur in a wide variety of clinical settings requiring immunosuppressive therapy (solid tumors, solid organ transplantation, gastrointestinal, and rheumatologic or dermatological inflammatory or autoimmune diseases). Recent findings also highlight the risk of HBV reactivation in patients with chronic hepatitis B and C infection who pharmacologically eradicate hepatitis C virus.

So far, minimal information is available on the molecular bases modulating the interplay between cccDNA transcriptioanl activity and the immune response. Unravelling this issue will offer the opportunity to unravel not only the biological correlates of HBV reactivation but also the mechanisms underlying the HBV functional cure. This is critical considering the novel upcoming pharmacological approaches aimed at achieving this important endpoint.

In this light, this Special Issue is aimed at providing a comprehensive overview and new insights into virological and immunological mechanisms underlying the HBV functional cure, persistence and factors promoting viral reactivation. This Special Issue will also provide insights and future directions to optimize the management of patients who are at risk of HBV reactivation.

Dr. Valentina Svicher
Guest Editor

Manuscript Submission Information

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Keywords

  • HBV persistence
  • HBV functional cure
  • cccDNA
  • immunology of HBV
  • HBV reactivation
  • immune-escape mutations

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