Hepatitis B virus (HBV) infection remains an urgent global health concern, affecting hundreds of millions of people and significantly heightening the risk of severe liver complications, including cirrhosis and hepatocellular carcinoma. Current antiviral treatments, such as nucleos(t)ide analogs, have significantly advanced HBV management; however, they rarely lead to complete viral clearance. Thus, unraveling the complex interactions between HBV and host-derived cellular factors governing the viral replication cycle—including entry, replication, assembly, and release—remains a critical challenge in antiviral research. Among existing therapeutic options, interferon (IFN) therapy is notable for its dual direct antiviral and immune-regulating activities. Nevertheless, IFN therapy is hindered by variable patient responses and commonly associated side effects, including flu-like symptoms, psychiatric disorders, and hematologic toxicity. While recent technological advances such as CRISPR screening, proteomics, and RNA interference have enabled the identification of potential host factors relevant to HBV's life cycle, the underlying molecular mechanisms detailing how interferon modulates these host–virus interactions remain incompletely defined.This Research Topic aims to deepen our understanding of host cellular factors involved in the HBV life cycle, particularly addressing how interferon therapy alters these interactions and their implications for therapeutic efficacy and adverse effects. Specific goals include the identification and mechanistic characterization of host factors essential in different stages of virus infection, determining how interferon treatment modulates these factors, elucidating the molecular basis for interferon-related side effects, and exploring novel therapeutic strategies aimed at host components to improve HBV treatment outcomes.To gather further insights within the scope of host-HBV interactions, their mechanistic regulation, and their relevance to interferon-based treatments, we welcome articles addressing, but not limited to, the following themes:- High-throughput studies such as CRISPR/Cas9 screening, RNA interference, and proteomic analyses to identify novel host factors critical for HBV infection processes.- Detailed mechanistic studies clarifying how specific host factors control HBV replication, viral assembly, and release, including protein-protein interactions and cellular signaling pathways.- Examination of interferon's mechanisms of action on host factors at molecular and cellular levels, particularly those modulating antiviral responses against HBV.- Investigation of host factor involvement in the adverse effects of interferon treatment on patients, aiming to elucidate pathways involved and identify potential interventions.- Evaluation of host cellular factors as therapeutic targets, including innovative approaches such as gene editing, small molecule inhibitors, or combination therapies to improve interferon treatment efficacy in HBV management.We welcome Original Research, Review, and Mini-review articles.
Hepatitis B virus (HBV) infection remains an urgent global health concern, affecting hundreds of millions of people and significantly heightening the risk of severe liver complications, including cirrhosis and hepatocellular carcinoma. Current antiviral treatments, such as nucleos(t)ide analogs, have significantly advanced HBV management; however, they rarely lead to complete viral clearance. Thus, unraveling the complex interactions between HBV and host-derived cellular factors governing the viral replication cycle—including entry, replication, assembly, and release—remains a critical challenge in antiviral research. Among existing therapeutic options, interferon (IFN) therapy is notable for its dual direct antiviral and immune-regulating activities. Nevertheless, IFN therapy is hindered by variable patient responses and commonly associated side effects, including flu-like symptoms, psychiatric disorders, and hematologic toxicity. While recent technological advances such as CRISPR screening, proteomics, and RNA interference have enabled the identification of potential host factors relevant to HBV's life cycle, the underlying molecular mechanisms detailing how interferon modulates these host–virus interactions remain incompletely defined.This Research Topic aims to deepen our understanding of host cellular factors involved in the HBV life cycle, particularly addressing how interferon therapy alters these interactions and their implications for therapeutic efficacy and adverse effects. Specific goals include the identification and mechanistic characterization of host factors essential in different stages of virus infection, determining how interferon treatment modulates these factors, elucidating the molecular basis for interferon-related side effects, and exploring novel therapeutic strategies aimed at host components to improve HBV treatment outcomes.To gather further insights within the scope of host-HBV interactions, their mechanistic regulation, and their relevance to interferon-based treatments, we welcome articles addressing, but not limited to, the following themes:- High-throughput studies such as CRISPR/Cas9 screening, RNA interference, and proteomic analyses to identify novel host factors critical for HBV infection processes.- Detailed mechanistic studies clarifying how specific host factors control HBV replication, viral assembly, and release, including protein-protein interactions and cellular signaling pathways.- Examination of interferon's mechanisms of action on host factors at molecular and cellular levels, particularly those modulating antiviral responses against HBV.- Investigation of host factor involvement in the adverse effects of interferon treatment on patients, aiming to elucidate pathways involved and identify potential interventions.- Evaluation of host cellular factors as therapeutic targets, including innovative approaches such as gene editing, small molecule inhibitors, or combination therapies to improve interferon treatment efficacy in HBV management.We welcome Original Research, Review, and Mini-review articles.