Interferon and interferon-stimulated genes in HBV treatment

Abstract

Human hepatitis B virus (HBV) is a small enveloped DNA virus with a complex life cycle. It is the causative agent of acute and chronic hepatitis. HBV can resist immune system responses and often causes persistent chronic infections. HBV is the leading cause of liver cancer and cirrhosis. Interferons (IFNs) are cytokines with antiviral, immunomodulatory, and antitumor properties. IFNs are glycoproteins with a strong antiviral activity that plays an important role in adaptive and innate immune responses. They are classified into three categories (type I, II, and III) based on the structure of their cell-surface receptors. As an effective drug for controlling chronic viral infections, Type I IFNs are approved to be clinically used for the treatment of HBV infection. The therapeutic effect of interferon will be enhanced when combined with other drugs. IFNs play a biological function by inducing the expression of hundreds of IFN-stimulated genes (ISGs) in the host cells, which are responsible for the inhibiting of HBV replication, transcription, and other important processes. Animal models of HBV, such as chimpanzees, are also important tools for studying IFN treatment and ISG regulation. In the present review, we summarized the recent progress in IFN-HBV treatment and focused on its mechanism through the interaction between HBV and ISGs.

CXCL10 and its receptor in patients with chronic hepatitis B and their ability to predict HBeAg seroconversion during antiviral treatment with TDF

“…In addition, it has been reported that CXCL10 has been shown to be an important marker of hepatic inflammatory response and may be involved in HBsAg and HBeAg clearance in CHB, 12,26 so CXCL10 in the liver may be related to the immunological process of HBeAg SC, although the details should be investigated in a future study. In addition, using data from GEO and GSEA analysis, we identified the genetic determinants of response to interferon‐alpha (IFN‐α) therapy, 34 revealing that immune‐related genes and pathways are the ascending host responses to chronic HBV infection and the major determinants of response to IFN‐α therapy 35,36 …”

“…In addition, using data from GEO and GSEA analysis, we identified the genetic determinants of response to interferon-alpha (IFN-α) therapy, 34 revealing that immune-related genes and pathways are the ascending host responses to chronic HBV infection and the major determinants of response to IFN-α therapy. 35,36 In summary, we determine the transform of CXCL10 or…”

Higher BST2 Expression Promotes the Anti‐HBV Effect of IFN‐α and BST2 Genetic Variant Predicts PegIFNα Treatment Response of HBeAg‐Positive Chronic Hepatitis B Patients

“…IFNs are essential for HBV transcription and replication through the induction of IFN-stimulated genes (ISGs). 29 For example, APOBEC3A was activated by IFNα and prevented HBV replication by reducing the transcription of pgRNA and subgenomic RNA. 26 Sajid et al 30 reported that IFN-a-inducible protein 6 restricted HBV replication by decreasing the level of HBV enhancer II and core promoter (EnhII/Cp) genes.…”

“…IFNs are essential for HBV transcription and replication through the induction of IFN‐stimulated genes (ISGs) 29 . For example, APOBEC3A was activated by IFNα and prevented HBV replication by reducing the transcription of pgRNA and subgenomic RNA 26 .…”

NEDD4-binding protein 1 suppresses HBV replication by degrading pgRNA

“…Interferon (IFN) and nucleos(t)ide analogs (NAs) are currently used as treatments for HBV infection, and both have shown efficacy in controlling viremia [7,8]. IFNs are involved in the inhibition of HBV replication, transcription, and other important processes by inducing the expression of various IFN-stimulated genes (ISGs) in host cells [9]. However, IFN treatment can cause considerable side effects, including liver damage, and is thus unsuitable for patients with severe liver dysfunction [10].…”