Interferons (IFNs) are a group of signaling proteins, induced and released by host cells in response to microbial infection. By binding to the Interferon receptor (IFNR), hundreds of IFN-stimulated genes (ISGs) are further produced and play direct or indirect roles in restricting the virus infection and replication. Based on the receptors to which they bind, three main categories of human interferons are classified, including type-I, type-II, and type-III. Herein, type-I interferon (IFN-a, IFN-ß, IFN-e, IFN-?, and IFN-?) has been approved to be the first-line drug for the clinical treatment of chronic HBV. However, poor response rates and substantial side effects of the interferon treatment were reported, which affect their clinical application.
It was reported that HBV could inhibit the expression of ISGs and the production of type-I IFN in HBV-infected patients, while type-III IFN (IFN-?s, including IL-29/IFN-?1, IL-28A/IFN-?2, and IL-28B/IFN-?3) but not type-I or type-II IFNs could be induced upon HBV infection. Hence, IFN-?s might play a critical role in anti-HBV processes. The induction of interferons in response to HBV infection remains controversial and the molecular mechanisms involved in the crosstalk between HBV and interferons still need to be fully clarified.
The goal of this Research Topic is to provide deep insights into the induction of the interferons after HBV infection and the interaction between HBV and interferons or interferon-stimulated genes. We aim to give more details about the crosstalk between HBV and the host, which might be helpful to ameliorate the side effects of interferon therapy.
We welcome the submission of Original Research, Review, and Mini-review articles focusing on, but not limited to, the following topics:
1) Induction of Interferons in response to HBV infection
2) Interactions between HBV and Interferon-stimulated genes (proteins, lncRNAs, microRNAs, etc.)
3) HBV immune tolerance in response to Interferon therapy
4) Clinical research on Interferon therapy of HBV-infected patients
Interferons (IFNs) are a group of signaling proteins, induced and released by host cells in response to microbial infection. By binding to the Interferon receptor (IFNR), hundreds of IFN-stimulated genes (ISGs) are further produced and play direct or indirect roles in restricting the virus infection and replication. Based on the receptors to which they bind, three main categories of human interferons are classified, including type-I, type-II, and type-III. Herein, type-I interferon (IFN-a, IFN-ß, IFN-e, IFN-?, and IFN-?) has been approved to be the first-line drug for the clinical treatment of chronic HBV. However, poor response rates and substantial side effects of the interferon treatment were reported, which affect their clinical application.
It was reported that HBV could inhibit the expression of ISGs and the production of type-I IFN in HBV-infected patients, while type-III IFN (IFN-?s, including IL-29/IFN-?1, IL-28A/IFN-?2, and IL-28B/IFN-?3) but not type-I or type-II IFNs could be induced upon HBV infection. Hence, IFN-?s might play a critical role in anti-HBV processes. The induction of interferons in response to HBV infection remains controversial and the molecular mechanisms involved in the crosstalk between HBV and interferons still need to be fully clarified.
The goal of this Research Topic is to provide deep insights into the induction of the interferons after HBV infection and the interaction between HBV and interferons or interferon-stimulated genes. We aim to give more details about the crosstalk between HBV and the host, which might be helpful to ameliorate the side effects of interferon therapy.
We welcome the submission of Original Research, Review, and Mini-review articles focusing on, but not limited to, the following topics:
1) Induction of Interferons in response to HBV infection
2) Interactions between HBV and Interferon-stimulated genes (proteins, lncRNAs, microRNAs, etc.)
3) HBV immune tolerance in response to Interferon therapy
4) Clinical research on Interferon therapy of HBV-infected patients
