Strategies to Eliminate HBV Infection

ABSTRACT: 

Chronic HBV infection is a major public health concern affecting over 240 million people worldwide. Although suppression of HBV replication is achieved in the majority of patients with currently available newer antivirals, discontinuation of therapy prior to hepatitis B surface antigen loss or seroconversion is associated with relapse of HBV in the majority of cases. Thus, new therapeutic modalities are needed to achieve eradication of the virus from chronically infected patients in the absence of therapy. The basis of HBV persistence includes viral and host factors. Here, we review novel strategies to achieve sustained cure or elimination of HBV. The novel approaches include targeting the viral and or host factors required for viral persistence, and novel immune-based therapies, including therapeutic vaccines.

KEYWORDS:

• covalently closed circular DNA
• cure
• elimination
• eradication
• HBV
• host
• IL-7
• IL-21
• immunity
• PD-1
• PD-L1
• receptor
• RNAi
• seroconvesrion
• therapeutic vaccination
• Toll-like receptor
• treatment
• vaccines
• viral entry
• virus

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The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government.

Financial & competing interests disclosure

S Kottilil is Federal Employee and R Kapoor is Government Contractor. This project has been funded in whole or in part with federal funds from the National Cancer Institute, NIH, under contract No. HHSN261200800001E. This research was supported (in part) by the National Institutes of Allergy and Infectious Diseases. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

S Kottilil is Federal Employee and R Kapoor is Government Contractor. This project has been funded in whole or in part with federal funds from the National Cancer Institute, NIH, under contract No. HHSN261200800001E. This research was supported (in part) by the National Institutes of Allergy and Infectious Diseases. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.