# Mechanisms of Hepadnavirus Assembly and Replication

> **NIH NIH R37** · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · 2020 · $380,803

## Abstract

Abstract
Hepatitis B virus (HBV) is a major cause of chronic viral hepatitis that increases dramatically the risk of liver
cancer and other end-stage liver diseases such as cirrhosis. The major obstacle to curing chronic HBV
infection is the persistence of the viral episome, the covalently closed circular DNA (cccDNA), in the infected
hepatocytes despite antiviral treatment. This application will address viral and host control of HBV cccDNA
formation at a prerequisite step for cccDNA formation, i.e., the disassembly of viral nucleocapsids (uncoating),
which releases the viral relaxed circular DNA (rcDNA) for conversion to cccDNA. Three Specific Aims are
proposed. Aim 1 will define the viral capsid determinants of uncoating. Aim 2 will define the host determinants
of uncoating. Aim 3 will seek to understand, and to overcome, the failure of mouse hepatocytes to support HBV
cccDNA formation, so as to render mouse hepatocytes fully permissive to HBV replication and facilitate the
development of fully susceptible mouse models of HBV infection and replication.

## Key facts

- **NIH application ID:** 10000008
- **Project number:** 5R37AI043453-23
- **Recipient organization:** PENNSYLVANIA STATE UNIV HERSHEY MED CTR
- **Principal Investigator:** Jianming Hu
- **Activity code:** R37 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $380,803
- **Award type:** 5
- **Project period:** 1999-02-15 → 2023-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10000008

## Citation

> US National Institutes of Health, RePORTER application 10000008, Mechanisms of Hepadnavirus Assembly and Replication (5R37AI043453-23). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10000008. Licensed CC0.

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