# HEPATITIS B LIKE VIRUS

> **NIH NIH R01** · INSTITUTE FOR CANCER RESEARCH · 1987 · $241,550

## Abstract

Human hepatitis B virus (HBV) is a cause of both acute and chronic liver
disease in man, and chronic infections are epidemiologically associated
with hepatocellular carcinoma.  HBV is the prototype of a new family of
hepatotropic DNA viruses (hepadna viruses) which includes woodchuck
hepatitis virus, ground squirrel hepatitis virus, and duck hepatitis B
virus (DHBV).  Our recent studies with DHBV indicate a novel mode of
replication for the hepadna viruses, involving reverse transcription of an
RNA intermediate occurring as a step in virion maturation.

The long term objective in studying the hepadna viruses is to understand
and prevent the phenomenon of viral pathogenesis.  An important aspect of
this problem is to understand the molecular biology of virus replication,
including the mechanism of initiation of infection and the control of virus
expression.  We have been studying these processes using DHBV as a model of
human hepatitis B virus.  During the next three years, our main objectives
will be in two areas.  First, we propose to characterize in detail the
initiation of infection in embryos and ducklings, and the basis for the age
dependent decline in susceptibility.  Second, we will continue work on the
mechanism of virus DNA synthesis, including the structure of the RNA
template for minus strand synthesis and the DNA template for plus strand
synthesis, and the mechanisms and timing for initiation and elongation of
both strands.  As a new area of research in our lab, we will also carry out
a pilot project on the induction and role of liver specific
immunoregulatory factors in viral hepatitis in Pekin ducks.

Towards these goals, we have demonstrated that infection is rapid (less
than 24h) in embryos and young ducklings, allowing a detailed
characterization of early steps in infection without recourse to tissue
culture systems, which are unavailable.  In addition, DNA synthesis
complexes are readily isolated from the liver, permitting analysis of
virion DNA synthesis in an in vitro system.  Cloned DNA as well as
antibodies have been prepared to assist both studies, and we have been able
to use the former to identify the origin and a potential primer (protein)
of reverse transcription.

## Key facts

- **NIH application ID:** 3128084
- **Project number:** 5R01AI018641-06
- **Recipient organization:** INSTITUTE FOR CANCER RESEARCH
- **Principal Investigator:** William Mason
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $241,550
- **Award type:** 5
- **Project period:** 1982-09-01 → 1989-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3128084

## Citation

> US National Institutes of Health, RePORTER application 3128084, HEPATITIS B LIKE VIRUS (5R01AI018641-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3128084. Licensed CC0.

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