A New Hepatitis B Treatment?

[Guest guest]

A New Hepatitis B Treatment?

by C.

Article Date: 04-07-04

An enzyme thought to only be effective against retroviruses like HIV may be

the key to a treatment for hepatitis B. That's what a recent study from

Switzerland suggests.1

Doctors at the University of Geneva discovered that the enzyme known as

APOBEC3G (abbreviated as A3G) can block reproduction of the HBV vaccine.

Based on that finding, they theorize that the enzyme may also be able to

halt HBV itself from reproducing in the body.

" We had done some work demonstrating the mechanism by which APOBEC3G blocks

retroviruses. " explained Didier Trono M.D., chairman of the department of

Microbiology and Molecular Medicine at the University of Geneva in

Switzerland, in an interview with Priority Healthcare. " Since HBV is also a

retro-element, we asked whether the innate antiviral might work on this

other pathogen. "

An HBV-Blocking Enzyme

In their in-vitro study, Trono and his team showed that A3G blocked

reproduction of the HBV vaccine in laboratory-grown cell lines. It was a

surprise finding because up until now, the enzyme had only been identified

as a molecule that defends against retroviruses that have RNA as their

genetic material. HIV is the best known retrovirus, and is spread in the

same way as hepatitis B, by infected blood and through sexual contact.

This is the first study, the authors say, which shows A3G can act against

hepatitis B, which contains DNA as its genetic material.

The DNA in the hepatitis B virus is the genetic material that HBV uses to

make copies of itself inside a liver cell. DNA causes the liver cell itself

to create these new copies of hepatitis B.2

Clinical Implications

Taking this study's findings and applying it to the clinical setting for

patients will require much more scientific study first, said Trono. He

says, hypothetically, the efficacy of this enzyme against HBV could be

harnessed into some sort of gene therapy. The therapy could express A3G in

the livers of chronically infected people, Trono said.

" It has to be inside the cells to work, " he explained. " So, it would have to

be introduced by gene therapy, or its expression would have to be activated

pharmacologically, if it is possible. "

How does the enzyme specifically block HBV replication? It's not yet known,

Trono explained. Finding the cause will be complicated because the hepatitis

B virus is a retrovirus in disguise, using RNA in its reproductive cycle.

It's possible that A3G blocks the assembly of the complex needed for

hepatitis B replication, Trono said, but that's not been proven.

Further studies to assess the role of the enzyme in halting HBV's ability to

replicate is ongoing, he said.

One next step would be to confirm this study's findings in animals, Trono

explained.

Hepatitis B Risk Factors

It's estimated that approximately 1.25 million Americans are chronically

infected with hepatitis B today, of whom 20% to 305 acquired their infection

in childhood. But the number of new infections has plunged from an average

of 260,000 in the 1980s to about 78,000 in 2001. The largest decrease has

occurred in children and adolescents due to routine hepatitis B

vaccination.3

Symptoms of HBV include jaundice, fatigue, abdominal pain, loss of appetite,

nausea and vomiting, and joint pain.

HBV is transmitted through unprotected sexual intercourse with an infected

person, sharing drugs or needles when shooting drugs, through needlesticks

or sharps exposures on the job, or through vertical transmission-from mother

to baby during birth.3

1. Turelli P et al. Inhibition of hepatitis B virus replication by APOBEC3G.

Science 2004 Mar 19;303(5665):1829.

2. Health On the Net Foundation.

3. Centers for Disease Control and Prevention (CDC).

is a long-time health journalist and an editor for Priority

Healthcare. His credits include coverage of health news for the website of

Fox Television's The Health Network, and articles for the New York Post and

other consumer and trade publications.