Androgen boosts hepatitis B virus replication

February 16, 2012, American Society For Microbiology

Androgen enhances replication of hepatitis B virus (HBV), rendering males more vulnerable than females to this virus, according to research published in the February Journal of Virology.

“Our studies allowed us to understand the gender disparity of HBV carriers, and why this virus tends to cause more severe liver disease in men than in women,” says principal investigator James Ou of the University of Southern California.

The researchers found no difference between levels of virus in prepubescent male and female mice. However, post-puberty, levels in males exceeded those in , in some cases by more than double, says Ou. Subsequently castrating male mice reduced the viral load, but injecting castrated mice with an androgen agonist resulted in a rising viral load again.

In a third set of experiments, the researchers removed the androgen receptor by genetic knockout, once again abolishing the androgen’s effect on . Then they drilled down still further, discovering elements within the HBV genome which are recognized by the host’s activated androgen receptor, which then boosts viral gene expression and replication.

Epidemiologic studies have shown that men are three to seven times more likely than women to become HBV carriers, and male HBV carriers are more likely to develop cancer of the liver (hepatocellular carcinoma) than female carriers.

is one of the most important human pathogens,” says Ou. “Approximately 350 million people worldwide are chronically infected, and roughly one million die annually.”

HBV can be transmitted sexually, as well as via non-sterile needles, and perinatally. In areas where the virus is endemic, it is frequently transmitted among young children. It is present in blood (including menstrual blood), vaginal secretions, saliva, semen, breast milk, and to a lesser extent in other bodily fluids. A vaccine is available for HBV.

More information: Y. Tian, C.f. Kuo, W.-l. Chen, and J.-h.J. Ou, 2012. Enhancement of hepatitis B virus replication by androgen and its receptor in mice. J. Virol. 86:1904-1910.

Related Stories

Recommended for you

Onions could hold key to fighting antibiotic resistance

January 22, 2018
A type of onion could help the fight against antibiotic resistance in cases of tuberculosis, a UCL and Birkbeck-led study suggests.

New long-acting approach for malaria therapy developed

January 22, 2018
A new study, published in Nature Communications, conducted by the University of Liverpool and the Johns Hopkins University School of Medicine highlights a new 'long acting' medicine for the prevention of malaria.

Virus shown to be likely cause of mystery polio-like illness

January 22, 2018
A major review by UNSW researchers has identified strong evidence that a virus called Enterovirus D68 is the cause of a mystery polio-like illness that has paralysed children in the US, Canada and Europe.

Creation of synthetic horsepox virus could lead to more effective smallpox vaccine

January 19, 2018
UAlberta researchers created a new synthetic virus that could lead to the development of a more effective vaccine against smallpox. The discovery demonstrates how techniques based on the use of synthetic DNA can be used to ...

Study ends debate over role of steroids in treating septic shock

January 19, 2018
The results from the largest ever study of septic shock could improve treatment for critically ill patients and save health systems worldwide hundreds of millions of dollars each year.

New approach could help curtail hospitalizations due to influenza infection

January 18, 2018
More than 700,000 Americans were hospitalized due to illnesses associated with the seasonal flu during the 2014-15 flu season, according to federal estimates. A radical new approach to vaccine development at UCLA may help ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.