There has always been a quest regarding the treatment of AIDS/HIV infection that has been haunting the world. Despite the initiation of a global research, AIDS still remains a puzzle to be tackled effectively. Approximately five percent of patients with HIV, or human immunodeficiency virus, do not develop AIDS, or do so very slowly.
Past research suggested that such patients maintain higher levels of an enzyme in white blood cells called APOBEC-3G (A3G), and the new study confirmed it in the first experiments on human cells. These patients remain healthy even after years of infection with HIV despite receiving no treatment. These results have confirmed the presence of an innate defense system present in such subjects.
It is believed that A3G "edits," or introduces changes in, the HIV genetic code every time the virus copies itself. By doing so, A3G corrupts the HIV gene code and prevents the virus from reproducing. However, the HIV virus overcomes this difficulty with the help of viral infectivity factor (Vif) that directs the body to destroy A3G. HIV is then free to overwhelm the immune system, leaving patients vulnerable to AIDS infections.
It has been hypothesized that people suffering from the effects of HIV infection do not make or produce sufficient amounts of the A3G protein to combat Vif and shut it down. Therefore protecting whatever amount of A3G that people do have from Vif represents a new way to attack HIV.
To confirm that A3G offers strong protection against HIV, researchers in the current study measured A3G levels in the immune cells of six people not infected with HIV and in 25 patients with the virus. It was found that higher levels of A3G closely corresponded to lower HIV viral levels.
Furthermore, the team determined that nonprogressors have the most A3G editing enzyme, followed by those not infected with HIV and lastly by those progressing toward full-blown AIDS.
The study has the potential to frame a new prognostic marker for AIDS by enabling the measurement of A3G levels in HIV-infected patients. It will also clarify a previously unrecognized mechanism that underlies slower disease progression in long-term nonprogressors. Lastly, the data suggest that protecting A3G from viral attack may be an important new way to treat AIDS and other viral infections.