Monday, September 15, 2008

Health Genetics and HIV

In a number of previous posts I have emphasized the importance of transcending the "disease model" of medicine. Whether it be "health genetics", or positive psychology , or the study of longevity genes, examining why some do not develop disease or become ill may actually help us better address human disease and suffering.

Tackling HIV may prove to be another great example of this point. Today, like yesterday, and like tomorrow, approximately 6 800 people will become infected with HIV, and more than 5 700 will die (see here). However, some individuals who are are at a very high risk of contracting the disease (like prostitutes) never contract HIV. Why is this? And how could this information better position us for tackling HIV?

The Sept 5th issue of Science has an important report that helps answer these questions here. Here is a sample:

The human Apobec3 family has been implicated in the control of HIV-1 infection, but HIV-1 encodes Vif, which thwarts the actions of Apobec3G (A3G) and Apobec3F (A3F) (23–26). Compromised A3G/A3F antiviral activity may therefore contribute to the generally poor neutralizing antibody response observed in HIV-1 infection (27). Vif antagonists, if and when they are available, may enhance the generation of effective humoral immune responses against HIV-1. Finally, studies exploring the apparent intrinsic resistance of individuals who are extensively exposed to HIV-1, yet remain uninfected, have genetically mapped this phenotype to chromosome 22q12-13 (12), a location distinguished by a tandem array of the seven human Apobec3 family members. Genome-wide studies of the entire human Apobec3 locus, with particular emphasis on functional differences induced by alternative splicing, are clearly merited to fully explore the potential contribution of this gene family to HIV resistance, neutralizing antibody production, and disease progression.

The NIH has a press release about the research here. The Apobec3 gene may influence anti-HIV antibody production, and this could explain why some at risk individuals do not develop the disease. These insights might help with the development of new HIV drugs and vaccines.