Our primary interest is to understand why HIV causes AIDS. This may sound like a naive question, but unfortunately it is a terribly complicated one. We believe that it is imperative to understand in more detail the relationship between HIV and the human immune system, and that in absence of this understanding it will be extremely difficult to develop a truly effective AIDS vaccine, or to find a way to eradicate HIV from an infected person. Indeed, one must think that there are over 40 viruses in the wild that are closely related to HIV and infect African monkeys species -- but despite this striking similarity none of these viruses causes any disease. Our approach is multi-pronged and involves: (i) studies of the comparative pathogenic and non=pathogenic models of Simian Immunodeficiency Virus (SIV) in macaques and mangabeys, respectively; (ii) studies of the host immune response to SIV, with emphasis on the direct antiviral role of CD4+ and CD8+ T cells; and (iii) studies of chronic immune activation as a determinant of both disease progression and size of reservoirs in HIV-infected individuals.

My vision is to make Atlanta and Georgia the number one place in the world for AIDS research within the next 5 to 7 years.

There are three areas that we think are just "incandescent". The first is the discovery that certain subsets of CD4+ T cells are more susceptible than others during the non-pathogenic SIV infection of sooty mangabeys. This discovery led us to formulate the highly innovative hypothesis that, in AIDS pathogenesis, it doesn't really matter how much virus is present in the body, or how many cells are killed by the virus, but rather what cells are infected (i.e., where the virus comes from). The second "hot" area is the discovery that CD8+ T lymphocytes, who are potentially the most effective immune cells against HIV and SIV, may reduce virus replication not just by directly killing the infected cells, but also by producing soluble factors that inhibit virus replication. Further defining what these factors are might have major implications for AIDS vaccine design. The third "hot" area is the recent discovery that a minor subset of HIV-infected individuals have learned to adapt to the infection in the same way of the African monkeys that remain healthy upon SIV infection. Understanding the mechanisms beyond this adaptation may lead to advances in how HIV infection is treated.

The vision and the support of the Georgia Research Alliance; the excellent environment of Emory University; the Emory Center for AIDS Research and the Emory Vaccine Center; and the unique resources of the Yerkes National Primate Research Center.