HIV molecular epidemiology: transmission and adaptation to human populations

Abstract

Purpose of review To provide an update on the origin of the HIV epidemic and insights into how the immune response is shaping virus evolution. Recent findings Characterization of archival samples showed that by the 1960s, HIV had already diverged within humans. It is now estimated that HIV has been in humans since at least the early 1900s. However, despite the potential for different divergent viruses to spread, surprisingly few viruses successfully expanded to cause the global epidemic. In approximately 80% of cases, productive infection is the result of infection with only a single virus or single virus-infected cell. After transmission, HIV evolves at a rapid rate driven by the immune pressure until the virus reaches a delicate survival balance: on one hand avoiding elimination through the development of cytotoxic T-cell immune escape mutations, and on the other sacrificing replication fitness as these mutations may come with a severe fitness cost to the virus. People infected with these ‘attenuated’ cytotoxic T-cell escape viruses can have a survival advantage. Cytotoxic T-cell responses are molding HIV diversity at a population level resulting in a loss of some of the common immune epitopes. Summary Insights into the origin of HIV and its evolution between populations and within individuals is essential to understanding HIV pathogenesis and imperative for the design of effective biomedical interventions such as vaccines.