PROGRESSION AND CLINICAL OUTCOME OF INFECTION DUE TO HUMAN-IMMUNODEFICIENCY-VIRUS

Ten years into the AIDS epidemic, how are we doing? Have we managed to significantly alter the course of infection with human immunodeficiency virus (HIV)? Have we defined factors that accelerate or decelerate the rate of progression of infection to clinical disease? Are we better able to predict who is most likely to develop AIDS, to substantially alter the course of infection, and to prevent or delay HIV-related morbidity and mortality? Advances made during the past decade that have furthered our understanding of the virus itself have been remarkable. We now understand a great deal about how the virus attaches to the CD4 cell receptor; how it is internalized, transcribed onto DNA of the host, and incorporated into the host’s genome; and how its expression is latently controlled by a series of regulatory genes. However, translating this basic understanding of the virus into significant clinical advances still seems tediously slow for clinicians caring for HIV-infected individuals. I asked Dr. Alan R. Lifson of the University of California San Francisco School of Medicine and his colleagues from the San Francisco Department of Public Health and the California Department of Health Services to summarize the current status of our attempts to alter the course of HIV infection. © 1992, by The University of Chicago.