Int Conf AIDS 1996 Jul 7-12; 11:208 (abstract no. Th.18) Coffin JM; Dept. of Molecular Biology and Microbiology, Tufts University, Boston, MA, USA. Fax: 617-636-8086.
Elucidation of the underlying rapid turnover of virus and HIV infected cells in vivo was perhaps the most informative and exciting discovery in HIV and AIDS in the last few years. This observation, based on the rapid drop in virus load following antiviral drug therapy promises to change significantly the way we view important aspects of interaction of the virus and its host. As a result, the paradigm for HIV infection has shifted from considering the long period of clinical latency as one of viral inactivity, to viewing it as an active steady state of constant virus replication and cell death. This period should also be viewed as an integral part of the disease process, not simply a prolog to frank AIDS. In this talk, I will discuss the theoretical basis of the steady state model of HIV infection as well as its important consequences for understanding and controlling HIV pathogenesis. These include: the significance of genetic variation and the establishment and evolution of the virus quasispecies; the evolution of resistance of the virus to antiviral therapy; and the theoretical and practical significance of virus load measurements. Emphasis will be on discussion of recent developments as well as areas where our understanding still has significant gaps.
Keywords: AEGIS, HIV, Viral Load, HIV Infections, Acquired Immunodeficiency Syndrome, Virus Replication, Antiviral Agents, HIV Core Protein p24, Variation (Genetics), virology, genetics, ICA11
