Elissa Pratt-Lowe

Molecular interactions between human immunodeficiency virus type 1 and human cytomegalovirus.

In humans infected with human immunodeficiency virus type 1 (HIV-1) and in rhesus macaques infected with simian immunodeficiency virus (SIV), the cause of death appears not to be a direct result of infection by either lentivirus; instead, fatality is due to any of a variety of secondary infectious agents brought about by the ablation of the hosts immune system. Persistent infections by these heterologous viral, bacterial, or fungal pathogens are a characteristic of individuals suffering from acquired immune deficiency (AIDS).* One such viral pathogen, cytomegalovirus (CMV), is a member of the herpesvirus family of viruses and is a frequent pathogen in HIV-infected human^.^ A large percentage of dually infected individuals suffer life-threatening complications as a direct result of CMV pathogenesi~.~.~ A critical point that requires further investigation is whether infections by heterologous pathogens are merely an opportunistic response to deterioration of the hosts immune system, or whether these agents might be important cofactors in the onset of AIDS. The issue of cofactors is vitally important because therapeutic agents directed against these secondary agents will not only alleviate suffering of the individuals, but also might delay onset of frank AIDS. A potential role for heterologous cofactors is not unique to humans infected with HIV. Rhesus macaques experimentally infected with SIV suffer an AIDS-like disease,6 and rhesus CMV in terminally ill SIV-infected macaques appears to contribute to pathogenesis (A. Lackner 8c P. Vogel, unpublished results). We have been examining molecular interactions of CMV with HIV-1 and SIV using in vitro transient expression assays to