Suppression of human immunodeficiency virus type 1 replication by human herpesvirus-6.
The pathogenesis of AIDS is complex and poorly understood despite intensive research efforts. One of the most puzzling aspects of the disease is the long interval between primary infection with human immunodeficiency virus (HIV) and the production of antiviral antibodies and onset of overt disease. Probably the most important factor that determines the length of these intervals is the rate at which HIV replicates within the infected host. Molecular studies have suggested that the replication of HIV can be enhanced by concurrent infection with other viruses, especially herpesviruses such as cytomegalovirus, herpes simplex virus, and Epstein-Barr virus. Presumably the presence of those viruses would serve to accelerate the progression of HIV-mediated disease. In contrast, studies reported here indicate that coinfection of cell populations with HIV and human herpesvirus-6 (HHV-6) leads to a near total suppression of HIV replication. The replication of HHV-6 is unaffected or minimally enhanced by the presence of HIV. These findings suggest that HHV-6 might serve to slow the progression of disease in some HIV-infected individuals.
Carrigan
D R
DR
Department of Pathology, Medical College of Wisconsin, Milwaukee 53226.
Knox
K K
KK
Tapper
M A
MA
D002478:Cells, Cultured; D015683:Gene Products, gag / Q000096:biosynthesis; D015488:HIV Antigens / Q000096:biosynthesis; D016655:HIV Core Protein p24; D015497:HIV-1 / Q000276:immunology / Q000502:physiology*; D015654:Herpesvirus 6, Human / Q000502:physiology*; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000382:microbiology*; D014758:Viral Core Proteins / Q000096:biosynthesis; D014779:Virus Replication
D015683:Gene Products, gag; D015488:HIV Antigens; D016655:HIV Core Protein p24; D014758:Viral Core Proteins