Herpesvirus may boost AIDS expression.Herpesvirus herpesvirus, any of the family (Herpesviridae) of common DNA-containing viruses, many of which are associated with human disease. See cytomegalovirus; Epstein-Barr virus; herpes simplex; herpes zoster. may boost AIDS expression A type of herpesvirus may accelerate the development of AIDS in people infected with human immunodeficiency virus human immunodeficiency virus n. HIV. Human immunodeficiency virus (HIV) A transmissible retrovirus that causes AIDS in humans. (HIV HIV (Human Immunodeficiency Virus), either of two closely related retroviruses that invade T-helper lymphocytes and are responsible for AIDS. There are two types of HIV: HIV-1 and HIV-2. HIV-1 is responsible for the vast majority of AIDS in the United States. ), new laboratory studies suggest. The finding may help explain why some HIV-positive people remain relatively healthy for long periods while others sicken and die within months. For years, scientists have been searching for a cofactor cofactor An atom, organic molecule, or molecular group that is necessary for the catalytic activity (see catalysis) of many enzymes. A cofactor may be tightly bound to the protein portion of an enzyme and thus be an integral part of its functional structure, or it may that increases an HIV-infected person's likelihood of getting full-blown AIDS (SN: 4/4/87, p.220). A team led by Paolo Lusso of the Bionetics Research Inc. in Rockville, Md., and Robert C. Gallo of the National Cancer Institute in Bethesda, Md., focused on herpesvirus-6 because it attacks the same T-cells that are depleted in AIDS patients and because most AIDS patients have active herpesvirus-6 infections. Herpesvirus-6 is a recently identified member of the herpes family (SN: 11/8/86, p.302). Lusso and Gallo studied cultured human T-lymphocytes infected with herpesvirus-6 and/or HIV. In the Jan. 26 NATURE, they report finding more dead T-cells in cultures infected with both viruses than in cultures infected with either agent alone. The data suggest the two viruses act synergistically syn·er·gis·tic adj. 1. Of or relating to synergy: a synergistic effect. 2. Producing or capable of producing synergy: synergistic drugs. 3. , attacking the immune system's T-cells in an accelerated fashion. By the sixth day of infection, the observed death of T-cells was up to three times greater than what would have been predicted by a simple additive effect additive effect n. An effect in which two substances or actions used in combination produce a total effect the same as the sum of the individual effects. . Lusso and Gallo's work suggests herpesvirus-6 starts a lethal cycle for T-cells by "turning on" the gene that triggers the HIV replicative cycle. The researchers hypothesize hy·poth·e·size v. hy·poth·e·sized, hy·poth·e·siz·ing, hy·poth·e·siz·es v.tr. To assert as a hypothesis. v.intr. To form a hypothesis. that HIV, in turn, can stimulate herpesvirus-6 to replicate. More work is needed to prove that the in vitro results extend to the human body, Gallo says. The National Cancer institute plans a trial comparing the progression of AIDS in HIV-infected people with and without herpesvirus-6 infection. But that may be difficult, LUSSO says, because most people have been infected by herpesvirus-6 in childhood. Researchers believe herpesvirus-6 is contracted via close contact, but in most cases it lies dormant and does not cause disease. If herpesvirus-6 is shown to be an HIV cofactor, scientists may be able to slow--but not prevent--the progression to full-blown AIDS by finding a drug that halts herpesvirus-6 replication, Lusso says. Acyclovir acyclovir /acy·clo·vir/ (a-si´klo-ver) a synthetic purine nucleoside with selective activity against herpes simplex virus; used as the base or the sodium salt in the treatment of genital and mucocutaneous herpesvirus infections. , a drug used to treat some herpes infections, does not seem effective against herpesvirus-6, he adds. Other researchers warn against too much optimism. HIV alone kills T-cells and causes full-blown AIDS in time, says Robert R. Redfield at the Walter Reed Army Research Institute in Washington, D.C. |
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