"What we call AIDS is actually a combination of the direct effects of HIV replication and the indirect effects brought about by the immune system dysregulation," he said. "In contrast, the absence of the indirect effects in the SIV infected mangabeys can at least be partially attributed to a reduced activation of the immune system, and an ability to maintain continued renewal of T cells."
These findings influence the way in which one might think about treating an AIDS patient or developing a therapy for AIDS, Sodora said.
"It has relevance with regard to how we think about people getting sick with AIDS," he said. "One potential treatment might be an approach to deactivate the immune system, in a very strategic and careful way."
HIV and AIDS began to be identified in the mid-1980s. The virus had been transmitted to humans from primates among which SIV is prevalent. The two types of HIV that exist today originated from two variations of SIV present in chimpanzees (HIV-1) and mangabeys (HIV-2). In both species of primates, the host becomes infected with SIV and replicates the virus in its own T cells, but does not become ill.
Dr. Richard Koup, former chief of infectious diseases at UT Southwestern who is now at the National Institutes of Health Vaccine Research Center, and researchers Guido Silvestri and Mark Feinberg of Atlanta's Emory University School of Medicine also contributed to the NIH-funded study.
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Contact: Rachel Horton
rachel.horton@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
17-Mar-2003