The study, published online in Science Translational Medicine, was conducted by researchers at the University of California, San Francisco (UCSF).
Kristina Abel, Ph.D., an assistant professor in the department of microbiology & immunology at UNC, who was a faculty member of the University of California, Davis (UCD), at the time of the study explained:
"The research involved a rhesus macaque model of HIV, monkeys who were infected with simian immunodeficiency virus, SIV. The course of SIV infection in these monkeys is quite similar to that of HIV in humans."
During early infection, both HIV and SIV infections cause severe CD4 T cell loss in the gut. This loss of cells impairs the intestinal mucosal barrier and causes the normal flora (bacteria) in the gut to migrate out and trigger the immune system throughout the body.
Abel said: "The immune activation contributes to higher replication of the virus. And so the question is, why do some patients progress from infection to AIDS faster than others?"
In order to find out the researchers examined the balance between certain immune cell populations and found that the presence of Th17 (a subtype of CD4-positive immune cells) cells in the gut "could influence disease outcome."
Th17 cells are usually found at mucosal surfaces and trigger epithelial or outer layer barrier cells to secrete antimicrobial molecules, therefore preventing disease-causing bacteria from penetrating.
In addition, the cells stimulate the generation of "tight junction" proteins. These proteins keep all the cells that make up the intestinal barrier in close contact, "so that bacteria of the normal flora or their products cannot leak out."
The researchers set out to determine whether infection with the AIDS virus would still significantly effect gut permeability if there was increase of Th17 cells in the gut. In addition, they also wondered if the intestinal barrier was kept intact during early infection with HIV, would it influence the severity of disease progression, on having less severe disease in the long run?
The team found that rhesus macaques with elevated amounts of Th17 cells in blood and intestinal tissue prior to SIV infection subsequently had lower SIV viral loads. Abel explained, "it appears they're more able to control the infection."
Furthermore, they found that disease progression occurred more rapidly among monkeys given a drug that increases regulatory T cells and prevents Th17 cell development. These animals also had elevated levels of SIV virus six months after becoming infected.
"The main message of the study is that the frequencies of certain immune cell populations in the normal, still uninfected individual are important in subsequent disease progression and outcome.
The paper also suggests that treatment aimed at increasing Th17 cells may improve the control of HIV growth by promoting an environment in which T cells having more anti-viral capabilities are produced."