|
The study was led by researchers at the University of California,San Francisco (UCSF) and included Kristina Abel, PhD, an assistantprofessor in the department of microbiology & immunology atUNC, at the time of the study a faculty member at the University ofCalifornia, Davis (UCD). "The research involved a rhesusmacaque model of HIV, monkeys who were infected with simianimmunodeficiency virus, SIV" Abel said. "The course ofSIV infection in these monkeys is quite similar to that of HIV inhumans." Both HIV and SIV infections cause severe CD4 T cell loss in the gutduring early infection. As a result, the intestinal mucosalbarrier, which is like the body's second skin or front line ofdefense against pathogens, is compromised. The "leakygut" causes bacteria that are normally located in the gut (thenormal flora) to migrate out and activate the immune systemthroughout the body with disastrous health consequences. "Theimmune activation contributes to higher replication of the virus.And so the question is, why do some patients progress frominfection to AIDS faster than others?" Abel asks. This new study looked at the balance between certain immune cellpopulations that might influence disease outcome. The study showsthe presence of a subtype of CD4-positive immune cells called Th17(T helper 17) cells in the gut "could influence diseaseoutcome." A report of the research appeared in the May 30, 2012 online issueof Science Translational Medicine . Th17 cells are commonly found at mucosal surfaces and activateepithelial or outer layer barrier cells to secrete antimicrobialmolecules, thus blocking disease-causing bacteria from entering.Abel points out that they also stimulate the production of"tight junction" proteins that keep all the cells thatmake up the intestinal barrier in close contact, "so thatbacteria of the normal flora or their products cannot leakout." The researchers wondered if there are more Th17 cells in the gut,would infection with the AIDS virus still have that early massiveeffect on gut permeability? And if you could keep the intestinalbarrier intact during early infection with HIV, would it have animpact on the severity of disease progression, on having lesssevere disease in the long run? Results of the study suggest that the answers may be yes. Rhesusmacaques with higher numbers of Th17 cells in blood and intestinaltissue before they are infected with SIV subsequently have lowerSIV viral loads. "It appears they're more able to control theinfection," Abel said. The study also found that among animals given a drug that increasesregulatory T cells and thereby suppresses Th17 cell development,disease progression occurred more rapidly, and they had higherlevels of SIV virus six months after infection. "The main message of the study is that the frequencies ofcertain immune cell populations in the normal, still uninfectedindividual are important in subsequent disease progression andoutcome," Abel said. "The paper also suggests thattreatment aimed at increasing Th17 cells may improve the control ofHIV growth by promoting an environment in which T cells having moreanti-viral capabilities are produced." The study's principal investigator was Dennis J. Hartigan-O'Connor,MD, PhD, from UCSF (now at UCD). Other investigators are Koen K.A.Rompay, from UCD; Bitoo Kanwar, from UCSF; and study senior authorJoseph M. McCune, MD, PhD, from UCSF. Support for the research came from the National Institutes ofHealth, the Bill and Melinda Gates Foundation, the CaliforniaNational Primate Research Center, the National Center for ResearchResources, and the Harvey V. Berneking Living Trust. I am an expert from multitouchscreenmonitor.com, while we provides the quality product, such as Touchscreen Panel PC Manufacturer , Portable Interactive Whiteboard, Electronic Interactive Whiteboard,and more.
Related Articles -
Touchscreen Panel PC Manufacturer, Portable Interactive Whiteboard,
|
