It was a surprising observation for a team of researchers studying sexually transmitted diseases among prostitutes in a Nairobi slum in the early 1990s: Despite being continuously exposed to HIV through unprotected intercourse with myriad partners, a small number of the women appeared to be resistant to the deadly virus.
For Keith Fowke, a University of Manitoba graduate student with the group who would later write his PhD thesis on the topic, it was the start of a journey that appears to be yielding a weapon in the fight to prevent AIDS. At root was the finding that those female sex workers in the Pumwani slum were apparently protected by inactive immune cells in the genital tract, preventing HIV infection.
Today, as head of the Department of Medical Microbiology and Infectious Diseases at the University of Manitoba and a visiting scientist at the University of Nairobi, much of Dr. Fowke's research has focused on the interaction between HIV and the immune system. A key conclusion involves the importance of "immune quiescence," the somewhat counterintuitive finding that "if you have immune cells in the genital tract that are resting and HIV comes into contact with them, it is not able to establish an infection in those cells."
Dr. Fowke is currently studying a relatively safe, cheap and available anti-inflammatory substance that can have a quietening effect on these immune cells and reduce the risk of HIV transmission: Aspirin.
A study among women in Nairobi has showed that a small amount of Aspirin reduced HIV target cells in the genital tract by 35 per cent. Dr. Fowke's team plans to do a similar study among high-risk sex workers there, and to further investigate the common drug's effects on HIV transmission in the wider population.
"This is another tool in the toolbox for HIV prevention," he says, noting that the approach also avoids the detrimental effects of HIV mutation. "We're targeting the immune cell, not the HIV."
Dr. Fowke's lab is also studying a "functional cure" for HIV, looking at how immune cells become overactive and don't function properly in people that have the virus. Their goal is to block a protein called LAG-3, which stops the body from fighting HIV.
Being at the leading edge of research that could change the way HIV is prevented or controlled "is rewarding and exciting," he says. "This could really make a difference in how we deal with this disease."
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