Thanks to antiretroviral therapy, HIV infection is no longer the life sentence it once was. But despite the effectiveness of drugs in managing and treating the virus, it can never be completely eliminated from the human body, persisting in certain deep cells of different human tissues where it goes unnoticed by the immune system.
Now, new research from University of Alberta immunologist Shokrollah Elahi reveals a possible answer to the mystery of why infected people cannot completely rid themselves of HIV.
Elahi and his team found that in HIV patients, killer T cells — a type of white blood cell responsible for identifying and killing cells infected with viruses — have very little or none of a protein called CD73.
Because CD73 is responsible for cell migration and movement in tissues, the lack of the protein compromises the ability of killer T cells to find and eliminate HIV-infected cells, Elahi explained.
“This mechanism explains a potential reason why HIV stays in human tissue forever,” he said, adding that the research also shows the complexity of HIV infection.
“This gives us the opportunity to come up with potential new treatments that would help killer T cells migrate better to access infected cells in different tissues. »
After identifying the role of CD73 – a three-year project – Elahi focused on understanding the potential causes of the drastic reduction. He found that this was partly due to the chronic inflammation that is common in people living with HIV.
“As a result of extensive studies, we found that chronic inflammation leads to increased levels of a type of RNA found in cells and in the blood called microRNA,” he explained. “These are very small types of RNA that can bind to messenger RNAs to stop them from making the CD73 protein. We found that this caused the deletion of the CD73 gene. »
The team’s finding also helps explain why people living with HIV have a lower risk of developing multiple sclerosis, Elahi noted.
“Our results suggest that reduced or eliminated CD73 may be beneficial in HIV-infected individuals to protect against MS. Therefore, targeting CD73 could be a potential new therapeutic marker for MS patients. »
Elahi said the next steps in her research include identifying ways to manipulate the CD73 gene to turn it on in patients living with HIV and turn it off in those with MS.
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Materials provided by University of Alberta. Original written by Tarwinder Rai. Note: Content may be edited for style and length.