Scientists at the University of Pittsburgh and National Institutes of Health (NIH) in the US have found a clue to why people living with HIV have double the likelihood of developing heart disease.
The increased heart disease risk is driven by a subset of immune cells in people with HIV which continue to express a protein that triggers blood clotting and inflammation even after the HIV virus is under control by medication, they said.
The researchers found that Ixolaris, an experimental drug isolated from tick saliva and previously tested to treat blood clots in animals, successfully reduced the inflammation in monkeys infected with SIV, the primate form of HIV.
"By uncovering one of the cellular mechanisms driving the heart disease, we can look for medications - such as Ixolaris - that specifically target and disrupt that mechanism," said Pandrea, senior author of the study published in the journal Science Translational Medicine.
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Irini Sereti, of the NIH's National Institute of Allergy and Infectious Diseases (NIAID), tested blood samples from people without HIV, people with HIV whose infections were well-controlled by antiretroviral therapy and people with HIV who were not on the medications.
These findings were confirmed by Pandrea and her team in monkeys that progress to AIDS after infection with SIV.
The same cells isolated from a different species of monkey that usually does not develop heart disease when infected with SIV do not produce tissue factor, thus reinforcing the role of this damaging protein in triggering cardiovascular disease in the HIV/SIV settings.
When tested in a small group of monkeys during early SIV infection, the treatment significantly lowered the levels of inflammatory proteins linked to cardiovascular diseases.