Tick saliva may prevent heart disease in people living with HIV
People living with HIV are twice as likely to develop heart disease. A multinational team of scientists may have found out why… and discovered a cure.
HIV, or human immunodeficiency virus, damages the cells in your immune system. When the immune system becomes too damaged, doctors say the person has developed AIDS (acquired immunodeficiency syndrome), and eventually the immune system will become unable fight even everyday infections.
For those lucky enough to receive it, antiretroviral therapy (ART) will profoundly slow the progression of HIV, and delay the onset of AIDS. Dr. Irini Sereti, at the National Institutes of Health in the USA, says that patients with ART are “doing very well now and have much lower morbidity… than they did in the past.”
But as people with HIV are alive longer, doctors have seen a “shift to more non-infectious complications” says Sereti. She explains that such treated patients have a 2-fold increased risk for heart disease.
Sereti believes these complications are alarming because “the HIV population is aging” and estimates “that more than 50% of the people living with HIV will be above the age of 50 by 2020.” In general, heart disease is an affliction of the old.
Some studies suggest that abnormal behaviour from the immune system may be responsible for the cardiovascular problems. A major goal of Sereti’s study was to interrogate this potential connection.
The scientists studied the blood of healthy people, people infected with HIV who hadn’t received ART and patients who had.
They were specifically investigating a type of immune cell called monocytes, which Sereti says is “part of the first line of defense of the immune system.”
Sereti and her colleagues observed that there was a population of these monocytes that “were big producers of inflammatory mediators” and high levels of a protein called tissue factor. Under the right conditions, tissue factor can trigger blood clotting.
They found that infected patients had far higher levels of these special monocytes.
Furthermore, there was no difference in the number of these monocytes or their behaviour between patients who had been treated by ART and those who hadn’t.
They then investigated the same thing in pigtail macaques that had been infected with simian immunodeficiency virus (SIV), which is similar to HIV. When the macaques are infected with SIV, they are much more likely to develop heart disease compared to uninfected individuals, just like humans.
Sereti explains that they also investigated African green monkeys because these primates “can get infected with SIV...yet do not progress to AIDS, so they remain healthy despite the fact that they have a lot of virus.”
The scientists tested the monocytes in both primate types. They found that the monocytes from pigtail macaques “reproduced the observations [they] had from the human samples” but the African green monkeys did not.
These observations strongly support the hypothesis that it’s these special monocytes that are responsible for the high cardiovascular risk in people living with HIV.
Interestingly, Sereti and her colleagues found that the drug “Ixolaris”, derived from tick saliva, can block the function of these rogue monocytes in pigtail macaques and in samples from humans with HIV.
The infected macaques were not given the drug or studied for long enough to determine whether blocking the monocyte behaviour is sufficient to limit the amount of heart disease seen in an infected population.
Furthermore, Sereti cautions they only studied a small number primates and that all the scientists “can say now is that [Ixolaris] didn’t have any big side effects and was tolerated.”
However, should scientists conclusively prove the link between these rogue monocytes, inflammation and heart disease risk in patients with HIV, Ixolaris could be a promising treatment.