Researchers led by Dr. Changyi Chen at Baylor College of Medicine discovered that HAART contributes to pulmonary hypertension in HIV-infected patients.
An estimated 33 million people were living with human immunodeficiency virus (HIV infection) in 2007. Without treatment, approximately 9 out of 10 HIV-infected people will progress to acquired immune deficiency syndrome (AIDS) with 5-10 years.
HAART is a combination therapy for HIV that consists of at least three antiretroviral drugs that suppress viral replication and restore CD4+ T cell numbers in HIV-infected patients. HAART dramatically improves the prognosis of HIV-infected patients; however, HAART drugs may increase the risk of cardiovascular disease.
Wang et al hypothesized that HAART drugs contribute to the risk for cardiovascular disease by impairing blood vessel-lining endothelial cell function. Their studies demonstrated that treatment of porcine pulmonary arteries with HAART drugs individually and in combination resulted in functional deficiencies in endothelial cells lining the blood vessels of the lungs. Therefore, HAART drugs may play a role in the high incidence of pulmonary artery hypertension in HIV-infected patients.
The research by Dr. Chen's group "showed that several HAART drugs including ritonavir, indinavir, lamivudine, abacavir and AZT can cause endothelial dysfunction through decreasing eNOS expression and increasing oxidative stress in porcine pulmonary arteries and [human pulmonary artery endothelial cells]. Consequently, reducing oxidative stress by selected antioxidants may be able to prevent HAART drugs-associated pulmonary artery hypertension."
- Wang, X, Chai H, Lin PH, Yao Q, Chen C. Roles and mechanisms of HIV protease inhibitor Ritonavir and other anti-HIV drugs in endothelial dysfunction of porcine pulmonary arteries and human pulmonary artery endothelial cells. Am J Pathol, 2009, 174: 771-781
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