The HIV protease inhibitor, ritonavir, dysregulates human platelet function in vitro

Thrombosis Research
Shannon G LoeliusSherry L Spinelli

Abstract

There are 37 million people globally infected with the Human Immunodeficiency Virus (HIV). People living with HIV can achieve nearly normal lifespans due to the use of antiretroviral drugs (ARVs). However, people living with HIV experience chronic inflammation and increased risk for cardiovascular diseases (CVD) relative to uninfected people. While the cause for this risk is unclear, some ARVs have been associated with CVD, and it is speculated that some ARVs potentiate inflammation in infected individuals. Platelets are a critical link between inflammation and the development and progression of CVD, but the effects of ARVs on platelets are largely understudied. In this study, we examined the effects of ARVs on human platelet function in vitro. Our data show that the ARV ritonavir, a protease inhibitor, severely altered human platelet lipid mediator production (prostaglandin E2 and thromboxane) in both resting and activated platelets. Further characterization revealed that ritonavir altered measures of platelet hemostatic and thrombotic function that included significantly decreased platelet spreading, increased platelet aggregation, and trended toward increased clot strength. These data provide proof-of-principle that ARVs can...Continue Reading

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