Divisions of Haematology, Department of Pathology, Stellenbosch University, Tygerberg, South Africa; Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville, South Africa
Nkambule, B.B., Divisions of Haematology, Department of Pathology, Stellenbosch University, Tygerberg, South Africa; Davison, G.M., Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville, South Africa; Ipp, H., Divisions of Haematology, Department of Pathology, Stellenbosch University, Tygerberg, South Africa
Introduction Human immunodeficiency virus (HIV) induces inflammation and platelet activation. People living with HIV are at increased risk of thrombotic events. Activated platelets link inflammation with thrombosis. However platelet function in HIV remains unclear. P-selectin (CD62P), a marker of platelet activation, and platelet glycoprotein GPIV (CD36) a marker of platelet aggregation, can be measured using flow cytometry. We raise a hypothesis that HIV alters the signalling pathways involved in normal platelet function. We evaluated platelet function in HIV using a whole blood platelet flow cytometry based assay. Materials and methods Fifty-eight antiretroviral therapy naïve HIV infected and 38 HIV negative individuals were recruited in a clinic in Cape Town. Platelet surface CD36 and CD62P were measured using flow cytometry. These were then correlated with CD4 count, viral load and %CD38 on CD8 + T-cells. Platelet function was evaluated using adenosine diphosphate, arachidonic acid and collagen at varying concentrations. Results The HIV group showed increased levels of %CD62P (median 5.51[3.03- 10.11] vs. Control group 2.14[0.19 - 3.59], p < 0.0001. This correlated with Viral load (r = 0.336, P = 0.008). The HIV group also showed increased levels of platelet %CD36 21.93[11.03-44.92] vs. Control 16.15[2.24-25.37], p = 0.0087) which correlated with viral load (r = 0.398, p = 0.024). The HIV group showed a hyper response to AA and collagen at various concentrations. Notably, the HIV group only showed a hyper response to ADP at a maximal concentration of 20 μM (median CD62P MFI, 1.91[1.64-4.95] vs. Control 1.75[1.45-2.44] p = 0.0279. Conclusion The measurement of platelet function using flow cytometry is a rapid technique for the evaluation of platelet signalling pathways that may be modified in HIV infected individuals. © 2015 Elsevier Ltd.
adenosine diphosphate; antiretrovirus agent; arachidonic acid; CD36 antigen; CD8 antigen; collagen; PADGEM protein; adult; antiviral therapy; Article; CD4 lymphocyte count; controlled study; disease course; female; flow cytometer; flow cytometry; human; Human immunodeficiency virus infected patient; Human immunodeficiency virus infection; major clinical study; male; priority journal; signal transduction; thrombocyte count; thrombocyte function; thrombocyte membrane; virus load