title: Platelet leukocyte aggregates and markers of platelet aggregation, immune activation and disease progression in HIV infected treatment naive asymptomatic individuals.
abstract: Platelet aggregates play a crucial role in the immune defence mechanism against viruses. Increased levels of lipopolysaccharide have been reported in human immunodeficiency virus (HIV) infected individuals. Platelets are capable of interacting with bacterial LPS and subsequently forming platelet leukocyte aggregates (PLAs). This study aimed at determining the levels of circulating PLAs in treatment naïve HIV infected individuals and correlating them, with markers of immune activation, disease progression and platelet aggregation. Thirty-two HIV negative and 35 HIV positive individuals were recruited from a clinic in the Western Cape. Platelet monocyte and platelet neutrophil aggregates were measured using flow cytometry at baseline and were correlated with markers of platelet activation (CD62P); aggregation (CD36); monocyte and neutrophil activation (CD69); monocyte tissue factor expression (CD142); immune activation (CD38 on T+ cells); D-dimers (a marker of active coagulation); CD4 count and viral load. Platelet monocyte aggregates were also measured post stimulation with lipopolysaccharide. PMA levels were higher in HIV 25.26 (16.16-32.28) versus control 14.12 (8.36-18.83), p = 0.0001. PMAs correlated with %CD38/8 expression (r = 0.54624, p = 0.0155); CD4 count (r = -0.6964, p = 0.0039) viral load (r = 0.633, p < 0.009) and monocyte %CD69 expression (r = 0.757, p = 0.030). In addition the %PMAs correlated with platelet %CD36 (r = 0.606, p = 0.017). The HIV group showed increased levels of %CD62P 5.44 (2.72-11.87) versus control 1.15 (0.19-3.59), p < 0.0001; %CD36 22.53 (10.59-55.15) versus 11.01 (3.69-26.98), p = 0.0312 and tissue factor (CD142) MFI 4.84 (4.01-8.17) versus 1.74 (1.07-9.3), p = 0.0240. We describe increased levels of circulating PMAs which directly correlates with markers of immune activation, disease progression and platelet aggregation in HIV treatment naïve individuals.
authors.affiliation: Divisions of Haematology, Department of Pathology, Stellenbosch University and NHLS, Tygerberg, South Africa. nkambuleb@gmail.com.
authors.forename: Bongani B
authors.initials: BB
authors.lastname: Nkambule
authors.affiliation: Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville, South Africa.
authors.forename: Glenda
authors.initials: G
authors.lastname: Davison
authors.affiliation: Divisions of Haematology, Department of Pathology, Stellenbosch University and NHLS, Tygerberg, South Africa. hipp@sun.ac.za.
authors.forename: Hayley
authors.initials: H
authors.lastname: Ipp
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D015658:HIV Infections / Q000097:blood / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007962:Leukocytes / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D008297:Male; D010974:Platelet Aggregation / Q000276:immunology*
chemical_list: D015415:Biomarkers
keywords: HIV; Immune activation; Platelet activation; Platelet function; Platelet leukocyte aggregates