HIV infection is associated with an immune activation and an inflammatory response - despite an active antiretroviral therapy - which may lead notably but not exclusively to cardiovascular diseases. It has been shown that the use of Protease Inhibitors (PI) instead of Non Nucleosidic Inhibitors (NNRTI) may increase the risk of myocardial infarction. Platelets may play a role in the occurrence of the inflammatory state: they contain big amounts of chemokines, growth factors, and adhesion proteins. Today, the contribution of platelets to the inflammatory state associated with HIV infection has been little studied. Thus, it has been shown that platelets in HIV patients are able to release interleukin (IL)-18. The group has shown with others that the platelet function could be altered during HIV infection. Inversely, it doesn't know how antiretroviral therapy interacts with platelets. The aim of the study is to evaluate, according to the antiretroviral therapy, the impact on the platelets activation markers.
Study Type
OBSERVATIONAL
Enrollment
133
Blood samples
CHU Saint-Etienne
Saint-Etienne, France
Plasmatic level of sCD40L
Comparison of plasmatic level of soluble Cluster Differentiation (sCD40L) between 2 groups : HIV patients treated by antiretroviral therapy and HIV patients untreated. sCD40L is measured by enzyme linked immunosorbent assay (ELISA) in ng/ml.
Time frame: day 1
sCD40L level
Comparison of plasmatic level of sCD40L between 2 groups : patients treated with 2 Nucleosidic analogs of Transcriptase Reverse Inhibitors (NRTIs ) and 1 Protease Inhibitors (PI) and patients treated with 2 NRTIs and 1 NNRTI. sCD40L is measured by ELISA in ng/ml.
Time frame: day 1
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