HIV infection has been associated with endothelial dysfunction, liver disease, and factors predisposing for hypercoagulable state including the presence of antiphospholipid antibodies and lupus anticoagulant, and deficiencies of protein C and protein S which cause activation and consumption of coagulation factors might be the possible reason for the occurrence prolonged PT and APTT in HIV-infected individuals [15, 27, 38–40]. This evidence concerns the gene PROS1 and thrombophilia.