This might include an altered cytokine milieu in individuals at different stages of disease e.g. raised plasma IL-10 and cortisol [23], [25], [54], [69], [70] (reviewed [71]), defects in cleavage of CD163 as a consequence of HIV-1 therapy, contribution from comorbid illness such as cardiovascular disease, or possibly alterations in gut lymphoid mass with resulting bacterial translocation [72], [73]. This evidence concerns the gene CD163 and cardiovascular disorder.