Since the virus itself may induce hypovitaminosis D through many mechanisms (increased levels of TNF-α, inhibition of renal hydroxylation and induction of 25-hydroxyvitamin D consumption by the macrophages and lymphocytes) [7,32,33], the abnormal biochemical features found in our HIV-infected subjects compared with the controls, in particular the lower vitamin D levels, may support the hypothesis that HIV per se might play a role in the pathogenesis of bone loss. This evidence concerns the gene TNF and rickets.