Further experiments demonstrated that the GR did not play arole, and that Vpr and PPARγ interacted directly in living cells.The authors of this study hypothesize that in vivo circulating Vpr, or Vpr produced as aresult of direct infection of adipocytes, could suppress differentiation ofpreadipocytes in a PPARγ dependent manner with obviousconsequences for the development of lipodystrophy and insulin resistance [80]. Here, PPARG is linked to infection.