Will killing the last HIV1 particle cure AIDS patients? Doesn't CMV activation and/or a graft-versus-host component of the disease, also have to be considered? .1. First of two parts

Before the discovery of HIV1 and HIV2, I proposed as the mechanism of HIV1-AIDS complex, a graft versus host reaction (GvH) induced by transfusion or seringe or sexual act blood transferred lymphocytes: this was based on the clinical, pathological and biological, and especially immunological similarities. I have treated ten HIV1-AIDS complex patients in the last phase with five virostatics, distributed in three week sequence combinations of 3 or 4, each differing from the preceeding and following ones. After follow-up between one and three and a half years, the results can be summarized as such: when the viral loads fall below the detectable level, the CD8(+) CD57(+) suppressor T-cell and CD8(+) CD57(-) cytotoxic T-cell numbers tend towards normal levels (similar or equal to 200/mL), bur the CD4 counts go up to a maximum of only 394, far from the normal level (800). Moreover, none of these subsets present a significant coefficient of correlation with the HIV1 load, which indicates that these immunologic markers and the viral one provide different information. I suggest the hypothesis according to which HIV1-AIDS complex comprises other components than HIV1 infection, such as a) the evoked GvH, which would occur early enough and might explain this CD4 incomplete restoration by virostatics, and b) cytomegalovirus (CMV) activation which occurs later. The second part of this editorial review will be published in a part II of the ''Dossier'' on AIDS. It will be devoted to the discussion of GVH and CMV infection systematic treatments.