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? I. First of two parts
Abstract
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 (approximately 200/mL), but 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...Continue Reading
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