Further HIV/AIDS Enlightenment out of Italy

That HIV does not cause AIDS is again demonstrated, this time in a doctoral thesis, “Endogenous retroviruses as confounding factors in the pathogenesis of AIDS”, by Chiara Matteuzzi, mentored by Dr. Stefania Pacini and Dr. Marco Ruggiero. The work has just been accepted (with maximum marks) at the University of Florence, is in English, and is publicly available. The presentation was in Italian.
The literature review mentions Montagnier’s longstanding view that sound immune systems withstand HIV, unpublished work of Dr. Christl Meyer suggesting that HIV is an evolutionary adapted and partly active variable and heritable gene construct of our immune (MHC/HLA)-system, De Harven’s discussion of human endogenous retroviruses as confounding factors in AIDS pathogenesis, and Yamamoto’s demonstration that stimulation of the immune system can eradicate HIV.
The experimental part of the thesis built on Yamamoto’s work, as described in the Abstract:
“Results
We demonstrated that GcMAF stimulated human monocyte proliferation and survival and  that this response was associated with VDR gene polymorphisms. Since these results were obtained in  peripheral blood mononuclear cells, an interplay between lymphocytes expressing VDR and GcMAF- stimulated monocytes producing vitamin D has to be assumed. The effect was dose-dependent and maximal  stimulation was achieved using 100 pg/ml. GcMAF sustained cell viability for about 98 h whereas un- stimulated cells were no longer viable after 48 h, as if GcMAF had rescued monocytes from apoptosis.  Heparin inhibited the stimulatory effect of GcMAF by binding the N-acetylgalactosamine moiety of  GcMAF. GcMAF stimulated cAMP formation in a dose-dependent manner. GcMAF inihibited PGE 2 – and  MCF-7 (human breast cancer cell)-stimulated angiogenesis in chick embryo chorionallantoic membrane  (CAM) assay.   Discussion
GcAMF-induced increase of cAMP formation could account for its anti-angiogenetic effect  since it was demonstrated that elevated cAMP level inhibited angiogenesis in CAM assay (J Vasc Res  31:195-204, 1994). GcMAF-induced inhibition of angiogenesis could then be crucial in determining its  therapeutic effects in conditions where angiogenesis plays a key role in the progression of the disease, from  cancer (Exp Cell Res 316:1304-8, 2010) to HIV infection (Angiogenesis 5: 141–151, 2002). In addition, the  CAM assay proved to be a rapid, simple and inexpensive method to determine the relative potencies of  different GcMAF preparations and their stability; for example, we observed that storage at room temperature  for 15 days decreased GcMAF potency by about 50%. These data could prove useful for upcoming clinical  trials on GcMAF. In fact, GcMAF is being sold over the internet and it appears that several people are  already assuming GcMAF to treat diseases as diverse as cancer and HIV infection.”