Now this is the problem of too much logic aka over thinking as a result of years of drilled schooling and online MBAs

Hmmm...quite some thinking there!

There is a link and its an aspect my research group has been following. However, HIV is a lethal virus so an injection of it to cure/control Leukemia will be the most ridiculous decision in science at this point in time. The work was published last year in New England Journal of Medicine, a journal with the highest 'impact factor' in medical sciences for the people who may be interested. As point of information do people know that there are group of people who cannot be infected with the viral strain that causes most of the primary infection (CCR5 virus). Unfortunately homozygotes are a small percentage of caucasian origin and in this population CCR5 viruses which seed most of the primary infections bounces off although rarely these group of people can be infected by the CXCR4 virus. However in Kenya we have a strain (D) which behaves exactly the opposite using CXCR4 early in infection and causing death rather faster.

Those interested in the scientific details can continue.............. it is also worthy noting that a follow up technology in phase 2 of trial creates a situation whereby we can isolate the non-infected CD4 T cells using various technologies from the patient, knock-down the CCR5 gene using zinc finger technology so that the protein is not expressed on cell surface, grow the cells in culture and back to the patient when we achieve approximately 1million cells per mm3. This way HIV is rather a chronic than a fatal disease.

Plagiarism is never tolerated in my profession so i present a case study and quote the author at the end.
'' A 40-year-old white man with newly diagnosed acute myeloid leukemia (FAB M4 subtype,with normal cytogenetic features) presented to our hospital. HIV-1 infection had been diagnosed more than 10 years earlier, and the patient had been treated with HAART (600 mg of efavirenz, 200 mg of emtricitabine, and 300 mg of tenofovir per day) for the previous 4 years, during which no illnesses associated with the acquired immunodeficiency syndrome (AIDS) were observed. At the time that acute myeloid leukemia was diagnosed, the patient’s CD4 T-cell count was 415 per cubic millimeter, and HIV-1 RNA was not detectable (stage A2 according to classification by the Centers for Disease Control and Prevention). Initial treatment of the acute myeloid leukemia consisted of two courses of induction chemotherapy and one course of consolidation chemotherapy.
During the first induction course, severe hepatic toxic effects developed and renal failure occurred. Consequently, HAART was discontinued, leading to a viral rebound (6.9×106 copies of HIV-1 RNA per milliliter). The therapy was resumed immediately, before a viral steady state was reached, and 3 months later, HIV-1 RNA was undetectable. Seven months after presentation, acute myeloid leukemia relapsed, and the patient underwent allogeneic stem-cell transplantation with CD34+ peripheral-blood stem cells from an HLA-identical donor who had been screened for homozygosity for the CCR5 delta32 allele. The patient provided informed consent for this procedure, and the protocol was approved by the institutional review board. The HLA genotypes of the patient and the donor were identical at the following loci: A*0201; B*0702,3501; Cw*0401,0702; DRB1*0101,1501; and DQB1*0501,0602. The patient underwent a conditioning regimen and received a graft containing 2.3×106 CD34+ cells per kilogram of body weight.5 Prophylaxis against graft-versus-host disease consisted of 0.5 mg of rabbit antithymocyte globulin per kilogram 3 days before transplantation, 2.5 mg per kilogram 2 days before, and 2.5 mg per kilogram 1 day before. The patient received two doses of 2.5 mg of cyclosporine per kilogram intravenously 1 day before the procedure and treatment with mycophenolate mofetil at a dose of 1 g three times per day was started 6 hours after transplantation. HAART was administered until the day before the procedure, and engraftment was achieved 13 days after the procedure. Except for the presence of grade I graft-versus-host disease of the skin, which was treated by adjusting the dosage of cyclosporine, there were no serious infections or toxic effects other than grade I during the first year of follow-up. Acute myeloid leukemia relapsed 332 days after transplantation, and chimerism transiently decreased to 15%.
The patient underwent reinduction therapy with cytarabine and gemtuzumab and on day 391 received a second transplant, consisting of 2.1×106 CD34+ cells per kilogram, from the same donor, after treatment with a single dose of whole-body irradiation (200cGy). The second procedure led to a complete remission of the acute myeloid leukemia, which was still in remission at month 20 of follow-up.

Hutter G et al., 2009.

this can be the best thing to happen if it were possible!

@BGL
YOur explanation was quite thorough but to deviate abit, what makes the HIV virus unreachable in the hideout by your treatment?

Very interersting discussion @ Selah you have brought up, and more dope given by BGL.

@ BGL, I have always wondered something: If a mosquito feeds on the blood of a sero-positive person, and proceeds to later bite a HIV-ve person, the negative person does NOT contract HIV, otherwise a good no. of us would be positive!

Ergo, it follows that something happens to the blood of the HIV+ person in the mosquito's digestive tract that makes it lose its ability to infect the negative person, its ability to attach to the CD4 cells of the negative subject. What is this? Is it a chemical - is it in the mosquito's salive, digestive enzymes? Or? Because am thinking (the layman that I am,remember) that if we can isolate this chemical them we could be staring at the cure or vaccine of HIV. Is there a flaw, a lacunae in this line of thinking? What say you?

Thanks BGL for the insight am wondering
rather than target the replication/polymerase enzyme
which is only expressed in active cells during replication why cant the activity/experssion of enzyme involved in intergration of the virus into the hosts DNA? be silenced and maybe address the issue of the virus remaining dormant and undetected.