By Sue Mueller & David Liu from? foodconsumer.org
Nov 15, 2008 – 2:13:45 PM
Why HIV vaccine fails
Dr. A. White of Duke University medical Center A published an article in the Sep 2, 2008 issue of Medical Hypotheses suggests that Merck’s V520 is destined to fail to prevent HIV infection in a recent trial.
Trial sponsored by Merck and the US government showed that the vaccine did not prevent infection in those not previously infected with HIV, nor did the vaccine reduce the virus load in those who did receive the vaccine.
As a matter of fact, those who received the vaccine were actually much more likely to become HIV positive, particularly among men who were also uncircumcised and had pre-existing immunity to adenovirus type 5, which was used as a carrier for the vaccine.
Dr. White said vaccines prior to V520 were intended to evoke strong anti-body-mediated immune response to prevent HIV virus from entering host cells. ? V520 however was meant to evoke a cell-mediated immune response to HIV, allowing HIV entering cells and then trying to conquer it in the infected cells.?
According to Dr. White, these two types immune response, antibody-mediated for extracellular infections and cell-mediated primarily for intracellular infections work in a teeter-totter manner. ? When one is suppressed the other is activated.?
V520 was well intentioned, White said. ? HIV quickly infects host cells right after entering the body, and a strong cell-mediated response is required to defeat the HIV virus.?
The problem, it seems to dr. White, is that the antibody-mediated immune response triggered by V520 suppressed the ability of the body to have the cell-mediated immune response that is needed to protect against HIV creating a window of opportunity for HIV infection. ? This is particularly the case for those who had exposed themselves to the adenovirus vector.
Dr. White acknowledged that the immune system uses antibodies to indentify extracellular pathogens, also said that it uses transfer factors to label infected host cells.
White suggested that “HIV-specific transfer factors could prove extremely useful, far more useful than vaccines, in preventing and treating HIV infections.” as hundred of studies indicated that pathogen -specific transfer factors can be used to stimulate the cell-mediated immune response against viruses. (by David Liu)
Bone marrow transplant cures man of AIDS??
Doctors in Berlin said a man was cured of AIDS after he received bone marrow transplant from a donor naturally resistant to HIV virus. ?? The man had been negative for HIV for nearly two years ever since the treatment.??
But the experts quickly warned that the treatment is not feasible for most AIDS patients or HIV carriers because for one thing donors with the genetic mutation that may be responsible for the miraculous cure are rare. ??? Only one in every 1,000 Europeans and Americans may carry the desirable mutation.
Other obstacles to successfully receiving the procedure are high risk of dying from the procedures itself. ?? Studies showed 20 to 30 percent of patients die from bone marrow transplant because the sick bone marrow needs to be killed by high doses of radiation and or medications.
Even if some people can find a HIV-resistant donor and be able to survive the procedure, bone marrow transplant is too costly for millions of HIV carriers and AIDS patients who live in Africa where the disease is most commonly seen.
The 42-year-old man suffered both leukemia and HIV. ?? Ever since he received the transplant at Berlin’s Charite clinic two years ago, he had been free of HIV virus as tests on the man’s bone marrow, blood and other organ tissues had been all clear.??
Scientists believe the mutated gene of concern, called Delta 32, prevents HIV from attaching itself to cells by blocking a receptor called CCR5.???
But doctors are not so sure if the man was cured because of the genetic mutation in the donated bone marrow. ?? But theoretically, knocking out the receptor by a gene therapy may be a future treatment for AIDS, Professor Andrew Sewell, University of Cardiff, was cited by BBC as saying.
This German case is an exceptional, said a health observer. Previous reports showed that bone marrow transplantation could be more likely to spread HIV than cure AIDS. (by Sue Mueller)
Vitamin C inhibits replication of HIV
S. Harakeh and R. J. Jariwalla at Linus Pauling Institute of Science and Medicine in Palo Alto, CA has done quite some research on the inhibitory effect of vitamin C on HIV replication and found that this vitamin along with other reducing agents may be used as a treatment to reduce the virus titer.
In a report published in the Dec 1991 issue of American Journal of Clinical Nutrition, Harakeh and Jariwalla said they tested calcium ascorbate and two thiol-based reducing agents (glutathione and N-acetyl-L-cysteine (NAC)) for their effect against the human immunodeficiency virus HIV-1 replication in chronically infected T lymphocytes.
They found that calcium ascorbate has the same magnitude of effect at reducing extracellular HIV reverse transcriptase as ascorbic acid or vitamin C does. But chronic exposure to ascorbate was necessary for HIV suppression. ? NAC, but not glutathione caused less than twofold inhibition of HIV reverse transcriptase and rendered a synergistic effect (about 8-fold inhibition) when tested together with vitamin C.
Later in 1994, the researchers published another study in the June 1994 issue of Chem Biol Interact saying that “the activity of an HIV LTR-directed reporter protein made in ascorbate-treated cells was reduced to approximately 11% relative to that of untreated control,” indicating that vitamin C “exerts a posttranslational inhibitory effect on HIV by causing impairment of enzymatic activity.”
In 1995, Harakeh and Jariwalla reported in the Sep-Oct issue of Nutrition that “exposure to 300 micrograms/ml ascorbate resulted in approximately 5- to 10-fold lowering of the extra-cellular RT (reverse transcriptase) titer. In contrast, no significant suppression in extracellular RT levels was seen with concentrations of AZT (an antiviral drug) in the range of 1-5 micrograms/ml.” (By David Liu)