Dr. Yamamoto treated 15 HIV patients with GcMAF, which eradicated the virus in all cases. These patients went into remission and remained disease free during 7 years of followup.
To sabotage the immune system and put macrophages to sleep, all viruses make Nagalase, the enzyme that blocks production of GcMAF. Without GcMAF (the protein that activates macrophages and jump-starts the entire immune response) HIV and other viruses can grow unimpeded. Nagalase puts the immune system to sleep. Dr. Nobuto Yamamoto demonstrated that GcMAF administration bypasses the Nagalase blockage and re-activates the macrophages, which then proceed to kill the HIV viruses and cure the infection.
Something to cheer about?
People infected with the Human Immunodeficiency Virus (HIV) have something to get excited about. They just don’t know it yet. In 2009 Dr. Nobuto Yamamoto published a landmark paper entitled: “Immunotherapy of HIV-Infected Patients With Gc Protein-Derived Macrophage Activating Factor (GcMAF)” in the Journal of Medical Virology in which he demonstrated that GcMAF cured 100% of nonanemic HIV infected patients. After seven years of followup, there were no recurrences. All patients maintained healthy CD+ counts.
Of course, this is just one study. And it had the disadvantage of containing some complex molecular biological chemo-speak. If the reader weren’t familiar with Yamamoto’s decades of background research (all of which was published in journals that HIV researchers and patients wouldn’t be likely to read), this study would fall on deaf ears. But Professor Yamamoto’s HIV study was no quirk. Based on a quarter-century of solid research that predicted success long before the actual human trials, it presented all the science one would need to understand exactly why these HIV patients were cured.
Though this study was published in 2009, there has been no informed discussion on this topic, no further GcMAF research as a therapy for HIV, and no media chatter. It’s as if this study never happened. Why is this?
How GcMAF destroys HIV
HIV—like all viruses—makes Nagalase, the enzyme that blocks GcMAF production. Without GcMAF, macrophages become indolent and the anti-viral immune response shuts down. This allows the HIV infection to spread. To remedy this situation, Dr. Yamamoto simply gave these patients GcMAF. This reactivated the sleeping macrophages, which then proceeded to phagocytize all of the viruses.
The precise molecular biological pathways and mechanisms involved with HIV, Nagalase, and GcMAF are identical to those for cancer cells, and need not be repeated here.
In his HIV study Yamamoto first showed that HIV patients had high Nagalase levels which correlated with their high HIV RNA levels (a way to measure the amount of HIV infection). Then, as he administered GcMAF (100 ng. once a week for 18 weeks), all patients’ Nagalase levels gradually went down to control levels, and, in tandem with the Nagalase, viral load went down to zero. Yamamoto wrote that these data “suggest that these patients were free of both HIV virions and HIV-infected cells.”
Professor Yamamoto followed these patients for seven years, and their viral load (HIV-1 RNA), CD4 counts (helper cells, a type of lymphocyte used to evaluate immunocompetence), p24 antigen (HIV-specific antigen), viral culture, and Nagalase levels remained normal. All patients continued to be free of disease. (Note: anemic HIV patients were excluded from this study. Anemia is common in HIV patients. The effect of GcMAF on anemic HIV patients is thus unknown.)