The winners of the 2008 Nobel Prize in Physiology or Medicine have been announced, and the prize has been awarded for early discoveries that have subsequently led to vaccines or treatments of two widespread virus-caused diseases. Half of the prize was awarded to Harald zur Hausen "for his discovery of human papilloma viruses causing cervical cancer" and one-fourth each was awarded to Francoise Barre-Sinoussi and Luc Montagnier "for their discovery of human immunodeficiency virus." For more, check out the official press release or the more detailed description of the prize-winning discoveries from the Nobel Committee.
This is an interesting subject for a Nobel Prize, since a huge number of scientists have contributed to the basic and applied research on HIV and HPV, leading to several significant clinical successes. The committee could have taken this in a few different directions, but they decided in both cases to give the award to just the scientists who made the initial discoveries: the initial descriptions of HIV and the identification of HPV as the predominant cause of cervical cancer. Thanks to the discoveries of Barre-Sinoussi and Montagnier (and an enormous quantity of research by a wide range of scientists that followed them), patients infected with HIV can be treated with a wide array of antiretroviral drugs that can greatly extend their lifespan and improve their quality of life. In the developed world, at least, AIDS is no longer the rapid death sentence it once was in the 1980s. Likewise, thanks to Hausen and the work that followed on his footsteps, we now have two effective vaccines for HPV--which are effectively vaccines for cervical cancer.
it is now 2011 and luckily we are using gcmaf on many infections/cancers
Hi Nick, I've got a post up on this too. The HIV history and the role of Robert Gallo are interesting in how the committee chose to split the prize for HPV and HIV instead of giving a prize just for HIV. It will be interesting to see what the other science blogs add.
What do you think of the following?
HIV ERADICATION IN HUMANS....
Immunotherapy of HIV-infected patients with Gc protein-derived macrophage activating factor (GcMAF).Yamamoto N, Ushijima N, Koga Y.
Division of Molecular Immunology and Immunotherapy, Socrates Institute for Therapeutic Immunology, Philadelphia, Pennsylvania 19126-3305, USA. firstname.lastname@example.org
Serum Gc protein (known as vitamin D3-binding protein) is the precursor for the principal macrophage activating factor (MAF). The MAF precursor activity of serum Gc protein of HIV-infected patients was lost or reduced because Gc protein is deglycosylated by alpha-N-acetylgalactosaminidase (Nagalase) secreted from HIV-infected cells. Therefore, macrophages of HIV-infected patients having deglycosylated Gc protein cannot be activated, leading to immunosuppression. Since Nagalase is the intrinsic component of the envelope protein gp120, serum Nagalase activity is the sum of enzyme activities carried by both HIV virions and envelope proteins. These Nagalase carriers were already complexed with anti-HIV immunoglobulin G (IgG) but retained Nagalase activity that is required for infectivity. Stepwise treatment of purified Gc protein with immobilized beta-galactosidase and sialidase generated the most potent macrophage activating factor (termed GcMAF), which produces no side effects in humans. Macrophages activated by administration of 100 ng GcMAF develop a large amount of Fc-receptors as well as an enormous variation of receptors that recognize IgG-bound and unbound HIV virions. Since latently HIV-infected cells are unstable and constantly release HIV virions, the activated macrophages rapidly intercept the released HIV virions to prevent reinfection resulting in exhaustion of infected cells. After less than 18 weekly administrations of 100 ng GcMAF for nonanemic patients, they exhibited low serum Nagalase activities equivalent to healthy controls, indicating eradication of HIV-infection, which was also confirmed by no infectious center formation by provirus inducing agent-treated patient PBMCs. No recurrence occurred and their healthy CD + cell counts were maintained for 7 years.
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