Researchers have made a remarkable new advance against the virus that causes AIDS.
![Scientists Announce Anti-HIV Agent Which Can Work in a Vaccine Scientists Announce Anti-HIV Agent Which Can Work in a Vaccine](https://images.medindia.net/health-images/1200_1000/anti-hiv-medications.jpg)
The research, which involved scientists from more than a dozen research institutions, was published February 18 online ahead of print by the prestigious journal Nature.
The study shows that the new drug candidate blocks every strain of HIV-1, HIV-2 and SIV (simian immunodeficiency virus) that has been isolated from humans or rhesus macaques, including the hardest-to-stop variants. It also protects against much-higher doses of virus than occur in most human transmission and does so for at least eight months after injection.
"Our compound is the broadest and most potent entry inhibitor described so far," said Michael Farzan, a TSRI professor who led the effort. "Unlike antibodies, which fail to neutralize a large fraction of HIV-1 strains, our protein has been effective against all strains tested, raising the possibility it could offer an effective HIV vaccine alternative."
Blocking a Second Site
When HIV infects a cell, it targets the CD4 lymphocyte, an integral part of the body's immune system. HIV fuses with the cell and inserts its own genetic material-in this case, single-stranded RNA-and transforms the host cell into a HIV manufacturing site.
The new study builds on previous discoveries by the Farzan laboratory, which show that a co-receptor called CCR5 contains unusual modifications in its critical HIV-binding region, and that proteins based on this region can be used to prevent infection.
With this knowledge, Farzan and his team developed the new drug candidate so that it binds to two sites on the surface of the virus simultaneously, preventing entry of HIV into the host cell.
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The team also leveraged preexisting technology in designing a delivery vehicle-an engineered adeno-associated virus, a small, relatively innocuous virus that causes no disease. Once injected into muscle tissue, like HIV itself, the vehicle turns those cells into "factories" that could produce enough of the new protective protein to last for years, perhaps decades, Farzan said.
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"This is the culmination of more than a decade's worth of work on the biochemistry of how HIV enters cells," Farzan said. "When we did our original work on CCR5, people thought it was interesting, but no one saw the therapeutic potential. That potential is starting to be realized."
In addition to Farzan, Gardner and Kattenhorn, authors of the study, "AAV-expressed eCD4-Ig provides durable protection from multiple SHIV challenges," include Hema R. Kondur, Tatyana Dorfman, Charles C. Bailey, Christoph H. Fellinger, Vinita R. Josh, Brian D. Quinlan, Pascal Poignard and Dennis R. Burton of TSRI; Jessica J. Chiang, Michael D. Alpert, Annie Y. Yao and Ronald C. Desrosiers of Harvard Medical School; Kevin G. Haworth and Paula M. Cannon of the University of Southern California; Julie M. Decker and Beatrice H. Hahn of the University of Pennsylvania; Sebastian P. Fuchs and Jose M. Martinez-Navio of the University of Miami Miller School of Medicine; Hugo Mouquet and Michel C. Nussenzweig of The Rockefeller University; Jason Gorman, Baoshan Zhang and Peter D. Kwong of the National Institutes of Health; Michael Piatak Jr. and Jeffrey D. Lifson of the Frederick National Laboratory for Cancer Research; Guangping Gao of the University of Massachusetts Medical School; David T. Evans of the University of Wisconsin; and Michael S. Seaman of Beth Israel Deaconess Medical Center.
Source-Newswise