Studying a substance produced by the human immunodeficiency virus (HIV-1) has revealed a powerful new therapeutic "anti-viral avenue".
Writing in Nature this week, University of Texas Southwestern Medical Center scientist Beth Levine and her colleagues were examining how a factor called "Nef" contributes to the virulence of HIV.
They found that it locks onto and inactivates a protein called beclin-1, which, under normal circumstances, activates the cellular equivalent of a waste disposal system.
Such a system, called autophagy, is potentially bad for viruses because it would lead to them and their products being chewed up inside cells, which is why HIV has evolved a way to stop it.
The Texas-based team discovered that the HIV-1 Nef locks onto just one part of the beclin-1 protein, so they produced a soluble, synthetic version of this small region. Administered to cells, it powerfully activated the autophagy process and inhibited the growth of HIV in culture.
Even better, it also worked against two other viruses the team tested, chikungunya and West Nile Virus, including in experimentally infected animals, and even against the bacterium Listeria monocytogenes, which invades cells, hence its susceptbility to this treatment.
This approach therefore represents and exciting new way to combat viral, and even some bacterial infections.
But more exciting still is that since certain neurodegenerative diseases, including Huntington's Disease, are in part caused by a build-up of pathological protein material inside cells, activating this waste-degrading autophagy pathway could help to treat these diseases too.
"I am cautiously optimistic that this approach really could work," Levine says.
It sounds a lot like computer viruses which are often programmed to disable the antivirus programs.
"The Texas-based team discovered that the HIV-1 Nef locks onto just one part of the beclin-1 protein, so they produced a soluble, synthetic version of this small region."
Actually, it's more clever than that; because the virus is switching down the rate of autophagy within the cell by deactivating an activating molecule. What the beclin-derivative peptide does is de-repress the autophagy rate, increasing the processing and virus dismantling. So it a positive effect on cell physiology, rather than a direct anti-viral effect. chris, Tue, 19th Feb 2013