By IANS, [RxPG] Washington, Nov 15 - Researchers have isolated a key protein that explains why antiviral drugs can fend off the HIV in the body, but not in the brain.
The new study traces how key steps taken by Tat, a protein that helps HIV operate, replicate and infect cells, enables HIV to attack the brain, bringing about severe inflammation.
Researchers identified the receptor that Tat uses to attack neurons, whose effects they reversed by blocking the receptor.
'Suddenly the brain environment turns from nurturing to toxic. Cells are on overdrive, spending a lot more energy to do the same things they used to do easily,' said Harris Gelbard, neurologist at Rochester University Medical Centre.
'The current medications give many patients a new lease on life. But the virus is still taking a toll on the brain, even when the virus appears to be much less active elsewhere in the body,' said Gelbard, the paper's co-author.
The discovery of a major molecular player in the process opens up new ways of exploring how to prevent or treat HIV's neurological effects, for which there is no currently approved treatment, said a Rochester release.
Much of the molecular action that underlies HIV's attack on the brain also occurs in other diseases, such as Parkinson's and Alzheimer's diseases, and the results spell progress for those conditions as well.
The powerful antiviral drugs that keep many HIV patients healthy for years don't completely eradicate the virus from the body, and in the brain, even the very low levels of that remain cause relentless damage.
Scientists have observed that a large percentage of HIV patients - perhaps up to half - show evidence of neurologic disease from the virus.
These findings were published online in the Nov 13 issue of PloS One.
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