December 3, 2008 (BRONX, NY) A new study led by researchers at Albert Einstein College of Medicine of Yeshiva University has clarified how two major variants of HIV differ in their ability to cause neurologic complications. The finding, published in Journal of Neuroscience, highlights a new target for drugs that could prevent HIV-associated dementia, an incurable and increasingly common complication in people with AIDS. Even with anti-retroviral drug therapies, up to one-half of people infected with HIV will develop mild to moderate neurological complications, according to some estimates.
Earlier this decade, scientists observed that people with AIDS in India developed dementia at a far lower rate than comparable populations in the U.S. and Western Europe. Most cases of AIDS in India are due to infection with a subtype or clade of HIV, known as clade C, while most cases in the U.S. and Western Europe are due to clade B.
Based on these observations, in 2004, a team of researchers led by Dr. Vinayaka R. Prasad, professor of microbiology and immunology at Einstein, began searching for genetic variations between the two clades that could explain the differing rates of HIV-related dementia. The team, in collaboration with Dr. Udaykumar Ranga of the Jawaharlal Nehru Centre for Advanced Scientific Research in Bangalore, India, focused their search on Tat, a protein that helps HIV replicate and leads the attack on the brain.
Dr. Prasad and colleagues compared the sequences of the Tat protein of the two clades and noted a key difference. Where the clade B Tat protein contained the amino acid cysteine at a specific position in the Tat protein, the clade C Tat had the amino acid serine. The next step, and the focus of the current study, was to compare the two viruses in a single host to determine whether this key change in the amino acid sequence makes a practical difference in HIV's neurotoxicity.
To find out, the researc
|Contact: Michael Heller|
Albert Einstein College of Medicine