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Gladstone investigators identify a new protective action for the powerful anti-HIV factor, APOBEC3G

sequestering them in the cytoplasm away from the nuclear machinery required for copying the RNA back into DNA and inserting the retro-element at a new chromosomal site.

Understanding A3G's role in activated CD4 T cells could lead to a new strategy against HIV.

"If we can find a way to partially block A3G assembly into the large complexes during CD4 T cell activation, we could both preserve the potent anti-HIV effect of the small form of A3G and the protective function of the large A3G complex against select mobile genetic elements," Greene said. Gladstone scientists are now exploring various ways to achieve this desired balance.


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Source:University of California - San Francisco


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