terplay between RNAi and SRS remains physiologically conserved from plants and invertebrates to higher vertebrate animals," explains Dr. Jeang. "Our finding that Tat is an SRS also helps explain the long-standing biological observation that when HIV-1 is engineered to be lacking Tat but contains alternative transcriptional activators, it fails to spread productively in human cells." The researchers also suggest that their findings raise a challenge to proposed therapeutic strategies making use of RNAi. "Because HIV-1 evades all other RNAi by point mutations, we reason that its requirement for an SRS is solely to shield this last 'Achilles' heel that we think HIV-1 cannot alter for functional reasons. The sequence we describe may represent a viable target for RNAi that HIV-1 cannot elude by using the point mutation mechanism, " explains Dr. Jeang.

The researchers include Yamina Bennasser and Kuan-Teh Jeang of the National Institute of Allergy and Infectious Diseases; Shu-Yun Le of the National Cancer Institute; and Monsef Benkirane of the Institut de Genetique Humaine, CNRS.

Bennasser, Y., Le, S.-Y., Benkirane, M., and Jeang, K.-T. (2005). Evidence that HIV-1 Encodes an siRNA and a Suppressor of RNA Silencing. Immunity, 22, 607-619. http://www.immunity.com

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Source:Cell Press


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