Molecular Mimicry Enhances Early Viral Infection

HTLV-1 is the viral cause of adult T-cell lymphoma, as well as at least two forms of neurologic disease. Investigators from Ohio State University (Columbus, USA; www.osu.edu) studying the molecular mechanism by which the virus successfully invades cells normally capable of resisting infection found that the HTLV-1 p12 protein caused T-lymphocytes to change from a normal resting state to an active state, thereby speeding up cell division which, in turn, allowed the virus to replicate. These findings were published in the May 2, 2003, issue of the Journal of Biological Chemistry.

Understanding of the mechanism came when it was found that a portion or motif of p12 was identical to a motif in a well-known cell protein called Nuclear Factor of Activated T-cells, or NFAT. This section of NFAT controls its binding to calcineurin, an enzyme that regulates calcium signals in T-cells.

"NFAT is a transcription factor that plays a critical role in all cells by binding to the enzyme calcineurin,” explained senior author Dr. Michael Lairmore, professor and chair of veterinary biosciences at Ohio State. "Once bound, it removes a phosphate group from the enzyme, allowing it to travel from the cell's cytoplasm into the nucleus. Once there, the cell becomes activated and begins the process of replication.”

The virus takes advantage of this burst of cell division to subvert the replicatory machinery and manufacture new virus particles.



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