January 1, 1970 (Vol. , No. )

Kevin Ahern

In a finding with analogies to Homeland Security at the cellular level, researchers at the University of Alberta have identified a host gene whose activity blocks viral “terrorists” like HIV from functioning properly inside the very cells they infect and may provide a foundation for a future anti-viral strategy. Writing in the Public Library of Science Pathogens, Dr. Stephen Barr and colleagues identify the gene as TRIM22 and it appears to augment the interferon response of the human innate immune system. Interferons have long been known to wreak havoc with early and late phases of HIV replication (1), but the mechanisms of their action are not fully understood. Barr and colleagues discovered TRIM22’s role by searching for genes most induced when cells are treated with interferon. The family of TRIM proteins, of which TRIM22 is a member, function cellularly by affecting trafficking of proteins inside of cells. TRIM22’s ability to stymie HIV is probably at least partly due to the gene’s disruption of the HIV gag gene’s normal migration to the plasma membrane during the infectious cycle. In cells expressing TRIM22, gag proteins are dispersed instead of accumulating at their proper cellular location. Since gag is necessary for making the viral protein shell, its absence from the site of HIV assembly prevents formation of proper viral particles. Scientists are investigating why TRIM22 is not protecting HIV patients in the same way it does in interferon-treated tissue culture cells and hope that by either activating or enhancing TRIM22 functions in patients, they may develop new tools for fighting HIV.


1. Agy MB, Acker RL, Sherbert CH, Katze MG (1995) Interferon treatment inhibits virus replication in HIV-1 and SIV-infected CD4+ T-cell lines by distinct mechanisms: evidence for decreased stability and aberrant processing of HIV-1 proteins. Virology 214: 379–386.


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