AIDSWEEKLY Plus; Monday, September 8, 2003
Staff Medical Writers

"The HIV-1 accessory protein Vif (virion infectivity factor) is required for the production of infectious virions by CD4+ lymphocytes," scientists in California explained. "Vif facilitates particle infectivity by blocking the inhibitory activity of APOBEC3G (CEM15), a virion-encapsidated cellular protein that deaminates minus-strand reverse transcript cytosines to uracils."

In a recent study, R. Miriani and colleagues at the Salk Institute for Biological Studies found that "HIV-1 Vif forms a complex with human APOBEC3G that prevents its virion encapsidation."

"HIV-1 Vif did not efficiently form a complex with mouse APOBEC3G," they wrote. "Vif dramatically reduced the amount of human APOBEC3G encapsidated in HIV-1 virions but did not prevent encapsidation of mouse or AGM APOBEC3G."

"As a result, these enzymes are potent inhibitors of wild-type HIV-1 replication," according to the report. "The species-specificity of this interaction may play a role in restricting HIV-1 infection to humans."

"Together these findings suggest that therapeutic intervention that either induced APOBEC3G or blocked its interaction with Vif could be clinically beneficial," the researchers concluded.

Mariani and coauthors published their study in Cell (Species-specific exclusion of APOBEC3G from HIV-1 virions by Vif. Cell. 2003 Jul 11;114(1):21-31.

For additional information, contact N.R. Landau, Salk Institute for Biological Studies, Infectious Diseases Laboratory, 10010 N. Torrey Pines Rd., La Jolla, CA 92037, USA.

The publisher's contact information for the journal Cell is: Cell Press, 1100 Massachusetts Avenue, Cambridge, MA 02138, USA.

The information in this article comes under the major subject areas of AIDS & HIV, Pharmaceutical & Drug Development and Proteomics.

This article was prepared by AIDS Weekly editors from staff and other reports.

Reference

Mariani R, Chen D, Schrofelbauer B, et al., "Species-specific exclusion of APOBEC3G from HIV-1 virions by Vif", Cell. 2003 Jul 11;114(1):21-31

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