AIDSWEEKLY Plus; October 28, 2002
Michael Greer, Senior Medical Writer

"The Vif (virion infectivity factor) proteins are encoded by primate immunodeficiency viruses, most notably human immunodeficiency virus-1 (HIV-1)," explained Ann M. Sheehy and colleagues at the Children's Hospital of Philadelphia and King's College in London.

HIV Vif interferes with a human gene whose activity disrupts viral replication, Sheehy and coauthors found.

Human T lymphocytes are capable of adopting a phenotype which prevents exported virions from infecting other cells, they said. However, exposure to HIV and other viral versions of Vif prevents T cells from expressing this phenotype.

The researchers idenitified a cellular gene, CEM15, which seems to play a key role in antiviral defense. CEM15 expression by cells that do not usually express this protein acts as a trigger for antiviral phenotype expression, even after transient CEM15 upregulation, according to the report.

However, CEM15 activity is inhibited by HIV Vif (Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. Nature 2002 Aug 8;418(6898):646-50.

"Because the Vif:CEM15 regulatory circuit is critical for HIV-1 replication, perturbing the circuit may be a promising target for future HIV/AIDS therapies," Sheehy and colleagues concluded.

The corresponding author for this report is Michael H. Malim, Department of Infectious Diseases, Guy's, King's and St Thomas' School of Medicine, King's College London, London SE1 9RT, UK. E-mail: michael.malim@kcl.ac.uk.

Key points reported in this study include:

• Humans carry a gene that could ward off HIV infection although its effects are countered by a key HIV protein

• The CEM15 gene triggers a T-cell phenotype that renders harmless HIV virions produced by infected cells

• However, the HIV Vif protein disrupts CEM15 function

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

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