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Indiana University discovery may provide new approach to HIV treatment

AIDSWEEKLY Plus; Monday, February 2, 2009
Staff Medical Writers


NewsRx -- Researchers at the Indiana University School of Medicine have identified a potential new target in the war on HIV/AIDS. The information was published in the Jan. 16 issue of the journal Molecular Cell – Mol Cell. 2009 Jan 16;33(1):87-96 (see also Indiana University).

The study revealed that a variant of a protein involved in HIV pathogenesis can suppress production of an HIV protein, known as Nef. Nef is required for the human immunodeficiency virus to develop into AIDS through a series of complex events involving viral elements and cellular proteins. Nef has never been a target for drug treatment in HIV patients.

Johnny J. He, Ph.D., principal author of the research and the director of the Indiana University Center for AIDS Research, said a drug affecting Nef could complement existing therapies to provide protection against the virus.

The current treatment for HIV/AIDS is highly active anti-retroviral therapy (HAART). It is a combination of drugs that target two HIV enzymes – reverse transcriptase (RT) and protease (PR) or RT or PR inhibitors.

Dr. He said another encouraging outcome of the research was the discovery that Nef could be suppressed on the molecular level to prevent it from translating into protein.

"These scientific advances have therapeutic potential to interrupt the progression of the virus into AIDS," said Dr. He, who also is a professor of microbiology and immunology and medicine.

Keywords: HIV/AIDS, AIDS, Acquired Immune Deficiency Syndrome, Acquired Immunodeficiency Syndrome, HIV, Human Immunodeficiency Virus, Immunology, Sexually Transmitted Disease, Therapy, Treatment, Virology, Indiana University.

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

Ref. He, JJ, et al. “Suppression of HIV-1 Nef translation by Sam68 mutant-induced stress granules and nef mRNA sequestration”, Mol Cell. 2009 Jan 16;33(1):87-96.

2009-02-02
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