AIDSWEEKLY Plus; Monday, October 27, 2003
Staff Medical Writers

"CCR5 is the major coreceptor for the HIV-1 strains responsible for primary infection," scientists in Madrid explained. "Individuals homozygous for a 32-bp deletion in the CCR5 coding region are resistant to HIV-1 infection. Strategies to delete CCR5 functionally could thus be of substantial benefit in preventing HIV-1 infection or delaying disease."

With this in mind, J.L. Abad and colleagues at the Centro Nacional de Biotecnologia in Madrid "evaluated new molecules for their ability to inhibit cell membrane CCR5 expression and to prevent HIV-1 infection."

"These inhibitors include several truncated forms of CCR5 that may act as negative transdominants, as well as bifunctional molecules resulting from the combination of a previously described anti-CCR5 ribozyme or a truncated CCR5 variant with an intracellular chemokine (RANTES-KDEL)," they wrote in the journal Molecular Therapy.

"These constructs efficiently blocked membrane CCR5 expression when cotransfected into HEK 293 cells," test results showed. "When expressed by retroviral transduction, some of these molecules significantly inhibited CCR5-dependent chemotaxis in the MCF-7 cell line and reduced CCR5 expression and HIV-1 infection in human T cells."

"Analysis of inhibitors with different efficiencies showed a strong linear correlation between CCR5 expression inhibition and prevention of HIV-1 infection," according to the report.

"This study indicates the potential clinical application of several new CCR5 inhibitory molecules for HIV-1 gene therapy," the researchers concluded.

Abad and coauthors published their study in Molecular Therapy (Novel interfering bifunctional molecules against the CCR5 coreceptor are efficient inhibitors of HIV-1 infection. Mol Ther. 2003 Sep;8(3):475-84.

Additional information can be obtained by contacting J.L. Abad, Centro Nacional de Biotecnologia/CSIC, Department of Immunology and Oncology, Campus Universidad Autonoma Cantoblanco, E-28049 Madrid, Spain.

The publisher of the journal Molecular Therapy can be contacted at: Academic Press Inc., Elsevier Science, 525 B St., Ste. 1900, San Diego, CA 92101-4495 USA.

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

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

Reference

Luis Abad J, Gonzalez MA, del Real G, et al. "Novel interfering bifunctional molecules against the CCR5 coreceptor are efficient inhibitors of HIV-1 infection", Mol Ther. 2003 Sep;8(3):475-84

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