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Discovery of an HIV inhibitor in human blood points to new drug class

A new study has pinpointed a natural ingredient of human blood that effectively blocks HIV-1, the virus predominantly responsible for human AIDS, from infecting immune cells and multiplying. The virus blocker might play a role in the progression of HIV to full-blown AIDS and—because it works in a different way than existing antiretroviral inhibitors—could lead to the development of another class of drugs in the fight against the pandemic disease, researchers reported in the April 20, 2007 issue of the journal Cell, a publication of Cell Press.

The research team found that fragments of a relatively abundant blood molecule, which they call VIRUS-INHIBITORY PEPTIDE, or VIRIP, acts as a broad-based inhibitor of HIV-1. Moreover, they showed that a few amino acid changes in the fragment enhanced its antiretroviral potency by two orders of magnitude. VIRIP and its derivatives remained effective against drug-resistant HIV strains, making them "highly promising for further clinical development," according to the researchers.

"The findings reveal a new target for inhibiting HIV that remains fully active against viral strains that are resistant to other drugs," said study author Frank Kirchhoff of the University of Ulm in Germany. "That's a big advantage."

Kirchhoff's group also provided evidence that HIV-1 does not easily develop resistance to VIRIP, at least in cell culture. Furthermore, their collaborators led by Wolf-Georg Forssmann of IPF PharmaCeuticals GmbH and Hannover Medical School found preliminary evidence showing that some derivatives of the peptide are highly stable in human blood plasma and are nontoxic even at exceedingly high concentrations.

According to the latest World Health Organization estimates, nearly 40 million people worldwide are living with HIV/AIDS, including more than 2 million children. Close to 4 million people became infected with HIV in 2006, and the virus was responsible for about 3 million deaths last yea
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Source:Cell Press


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