Drug aimed at 2 bioterror agents blocks live viral infection, Weill Cornell te...( NEW YORK (Dec. 19 2007) -- Two deadl...)

NEW YORK (Dec. 19, 2007) -- Two deadly and highly infectious viruses -- both potential bioterror threats -- may have met their match in a new drug developed by scientists at Weill Cornell Medical College in New York City.

Hendra and Nipah viruses are related, newly recognized zoonotic viruses that can spread from their natural reservoir in fruit bats to larger animals -- including pigs, horses and humans.

The mode of transmission isn't clear, but is thought to be relatively easy -- either by close contact with an infected host or by breathing in the microscopic pathogens. Infection often leads to a fatal encephalitis, and there is currently no effective treatment against these illnesses.

However, in breakthrough research conducted last year, researchers at Weill Cornell manipulated a peptide (protein) related to a third pathogen, parainfluenza virus, that appeared to block "pseudo" Hendra and Nipah viruses from entering and infecting human cells.

Now, this "entry inhibitor" approach has proven effective in blocking the infection of live virus in animal cells, pointing the way to a drug that could be stockpiled to help stop an outbreak in humans.

Those findings appeared recently in the Journal of Virology.

"We have now tested the peptide-based entry inhibitor in monkey cells to show that it does effectively block infection with both live Hendra and Nipah," explains study senior researcher Dr. Anne Moscona, a professor of pediatrics and of microbiology and immunology at Weill Cornell Medical College, and an attending physician at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

Public health officials have sounded alarm bells ever since Nipah virus first emerged in pigs and then humans living in Southeast Asia. More recently, cases of Hendra virus began to show up in horses and their human handlers in Australia.

Experts who drew up the U.S. National Institute of Allergy and Infe
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