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UCLA scientists reveal how Nipah virus infects cells

to part of a human antibody, like a worm on a fishing hook. When they placed this bait on cells at risk for Nipah infection, the antibody attached to a receptor on the cell surface. When placed on Nipah-resistant cells, however, the bait did not bind to the cell.

The scientists used an instrument that sorts molecules by weight to identify Ephrin-B2 as the receptor that bound to the bait.

To confirm their findings, the UCLA team engineered a harmless virus with Nipah virus proteins embedded in its coat. The decoy virus successfully infected cells vulnerable to the Nipah virus, but could not infect Nipah-resistant cells.

In the final step, the decoy virus entered nerve cells and cells lining blood vessels by latching onto Ephrin-B2, proving that the receptor is the same doorway that the real Nipah virus enters to infect these cells.

"We now can screen for small molecules that will block viral entry via Ephrin B-2 and develop them as therapeutic drugs," said Lee. "Because pigs are particularly susceptible to Nipah infection, public health officials could use these drugs to protect the animals, pig farmers and first-line responders, like paramedics, from a Nipah virus outbreak."

In the United States, agricultural experts estimate the value of pigs alone in the hog-farming industry at $8.6 billion.

The first reported outbreak of Nipah virus in Malaysia occurred between 1998 and 1999, sickening 265 people and killing 105. Spread from bats to pigs to humans, the outbreak infected more than 200 pig farmers and killed 40 percent. Desperate to contain the outbreak, the government ordered its military to kill more than 1 million pigs, resulting in economic devastation to the country.

In Bangladesh, death rates of repeated outbreaks of Nipah virus in the past four years have risen to 70 percent, suggesting that the virus is growing more lethal.


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Source:University of California - Los Angeles


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