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German scientists detect weak point in SARS virus


Althalus

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WASHINGTON (AFP) - German scientists announced that they have discovered a weakness in the SARS virus which could help speed up the development of a treatment to counter the infection.

The scientists said they had tracked down an enzyme that helps the spread of the virus that has killed about 560 people around the world and infected more than 7,400.

The breakthrough has started a race against time to develop a protease inhibitor -- a treatment that could block enzymes from the severe acute respiratory syndrome coronavirus and keep it from strengthening and infecting other cells in the human body.

The scientists, led by Rolf Hilgenfeld of the University of Lubeck's Institute of Biochemistry, announced the developments in a telephone press conference from Germany and on the Internet site of the US review Science (www.sciencemag.org).

Hilgenfeld worked with experts from other German universities: the Institute of Molecular Biology in Jena and the Institute of Virology and Immunology at the University of Wurzburg.

Hilgenfeld said a good inhibitor could be developed in a few months but that did not mean a treatment would be ready so quickly.

"It will probably be a couple of years until a drug is approved to treat SARS," he said.

To find the enzyme responsible for the spread of SARS, the researchers studied the crystal structure of an enzyme in the human coronavirus which causes the common cold, and an enzyme from a pig coronavirus.

"We have determined the crystal structure of the essential enzyme involved in the replication of this virus," Hilgenfeld said in the teleconference from Germany.

The researchers recommended first working on a molecule, codenamed AG7088, which is already being used in clinical trials on the the rhinovirus, the main cause of the common cold.

The German team hopes to make speedy progress because of the similarities between the enzymes in the two viruses.

Hilgenfeld said a drug being developed by US pharmaceutical giant Pfizer at San Diego in California "may be a good starting point" to create an inhibitor for the SARS coronavirus. He added that his team was not working with Pfizer.

"There are some minor clashes between the inhibitor AG7088 and the structure of SARS coronavirus main protease," said Hilgenfeld.

"This compound, AG7088, is unlikely to be a drug active against coronavirus infections. It needs to be modified. However, the new crystal structures, together with the modeled inhibitor, provide a good starting point for the design of such modifications."

Yahoo News

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