Chink discovered in armour of the common cold

SCIENTISTS HAVE discovered a vital chink in the armour of the common cold virus that they say could one day lead to a cure for the infection.

Medical researchers at the Brookhaven National Laboratory in Upton, New York, have found out how one form of the cold virus attacks human tissues in the nose and throat.

The discovery, reported in the journal Science, could lead to the development of new drugs that can block the virus from binding to human cells, said Paul Freimuth, a biologist at Brookhaven and a member of the research team.

"Viruses have to bind to cells to infect them. If you could interrupt that binding, the virus would be dead in the water," Dr Freimuth said. "That, in essence, is what the body's immune system does when it produces antibodies. The antibodies bind to the virus so the virus can't bind to the cell."

However, for the immune system to launch an attack on an invading virus takes time, allowing it to multiply within the respiratory tract, which is why the symptoms of a cold can linger for days or even weeks.

Dr Freimuth, working with John Flanagan and other colleagues at Brookhaven, used high-intensity X-rays to show the structure of proteins used by one type of common cold virus, called adenovirus, which are used as "grappling hooks" for attacking human cells.

From there, they worked backwards to discover the dimensions of the human proteins which the virus uses to grip the respiratory tract cell it is infecting. By determining the structure of these proteins, the scientists should be able to design drugs that mimic the effect, causing the virus to lose its vital grappling hooks.

Dr Freimuth believes the research will help other scientists working on gene therapy and cancer treatments. "If you understand the way a virus attaches to a specific cell, you might be able to modify the virus to precisely target specific cells, such as those that make up a tumour," he said. It would also help in the design of more effective vaccines directed at binding sites.

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