Common cold virus is foiled by a decoy

No one is claiming victory yet, but scientists have won a skirmish in the war against the common cold. By giving a drug that mimics a molecule that cold viruses use to invade cells, researchers have reduced cold symptoms in some people and prevented colds in others.

 A cure for the common cold has been so elusive that it has become a 20th-century symbol of futility. As funding for cold research dropped sharply in the past decade, many researchers gave up on finding a successful treatment. Nonetheless, colds continue to be more than an annoyance. They can lead to ear infections in children, aggravate asthma attacks, and spawn sinus infections.

 For 15 years, scientists have known that the rhinovirus, which causes roughly half of all colds, latches onto cells at a surface molecule called ICAM-1. This molecule provides the virus with a means to enter the cell. Once inside, rhinovirus commandeers the cell's machinery and replicates itself.

 To turn this exploitation to peoples' advantage, scientists at Boehringer Ingelheim Pharmaceuticals in Ridgefield, Conn., devised a truncated version of ICAM-1. The virus latches onto this decoy, called tremacamra, reducing the likelihood of infecting a cell.

 After the approach succeeded in chimpanzees scientists tried it on 177 volunteers aged 18 to 60. Each received nose drops containing rhinovirus and remained isolated in a hotel room for 8 days to limit contact with other viruses.

 Among the 81 people who also received tremacamra-in capsules or a nose spray-six times a day for 7 days, less than half developed a cold, the researchers report in the May 19 Journal of the American Medical Association (JAMA).

 Of 96 people getting an inert substance while exposed to the same virus, two-thirds came down with a cold within a week, says coauthor Frederick G. Hayden of the University of Virginia School of Medicine in Charlottesville. During the test, volunteers and researchers didn't know which treatments were placebos.

 Some participants were exposed to the virus shortly before getting the drug; some, 12 hours afterward. It didn't matter greatly. During the first week after exposure, people getting a placebo recorded roughly double the severity of cold symptoms-such as chills, cough, headache, and sore throat-as the people in the treated group did. Participants also collected their mucus-laden tissues in sealed containers, which revealed that untreated participants produced about twice as much mucus as those getting tremacamra did.

 Side effects of the medication were limited to nasal irritation in some participants.

 Tests on the participants' mucus discharge revealed less interleukin-8, an immune-system protein, in the treated group. Interleukin-8 rushes to the site of rhinovirus infections as a helper, but it actually can lead to some cold symptoms, such as the inflammation associated with sore throats. Reduction in interleukin-8 lessened such inflammation and indicated that the virus was replicating less extensively, Hayden says.

 Of course, the study doesn't precisely mirror reality. These people took medication within a day of being exposed to the virus. Normally, a person doesn't know a cold virus has struck until symptoms arise, which can take several days.

 While the study offers hope, "it remains to be seen whether tremacamra will have effects when given after symptoms have started, particularly in naturally occurring colds," says Kenneth McIntosh of Children's Hospital in Boston, also writing in JAMA. "Despite the encouraging findings," he concludes, "it is clear that the cure for the common cold is not yet in hand."