NEW YORK (Reuters Health) - Researchers may have found a way to treat one of the most common forms of muscular dystrophy by using a stripped-down version of a cold virus to carry gene therapy to damaged muscles.

A month after researchers injected the modified virus into adult mice with a condition similar to Duchenne muscular dystrophy, the mice showed significant improvements in muscle strength, according to the study published in the Proceedings of the National Academy of Sciences ( news - web sites).

"Now we know that there is a great potential to reverse muscle damage in boys who have already developed significant weakness," study co-author Jeffrey S. Chamberlain, a professor in the department of neurology at the University of Washington School of Medicine in Seattle, said in an interview with Reuters Health.

Duchenne muscular dystrophy is a fatal muscle-wasting disease that strikes approximately 1 in every 3,500 boys. The disease is caused by defects in the dystrophin gene, which is found on the X chromosome.

Previous attempts to treat the disorder with gene therapy have failed because of immune responses to the virus carrying the corrected copy of the dystrophin gene, Chamberlain noted.

For the new study, researchers created a "gutted" version of the cold virus. "The only thing remaining from the original virus is a piece of DNA that is required for both replication--making more of it--and assembling the viral DNA into an infectious shell of proteins," Chamberlain explained. "This shell allows the vector to enter the cell, as it binds to specific proteins on the surface of the muscle cells and allows it to be pulled inside the cell."

Once inside the cell, the corrected gene for dystrophin is transported into the cell's nucleus and the cell begins making the dystrophin protein, Chamberlain said.

"By removing the viral genes, we created a 'stealth' virus that no longer triggers an immune response," Chamberlain said.

Chamberlain and his colleagues injected the gutted virus carrying the dystrophy gene into a leg muscle in each mouse in the study. Within a month, the researchers found dystrophin production in the treated muscle was up by 25% to 30%. They also found an improvement in symptoms related to the disease.

And the effects of the therapy seem to be relatively long-lasting. "So far, we see persistence for 6 months," Chamberlain said. "But I suspect it will slowly go away over 2 years. Thus, we need to either find a way to repeat the injections, or get the dystrophin gene to remain stable in the muscle. We are pursuing both approaches."