Dr. Liggett adds that while anti-viral drugs seem to be the most likely to succeed, "the data gathered from these full genome sequences gives us an opportunity to reconsider vaccines as a possibility, particularly as we gather multiple-patient samples and sequence the entire genomes, to see how frequently they mutate during a cold season. That work is underway now."
The researchers also found that the human rhinovirus skips a step when it makes its protein product, a shortcut that probably speeds up its ability to make a person feel sick soon after infection. "This is a new insight," says co-investigator Claire M. Fraser-Liggett, Ph.D., director of the Institute for Genome Sciences and professor of medicine and microbiology at the University of Maryland School of Medicine. "We would not have had any sort of intuition about this had it not been revealed through genome analysis. Information that comes from this discovery might present a completely different approach in terms of therapy."
The analysis shows that some human rhinoviruses result from the exchange of genetic material between two separate strains of the virus that infect the same person. Such a swap, known as recombination, was previously not thought possible in human rhinovirus. During cold season, when many different strains of rhinovirus may be causing infections, recombination could rapidly produce new strains.
Multiple mutations (as many as 800) were evident in virus samples taken recently from patients with colds, compared to older rhinovirus reference strains. Some viruses mutate by making slight changes in certain proteins to avoid being destroyed by antibodies from a person's immune system. "Mutations were found in every area of the genome," says Dr. Liggett.
The study's lead author, Ann C. Palmenberg, Ph.D., professor of biochemistry and chair of the Insti
|Contact: Bill Seiler|
University of Maryland Medical Center