Washington, October 24 : A team of researchers have found that the human rhinovirus (HRV), which causes 30 to 50 per cent of common colds, can manipulate the host's genes to cause some of the most annoying symptoms.
The researchers say that HRV hijacks many of your genes, and causes an overblown immune response that ends up with the host's nose being overblown.
"The study's findings are a major step toward more targeted cold prevention and treatment strategies while also serving as a valuable roadmap for the broader respiratory science community," said Dr. David Proud, a professor in the Department of Physiology and Biophysics at the University of Calgary.
Proud, lead author of the study published in the American Journal of Respiratory and Critical Care Medicine, has revealed that he made these findings while working with collaborators from the University of Virginia and the Procter and Gamble Company.
He said that colds, though usually considered to be minor infections of the nose and throat, could have much more serious health repercussions.
"Rhinovirus is the major cause of the common cold, but it is also an important pathogen in more serious conditions, such as asthma and chronic obstructive pulmonary disease (COPD)," he said.
Dr. Ron Turner of the University of Virginia, one of the study's authors, added: "Advances in our understanding of the biology of the common cold may eventually lead to improvements in treatment or methods for prevention of colds."
For their study, the researchers recruited volunteers who were inoculated with either HRV or a sham inoculation and obtained cell scrapings from the nasal passages 8 and 48 hours after inoculation, and assessed the genetic changes by microarray, also know as gene chip technology.
After eight hours, there were virtually no differences between the control and the HRV-inoculated group, but by the 48-hour mark, more than 6500 genes has been significantly up- or down-regulated in the HRV subjects-many of the more highly up-regulated genes fell into two major categories: genes making antiviral proteins, including viperin (genes making pro-inflammatory cytokines).
"This is the first comprehensive picture to identify several groups of genes that are likely to contribute to the pro-inflammatory and antiviral response," said Dr. Proud.
The study also revealed that viral titer more than doubled in cells that had had the viperin-producing gene "knocked down", showing that HRV replication was hampered by viperin.
"This had never been examined during rhinovirus infections. Some evidence existed that this protein (only discovered a few years ago) had effects on influenza, but nothing was known about its role in rhinovirus infections. So it was a bit unexpected," said Dr. Proud.
"Overall these data provide new insights into the host response to HRV infection and identify several novel candidate genes that require further study to clarify their role in disease pathogenesis. This may identify proinflammatory, or host defense pathways that could be targeted for drug development, not only as treatments for colds but also for viral exacerbations of asthma and COPD.
"The fact that genes associated with structural 'remodeling' or the airways were also altered, supports further study of the role of rhinovirus infections in airway remodeling in asthma," he added.