After infection, researchers scraped small samples of nasal epithelial cells, which line the passages of the nose, from the volunteers. Rhinovirus-16 and other cold viruses infect these nasal cells, which are the body's first line of defense against airborne pathogens. The researchers then used microarray gene chip technology to compare the gene expression levels between the infected volunteers and the control group.
"Advances in genomics technology now allow us to analyze tens of thousands of genes in the same amount of time required to analyze just a handful of genes just a decade ago," said Jay Tiesman, P&G Genomics Group Leader and study author.
Forty-eight hours after inoculation, the expression of 6,530 genes in infected volunteers were significantly either up-regulated or down-regulated compared to the same genes in the control group. In other words, rhinovirus infection triggered a massive immune response in the nasal mucosa. Because rhinovirus is not as destructive as other more serious viral infections, this response appears to be disproportionate to the threat.
The researchers classified the active genes according to function, and found many involved in a process known as chemotaxis, which recruits various immune cells to the site of infection. These particular genes have been correlated with symptoms such as inflammation, congestion and runny nose. Other groups of active genes have also been classified; among them are genes which make antiviral compounds thought to help thwart infections.
"This study shows that after rhinovirus infection, cold symptoms develop because parts of our immune
|Contact: Shellie Byrum|
Procter & Gamble