A team of researchers at the University of Wisconsin School of Medicine and Public Health in Madison have discovered a way to loosen the foothold of Rhinovirus C (RV-C) in the human body. RV-C is among the most common viral infections in humans and is also the leading cause of the common cold. We haven’t been able to do much to change that so far, but the UW work presents a new understanding and method of attacking the virus.
The study was led by Dr. James Gern (pictured left, courtesy UW Madison), professor in the departments of pediatrics and medicine at the UW School of Medicine and Public Health. He knew that RVC binds to a specific protein on the cell, but had been vexed with the challenge of finding which one.
“This virus had been hard to study because none of the standard cell lines in the laboratory would permit growth of RV-C because the virus bound to an unknown receptor on the surface of cells,” said Gern in a recent UW Madison article.
“But our research describes the protein (CDHR3) that enables RV-C viruses to bind to cells, enter them and ultimately start the replication process.”
In particular, only cells with this protein allow RV-C to replicate. The team found that engineering cells to produce CDHR3 made them susceptible to RV-C. Conversely, they also found that engineering cells to not produce CDHR3 made them resistant to RV-C and stopped the virus from replicating.
(A rendering of a rhinovirus. The dark grey areas are “protein spikes” used to bind to healthy cells. Image courtesy Wikimedia Commons)
Beyond the common cold, Rhinovirus C is responsible for several childhood wheezing illnesses, most notably asthma. Gern hopes to develop drugs that can block CDHR3 in order to help treat these illnesses.
The study was funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. For further reading regarding funding for the University of Wisconsin, Madison and its studies, click on the link below:
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