Receptor for asthma-associated virus identified

Researchers led by James Gern, M.D., at the University of Wisconsin-Madison, discovered that CDHR3 recognizes and binds rhinovirus C, enabling the virus to enter human cells. Like all viruses, rhinovirus C uses the molecular machinery of host cells to replicate and become infectious. While the cellular receptors for other rhinovirus types are known, the rhinovirus C receptor had remained elusive. The scientists identified CDHR3 as a potential candidate by analyzing cells that either were or were not susceptible to rhinovirus C infection. When engineered to produce CDHR3, cells that normally were not susceptible to rhinovirus C could bind the virus and support its replication.

Notably, cells bearing a specific CDHR3 gene variant showed greatly enhanced rhinovirus C binding and produced more progeny virus than cells with normal CDHR3. In previous genetic studies, this variant had been linked to a greater risk of wheezing illnesses and asthma hospitalizations during childhood. The new findings suggest that this gene variant could be a risk factor for childhood wheezing illnesses caused by rhinovirus C, which in turn may increase the risk of developing asthma. In the future, development of drugs that block CDHR3 potentially could help prevent and treat illnesses caused by rhinovirus C.