Scientists funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have identified a cellular receptor for rhinovirus C, a cold-causing virus that is strongly associated with severe asthma attacks. A variant in the gene for this receptor previously had been linked to asthma in genetic studies, but the potential role of the receptor, called CDHR3, in asthma was unknown. The new findings help clarify the function of CDHR3 and point to a novel target for the development of prevention and treatment strategies against rhinovirus C-induced colds and asthma attacks.
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.
YA Bochkov et al. Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication. Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1421178112 (2015).
Alkis Togias, M.D., chief of the Allergy, Asthma and Airway Biology Branch in NIAID's Division of Allergy, Immunology and Transplantation, is available to comment on the findings.