Rhinovirus C, Asthma, and Cell Surface Expression of Virus Receptor CDHR3

J Virol. 2017 Mar 13;91(7):e00072-17. doi: 10.1128/JVI.00072-17. Print 2017 Apr 1.

Abstract

Human rhinoviruses (RVs) of the A, B, and C species are defined agents of the common cold. But more than that, RV-A and RV-C are the dominant causes of hospitalization category infections in young children, especially those with asthma. The use of cadherin-related family member 3 (CDHR3) by RV-C as its cellular receptor creates a direct phenotypic link between human genetics (G versus A alleles cause Cys529 versus Tyr529 protein variants) and the efficiency with which RV-C can infect cells. With a lower cell surface display density, the human-specific Cys529 variant apparently confers partial protection from the severest virus-induced asthma episodes. Selective pressure favoring the Cys529 codon may have coemerged with the evolution of RV-C and helped shape modern human genomes against the virus-susceptible, albeit ancestral Tyr529.

Keywords: asthma; cadherin structure; common cold; paleogenetics; rhinovirus C.

MeSH terms

  • Animals
  • Cadherin Related Proteins
  • Cadherins / genetics
  • Cadherins / metabolism*
  • Common Cold / virology*
  • Evolution, Molecular
  • Gene Expression
  • Host-Pathogen Interactions
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Rhinovirus / genetics*
  • Rhinovirus / metabolism
  • Virus Attachment

Substances

  • CDHR3 protein, human
  • Cadherin Related Proteins
  • Cadherins
  • Membrane Proteins