[Evolution and host variation of the canine parvovirus: molecular basis for the development of a new virus].
Canine parvovirus (CPV) evolved as a new pathogen in dogs between 1976 and 1978 from feline panleukopenia virus (FPV). The new virus hit an unprotected population, caused a dramatic pandemic and infected virtually all populations of domestic and wild carnivores worldwide. The great similarity between the two viruses and their differences in host range, both in vivo as well as in vitro, make it a good model system for emerging diseases and host range shifts of viruses. Recent results showed that CPV expanded its host range by binding to the canine transferrin receptor (Tfr). Residues in the capsid protein that had been defined as host range controlling regions also control the binding to the canine transferrin receptor. These residues are located on a raised region of the capsid at the three-fold axis of symmetry. Interestingly, adaption of the new virus to the new host appears to correlate with an improved binding to the Tfr receptor.
Hueffer
Karsten
K
J. A. Baker Institute for Animal Health, Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University Ithaca, New York, USA.
Truyen
Uwe
U
Parrish
Colin R
CR
D000818:Animals; D005075:Biological Evolution; D036022:Capsid Proteins / Q000737:chemistry / Q000378:metabolism; D002415:Cats; D004285:Dogs; D028301:Feline Panleukopenia Virus / Q000472:pathogenicity / Q000502:physiology*; D017993:Parvovirus, Canine / Q000472:pathogenicity / Q000502:physiology*; D011990:Receptors, Transferrin / Q000378:metabolism; D013045:Species Specificity
D036022:Capsid Proteins; D011990:Receptors, Transferrin