Rapid antigenic-type replacement and DNA sequence evolution of canine parvovirus

Abstract

Analysis of canine parvovirus (CPV) isolates with a panel of monoclonal antibodies showed that after 1986, most viruses isolated from dogs in many parts of the United States differed antigenically from the viruses isolated prior to that date. The new antigenic type (designated CPV type 2b) has largely replaced the previous antigenic type (CPV type 2a) among virus isolates from the United States. This represents the second occurrence of a new antigenic type of this DNA virus since its emergence in 1978, as the original CPV type (CPV type 2) had previously been replaced between 1979 and 1981 by the CPV type 2a strain. DNA sequence comparisons showed that CPV types 2b and 2a differed by as few as two nonsynonymous (amino acid-changing) nucleotide substitutions in the VP-1 and VP-2 capsid protein genes. One mutation, resulting in an Asn-Asp difference at residue 426 in the VP-2 sequence, was shown by comparison with a neutralization-escape mutant selected with a non-CPV type 2b-reactive monoclonal antibody to determine the antigenic change. The mutation selected by that monoclonal antibody, a His-Tyr difference in VP-2 amino acid 222, was immediately adjacent to residue 426 in the three-dimensional structure of the CPV capsid. The CPV type 2b isolates are phylogenetically closely related to the CPV type 2a isolates and are probably derived from a common ancestor. Phylogenetic analysis showed a progressive evolution away from the original CPV type. This pattern of viral evolution appears most similar to that seen in some influenza A viruses.

Occurrence of severe gastroenteritis in pups after canine parvovirus vaccine administration: A clinical and laboratory diagnostic dilemma

“…This new variant appears to be replacing CPV-2b in the Italian dog population [6][7][8][9][10][11]. The CPV variants differ in amino acid changes occurring at residue 426 of the capsid protein, with types 2a-2c displaying amino acids Asn, Asp and Glu, respectively [2,3]. This residue is located in a major antigenic site close to epitope B, i.e., over the shoulder region of the capsid in a region considered to affect viral immunogenicity.…”

“…CPV-2, first identified in the late 1970s, was replaced a few years after its emergence by two antigenic variants, CPV-2a and CPV-2b. Those two types are now distributed worldwide [2]. More recently, a third antigenic variant, CPV-2c, was first reported in Italy [3].…”

Review of companion animal viral diseases and immunoprophylaxis

“…Evidence suggests that the CPV arose from the long recognised FPLV or related virus infecting another carnivore such as mink, raccoon, artic fox or other. The new virus differed from FPLV like viruses in less than 1% in genomic sequence [20][21][22][23]. However, the life of firstly identified CPV variant in nature was brief [24].…”

“…In each case the replacement was global. Interestingly, CPV-2 and its 2a and 2b variants differed by less than 0.2% in their genome sequence and involved substitution of 3-4 amino acids in virus capsid protein VP2 [20][21][22][23]25]. This change was ongoing with the identification of CPV-2c in late 1990s [26].…”

Isolation and characterization of feline panleukopenia virus from a diarrheic monkey

“…Evidence suggests that the original type 2 (CPV-2) came from FPV infecting only cats in 1978, and gave rise to the antigenic variant CPV-2a through five or six amino acid mutations in the major capsid protein VP2 during 1979-1981(Parrish et al, 1988Parrish et al, 1985). A second variant, CPV-2b, was identified in 1986, which naturally infects dogs and cats (Parrish et al, 1991). A third variant, CPV-2c, was discovered in Italy in 2000, displaying an exceptional ability to spread rapidly through the canine population in that country (Buonavoglia et al, 2001;Martella et al, 2005), as well as in other European countries, Asia (Nakamura et al, 2004) and America (Kapil et al, 2007).…”