A Porcine Circovirus Type 2 (PCV2) Mutant with 234 Amino Acids in Capsid Protein Showed More Virulence In Vivo, Compared with Classical PCV2a/b Strain

Abstract

BackgroundPorcine circovirus type 2 (PCV2) is considered to be the primary causative agent of postweaning multisystemic wasting syndrome (PMWS), which has become a serious economic problem for the swine industry worldwide. The major genotypes, PCV2a and PCV2b, are highly prevalent in the pig population and are present worldwide. However, another newly emerging PCV2b genotype mutant, which has a mutation in its ORF2-encoded capsid protein, has been sporadically present in China, as well as in other countries. It is therefore important to determine the relative virulence of the newly emerging PCV2b genotype mutant, compared with the existing PCV2a and PCV2b genotypes, and to investigate whether the newly emerging mutant virus induces more severe illness.Methodology/Principal FindingsTwenty healthy, 30-day-old, commercial piglets served as controls or were challenged with PCV2a, PCV2b and the newly emerging mutant virus. A series of indexes representing different parameters were adopted to evaluate virulence, including clinical signs, serological detection, viral load and distribution, changes in immune cell subsets in the peripheral blood, and evaluation of pathological lesions. The newly emerging PCV2 mutant demonstrated more severe signs compatible with PMWS, characterized by wasting, coughing, dyspnea, diarrhea, rough hair-coat and depression. Moreover, the pathological lesions and viremia, as well as the viral loads in lymph nodes, tonsils and spleen, were significantly more severe (P<0.05) for piglets challenged with the newly emerging mutant compared with those in the groups challenged with PCV2a and PCV2b. In addition, a significantly lower average daily weight gain (P<0.05) was recorded in the group challenged with the newly emerging PCV2 mutant than in the groups challenged with the prevailing PCV2a and PCV2b.ConclusionsThis is believed to be the first report to confirm the enhanced virulence of the newly emerging PCV2 mutant in vivo.

A Novel Porcine Circovirus Distantly Related to Known Circoviruses Is Associated with Porcine Dermatitis and Nephropathy Syndrome and Reproductive Failure

“…Epidemiological studies suggest that a genotype shift similar to that seen with PCV2b is in progress, with resulting reports of PCV2 vaccine failure and increased clinical disease (70,71). PCV2d has been implicated in more severe clinical signs and lesions (72).…”

Complete Genome Sequence of a Novel Porcine Circovirus Type 2b Variant Present in Cases of Vaccine Failures in the United States

“…Further sequence BLAST and comparison showed that both U.S. PCV2 strains had a high level of identity (99.9%) with the PCV2 strain BDH, which is sporadically found in China, reported to belong to genotype PCV2d, and suggested to be of increased virulence (4,5). One silent mutation (1677A¡1677T) in ORF1 was found between BDH and the two U.S. mutant PCV2s.…”

In silico analyses of antigenicity and surface structure variation of an emerging porcine circovirus genotype 2b mutant, prevalent in southern China from 2013 to 2015

“…As this isolate was located between PCV2b-1A/1B and PCV2b-1C within the phylogenetic tree, the cap gene of the isolate was compared with the strains from clusters of PCV2b-1A/1B (strain WH; GenBank accession number FJ598044), PCV2b-1C (strain rBDH; GenBank accession number HM038017) and PCV2a (strain LG; GenBank accession number HM038034), previously reported in China (Guo et al, 2012;Zhai et al, 2014). This recombination analysis revealed that a potential breakpoint might be located at position 296 (position in alignment of cap gene; Fig.…”

“…Of note, a newly emerging mutant of PCV2b (designated PCV2b-1C) has been frequently isolated from PCV2-vaccinated farms in the USA, Korea and Germany (Eddicks et al, 2015;Opriessnig et al, 2013;Reiner et al, 2015;Seo et al, 2014;Xiao et al, 2012). An extra lysine present at the C terminus (CT) of PCV2 Cap is a unique feature of this mutant; furthermore, the presence of this additional amino acid increases virus titre in sera (Opriessnig et al, 2014b) and pathogenicity (Guo et al, 2012).…”