PLoS ONE (Jan 2012)

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.

  • Longjun Guo,
  • Yujie Fu,
  • Yiping Wang,
  • Yuehua Lu,
  • Yanwu Wei,
  • Qinghai Tang,
  • Peihu Fan,
  • Jianbo Liu,
  • Long Zhang,
  • Feiyan Zhang,
  • Liping Huang,
  • Dan Liu,
  • Shengbin Li,
  • Hongli Wu,
  • Changming Liu

DOI
https://doi.org/10.1371/journal.pone.0041463
Journal volume & issue
Vol. 7, no. 7
p. e41463

Abstract

Read online

BACKGROUND: Porcine 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 FINDINGS: Twenty 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. CONCLUSIONS: This is believed to be the first report to confirm the enhanced virulence of the newly emerging PCV2 mutant in vivo.