Figure 1.
Clinical pictures of inguinal (A) and submandibular (B) lymph nodes in the different challenge groups.
Moderate to severe atrophy, enlargement and hemorrhage were observed in the inguinal and submandibular lymph nodes, respectively, compared with the control group. More severe clinical signs were observed in the PCV2b/rBDH-challenged group, such as simultaneous presence of atrophy, enlargement and hemorrhage of inguinal and submandibular lymph nodes. a: PCV2a/rCL challenge group; b: PCV2b/rJF challenge group; c: PCV2b/rBDH challenge group; d: control group.
Table 1.
Scored values for clinical condition and pathological lesions for piglets in different challenge groups and the control group.
Figure 2.
Weight of individual animals from each group (A) and ADWG (B).
A: Weight of individual animals from each group at days 0 and 35, respectively. B: ADWG±SD was calculated for each treatment group throughout the experiment, with (*) indicating significant differences between the specified pairs. ADWG was significantly higher in the control group compared with the challenged groups (P<0.05). A significantly lower ADWG was observed in the PCV2b/rBDH-challenged group than in both the PCV2a/rCL- and PCV2b/rJF-challenged groups (P<0.05). No significant difference was seen between the PCV2a/rCL- and PCV2b/rJF-challenged groups (P>0.05).
Table 2.
Detection of PCV2 viral DNA using PCR in sera of pigs challenged experimentally with different PCV2 strains at different time points post challenge.
Table 3.
Titers of PCV2-specific antibodies in sera at different time points.
Figure 3.
Quantification and distribution of viral DNA loads.
Detection and quantification of viral DNA loads in lymphoid tissues, as well as spleen and lung, in pigs challenged experimentally with the PCV2a/rCL, PCV2b/rJF or PCV2b/rBDH virus. Group mean logarithm viral genomic copies/gram of tissue (±SD) was calculated as the corresponding value on the x axis for each treatment group. All samples from MEM-challenged pigs were negative. Pairs of treatments with (*) were significantly different (P<0.05).
Figure 4.
Histopathological detail of inguinal lymph nodes showing different degrees of severity of lymphocyte depletion.
(A) Inguinal lymph node from PCV2a/rCL-challenged group with mild lymphocyte depletion. (B) Inguinal lymph node from PCV2b/rJF-challenged group with moderate lymphocyte depletion. (C) Inguinal lymph node from PCV2b/rBDH-challenged group with significant lymphocyte depletion. (D) Normal inguinal lymph node from control group with normal lymphocyte count. Hematoxylin & eosin staining (400×).
Figure 5.
Proportion of monocytes and granulocytes in leukocyte subpopulations.
The proportion of monocytes and granulocytes in leukocyte subpopulations was significantly higher in the three PCV2 challenge groups compared with that in the control group, but no significant differences were observed among the three PCV2 challenge groups. Pairs of treatments with (*) were significantly different (P<0.05).
Figure 6.
Changes of CD4+/CD8+ cells in peripheral blood of infected piglets.
Ratio of CD3+CD4+CD8− cells to CD3+CD4−CD8+ cells (CD4+/CD8+) in PCV2b/rBDH-challenged group was significantly lower than that of the other two challenge groups at 3 and 7 DPC (P<0.05). When evaluated as a whole, all the PCV2 challenge groups showed a significant continuous decrease in the CD4+/CD8+ ratio, when compared with the control group from 21 DPC. Pairs of treatments with (*) were significantly different (P<0.05).
Figure 7.
Schematic diagram of PCV2 strains used in this study.
For the PCV2b/rBDH strain, a shift from TTA to CTT in the genomic sequence resulted in a stop codon mutation (from UAA to AAG) in ORF2 (in the antisense chain of the genomic sequence of PCV2), giving an ORF2 gene of 705 nt with another stop codon, compared with the classical PCV2a and PCV2b genotypes.
Table 4.
Characteristics of PCV2 strains used for the infection experiment in this study.