Reactivity to PCV1 antigen by IFA was found in serum from mice (Tischer et al., 1995). Seventy-three mice were tested and found to be negative for PCV2-specific antibodies by IPMA (Rodríguez-Arrioja et al., 2003) and 50 mice were found to be negative for PCV1-specific antibodies as determined by IFA (Allan et al. 1994).
Several studies have investigated the susceptibility of mice for PCV2-infection. One study using BALB/c mice found detectable PCV2 antigen in the nuclei and cytoplasm of histiocytes and apoptotic cells in germinal centers of lymph follicles as well as in hepatocytes in the liver (Kiupel et al., 2001). This group also showed mild lymphoid depletion and histiocytic infiltration of lymphoid follicles. The mice in this study were infected intraperitoneally as well as intranasally with a PCV2-isolate that had been passaged four times in cell culture and originated from a case with naturally occurring PMWS. Four mice were necropsied at 7, 14, 28, and 42 DPI, respectively. Microscopic lesions were first detected at 7 DPI, were most prominent at 14 and 21 DPI in bronchial and mesenteric lymph nodes and spleen and Peyer’s patches, and were less severe at 42 DPI (Kiupel et al., 2001). PCV2 replicated in the mice and upregulated caspase 1, 2, 3, 6, 7, 8, 11, and 12, the transcripts of apoptosis inhibitors bcl-2, bcl-w, bcl-X, and apoptosis promoters bax, bak and bad, and was associated with apoptosis in spleens, Peyer’s patches and lymph nodes of infected BALB/c mice (Kiupel et al., 2005).
Another study infected ICR-CD1 mice with the 4th cell culture passage of a PCV2-isolate from another case of naturally occurring PMWS (Quintana et al., 2002). Three intraperitoneally PCV2-infected mice were necropsied at 3, 7, 10, 14, and 20 DPI, respectively. Despite the detection of PCV2-DNA in sera, there was no evidence of PCV2 antigen or nucleic acids in microscopic sections; however, this group apparently did not examine the relevant lymphoid tissues (lymph nodes, spleen) that are the major sites of PCV2-associated lesions in pigs (Quintana et al., 2002).
Three different mouse lines (BALB/c, C57BL/6, and C3H/HeN) were used to investigate possible differences in host susceptibility to PCV2 (Opriessnig et al., 2004). C57BL/6 and C3H/HeN were selected based on markedly different responses to certain pathogens compared to BALB/c mice. Forty-eight mice of each line were purchased at 4 weeks of age. Thirty-six mice in each line were inoculated with 104TCID50 PCV2-isolate ISU-40895. The inoculation was done twice intranasally and intramuscularly at 5 and 6 weeks of age. At the time of inoculation, half of the mice in each line received additional immunostimulation in the form of subcutaneous injections with keyhole limpet hemocyanin in incomplete Freund’s adjuvant. Necropsies were performed at 12, 17, 22, 27, 32, and 37 DPI. Mice within all breeds were found to be positive for PCV2-nucleic acids based on PCR performed on tissue homogenates. There was a trend towards more PCR positive mice in the BALB/c group. PCV2-associated microscopic lesions were not observed and efforts to detect PCV2 antigen by IHC and PCV2 nucleic acids by ISH were unsuccessful (Opriessnig et al., 2004).
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