Date Full Report Received


Date Abstract Report Received



Primary Investigator:

The objectives of the project were to determine if 1) SIV infection (H1N1, not pandemic H1N1) could initiate clinically significant porcine circovirus associated respiratory disease (PCVAD-respiratory) or the severe form of systemic PCVAD (PCVAD systemic) in pigs subclinically infected with PCV2b; and, 2) a pre-existing, subclinical PCV2b infection would have any effect on the duration or severity of the SIV infection.   In order to test these hypotheses, we chose a PCV2-SIV co-infection model using caesarean-derived, colostrum-deprived (CD/CD) pigs to compare the clinical, serological, virological and pathological parameters. Pigs were housed by experimental group in separate rooms in a biosafety level 2 isolation facility. Pigs inoculated intranasally on day 1 with PCV2b, followed 17 days later by an intra-tracheal inoculation of SIV. Appropriate control groups (sham-inoculated, PCV2b only and SIV only) were used. PCV2b infection was confirmed by serum PCR and serology. SIV infection was confirmed by identifying virus shed in nasal secretions. Under the conditions of this study, subclinical PCV2b infection plus SIV infection resulted in increased severity of clinical respiratory signs, an increased amount of SIV shed in nasal secretions of dual-infected pigs, and shedding was sustained for 9 days longer than the SIV-only group. SIV initiated the severe form of PCVAD in 20% of the dual-infected pigs, but did not increase the PCV2b load in nasal secretions or tissues of pigs without the severe form of the disease. These results indicate that there are reciprocal effects between SIV and PCV2b when the PCV2b infection precedes SIV by approximately 17 days, and, at least in part, help to explain anecdotal observations of increased duration and severity of disease in field cases of SIV in PCV2-infected herds.