Infection of Cesarean-Derived Colostrum-Deprived Pigs with Porcine Circovirus Type 2 and Swine Influenza Virus

Porcine circovirus type 2 (PCV2) and swine influenza virus (SIV) are important pathogens for porcine respiratory disease complex, which is economically significant worldwide. The pathogenesis of PCV2–SIV coinfection is unknown. In this study, we focused on establishing a challenge model for PCV2 to determine whether SIV influences PCV2 replication and increases the severity of PCV2-associated disease. Cesarean-derived colostrum-deprived pigs were inoculated intratracheally with cell culture medium only (negative control group), PCV2 only, or PCV2 followed 1 wk later with SIV H1N1. Two pigs from each group were necropsied at 12, 21, 28, and 35 d after inoculation. Coinfection with SIV did not increase the number of PCV2 genomic copies in serum or target tissues or the severity of microscopic lesions associated with PCV2 in lung or lymph node. The antibody titer to PCV2 did not differ significantly between PCV2–SIV- and PCV2-infected groups. In conclusion, SIV H1N1 did not influence PCV2 replication in dually infected pigs in this study.Abbreviations: PCV2, porcine circovirus type 2; PRDC, Porcine respiratory disease complex; SIV, Swine influenza virusPorcine respiratory disease complex (PRDC) is an economically significant problem characterized by slow growth, poor food utilization, lethargy, anorexia, fever, cough, and dyspnea in pigs 16 to 22 wk of age.^14,38 PRDC is associated with complex sequential or concurrent infections with multiple viral or bacterial respiratory pathogens.^6,8,17,29 Field investigations and case-trend analyses demonstrate that porcine circovirus type 2 (PCV2) plays a role in PRDC.^12,17,24PCV2 belongs to the family Circoviridae, which contains the smallest nonenveloped, single-stranded, circular DNA viruses.^21,39 In the late 1990s, a pathogenic circovirus designated PCV2 was isolated, which differed from the nonpathogenic PCV1.^2,21 PCV2 is considered ubiquitous and can be detected in both diseased and clinically healthy pigs.¹ Infection induces various degrees of lymphoid depletion and immune suppression, demonstrated by experimentally infecting pigs with PCV2 infectious DNA clones.¹⁰ However, the factors that contribute to the pathogenicity of PCV2 remain unknown.²⁴ Generally, infection with PCV2 alone is limited in its ability to induce the full spectrum of symptoms associated with PRDC; the role of PCV2 in PRDC always involves interaction or synergism with other respiratory pathogens.^4,17Swine influenza virus (SIV) is a common pathogen associated with PRDC.^6,8 SIV is an enveloped, negative-sense, segmented RNA virus belonging to the family Orthomyxoviridae.³⁶ SIV infects the epithelium of the respiratory tract of pigs, causing an acute infection with clinical signs of cough, fever, lethargy, and anorexia beginning 1 to 2 d after experimental infection and lasting for 3 to 4 d.^14,44 High morbidity and low mortality are quite common in uncomplicated disease, but mortality usually is high when other infectious agents are present along with SIV.³⁶ Together with PCV2, SIV frequently is found in pigs with clinical signs of PRDC. At one farm, mortality reached as high as 10% in pigs coinfected with PCV2 and SIV, and 5% of the coinfected pigs failed to reach market weight.¹⁵ In a cross-sectional study, SIV infection was 11 times more likely to occur in PCV2-positive pigs compared with PCV2-negative pigs.⁸ Field studies on pigs with PRDC conducted in different years showed a 1.9% to 13% rate of coinfection with PCV2 and SIV.^{6,9,15,17,28,29} Clinical evidence suggests that SIV acts synergistically with PCV2 to cause PRDC. However, the pathogenesis of PCV2–SIV coinfection is unknown.In this study, our goal was to establish a challenge model for PCV2 and PCV2–SIV and to determine whether SIV influences PCV2 replication and increases the severity of PRDC. Throughout the study, microscopic lesions attributable to PCV2 and PCV2 viral load in serum, nasal swab, lung, and lymph node did not differ between PCV2- and PCV2–SIV-inoculated pigs. On the basis of these findings, we conclude that SIV H1N1 did not influence PCV2 replication in dually infected animals.