14:515-519. SDSU73. All pigs were necropsied 14 days after PRRSV challenge. PCV2-infected, PRRSV-vaccinated, and PRRSV-challenged pigs had significantly ( 0.05) more-severe macroscopic lung lesions than did the PRRSV-vaccinated and PRRSV-challenged pigs that were not exposed to PCV2 prior to PRRSV vaccination. Nonvaccinated PRRSV-infected pigs had a significantly ( 0.001) higher incidence of PRRSV antigen in lungs than did all other groups except the group infected with PCV2 prior to PRRSV vaccination and challenge. The nonvaccinated PRRSV-challenged group and the group challenged with PCV2 prior to PRRSV vaccination and challenge had significantly ( 0.001) lower average daily weight gain than did the control and the vaccinated groups. This work suggests that PCV2 infection has an adverse effect on the development of protective immunity induced Fenofibric acid by PRRSV vaccine. Porcine circovirus type 2 (PCV2), a small, nonenveloped, single-stranded DNA virus with a circular genome (48), is Fenofibric acid ubiquitous in the global swine population (2). The hallmark microscopic lesions of PCV2 infection are lymphoid depletion and histiocytic replacement of lymphoid follicles in the lymphoid tissues and variable degrees of lymphohistiocytic inflammation in a variety of organs (45). PCV2 is associated with postweaning multisystemic wasting syndrome (PMWS) (1, 12), which is characterized by moderate to excessive loss of body condition often accompanied by respiratory disease in nursery and grow-to-finish pigs (17). The incidence of PCV2-associated disease in affected herds generally varies from 4% to up to 30% in individual farms (2, 17, 23). On most farms, PCV2 infection is widespread and subclinical. Studies on pigs with naturally acquired PMWS and PCV2 infection showed leukopenia characterized by decreased lymphocyte counts compared to those of healthy control pigs (10, 42, 43). Segals et al. (42) found a Mouse monoclonal to TYRO3 significant decrease in the number of CD3+ and CD4+ cells in PMWS-affected pigs compared to numbers in clinically healthy pigs, whereas no difference was found in the numbers of CD8+ cells. Darwich et al. (10) compared clinically PMWS-affected pigs that were infected by PCV2, wasted pigs that were not infected by PCV2, and healthy control pigs and found that, regardless of PCV2 infection status, wasted pigs in general had decreased CD4+ cells. However, only PMWS-affected and PCV2-infected pigs had decreased numbers of CD8+ and double-positive cells. The amount of PCV2 in lymphoid tissues was correlated to the degree of lymphoid depletion and to the decrease in immunoglobulin M-positive and CD8+ cells in peripheral blood (10). Further detailed assessment of PCV2-induced alteration of cells of the immune system in pigs experimentally infected with PCV2 demonstrated a PCV2-induced lymphopenia present only in pigs that developed clinical PMWS but not in those that were subclinically infected (29). The mean lymphocyte levels of PCV2-infected pigs decreased below that of the control pigs, which was most evident at 10 days postinoculation (DPI). A prominent lymphopenia was present in PMWS-affected pigs starting from DPI 14 until the death of the pigs. All T-cell subpopulations were found to be susceptible to PCV2-induced lymphopenia (29). Lymphoid depletion is a necessary and hallmark lesion of PCV2-associated PMWS (45); however, lymphoid depletion, to some degree, can also be observed in subclinically infected pigs (38). Studies on pigs with naturally acquired PMWS revealed that there was a reduction in the number of interfollicular dendritic cells and a reduction or absence of B cells and CD4+ cells (40). Chianini et al. (8) graded lymphoid lesions in pigs with natural PMWS as mild, moderate, and severe and showed a reduction or loss of B and T lymphocytes. It has been suggested that PCV2-associated lymphoid depletion compromises the immune system of the pig. This is supported by case reports describing PCV2 infection associated with coinfecting pathogens that are typically indicative of an immunosuppressed stage of the host, such as (9), spp. (6), pulmonary aspergillosis (44), and (30). Porcine reproductive and respiratory syndrome disease (PRRSV) is the major contributor to the porcine respiratory disease syndrome complex (PRDC) in the United States (18) and is estimated to cost the U.S. swine market $560 million yearly (28). PRRSV is an enveloped, positive-sense, single-stranded RNA disease classified in Fenofibric acid the order (7). Clinical indications of PRRSV illness in growing pigs include fever, sneezing, dyspnea, tachypnea, anorexia, and decreased weight gain. Vaccination is definitely a common process to minimize.