Zhenguang Li1,2, Yanliang He1, Xiaoqin Xu3, Xue Leng2, Shufen Li1, Yongjun Wen2, Fengxue Wang2, Mingqi Xia1, Shipeng Cheng2, Hua Wu4,5. 1. Sinovet (Beijing) Biotechnology Co., Ltd., Kaituo Road 5, Haidian District, Beijing, 100085, China. 2. State Key Laboratory of Special Economic Animal Molecular Biology, Institute of Special Economic Animal and Plant Sciences, Chinese Academy of Agricultural Sciences,, Juye Street 4899, Changchun, Jilin, 130122, China. 3. Jiangyan Animal Health Inspection Institute, Jiangguan Road 251, Taizhou, Jiangsu, 225529, China. 4. Sinovet (Beijing) Biotechnology Co., Ltd., Kaituo Road 5, Haidian District, Beijing, 100085, China. wuhua@sinovetah.com. 5. State Key Laboratory of Special Economic Animal Molecular Biology, Institute of Special Economic Animal and Plant Sciences, Chinese Academy of Agricultural Sciences,, Juye Street 4899, Changchun, Jilin, 130122, China. wuhua@sinovetah.com.
Abstract
BACKGROUND: Porcine reproductive and respiratory syndrome (PRRS) remains a major threat to swine industry all over the world. The aim of this study was to investigate the mechanism of pathogenesis and immune responses caused by a highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV). RESULTS: All piglets experimentally infected with a HP-PRRSV TJ strain virus developed typical clinical signs of PRRS. The percentages of CD3+, CD4+, and CD8+ lymphocytes significantly decreased in the infected group as compared to the uninfected control animals (p < 0.01). Total WBC dropped in the infected animals during the experiment. The level of ELISA antibody against PRRSV increased in 7-10 days after infection and then started to decline. Pathological observations demonstrated various degree lesions, bleeding and necrosis in the lungs of the infected piglets. CONCLUSIONS: These results clearly indicated that HP-PRRSV TJ strain infection would activate host humoral immune response at the early period post infection and cause severe pathological damages on lungs and inhibit cellular immune response after infection.
BACKGROUND:Porcine reproductive and respiratory syndrome (PRRS) remains a major threat to swine industry all over the world. The aim of this study was to investigate the mechanism of pathogenesis and immune responses caused by a highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV). RESULTS: All piglets experimentally infected with a HP-PRRSV TJ strain virus developed typical clinical signs of PRRS. The percentages of CD3+, CD4+, and CD8+ lymphocytes significantly decreased in the infected group as compared to the uninfected control animals (p < 0.01). Total WBC dropped in the infected animals during the experiment. The level of ELISA antibody against PRRSV increased in 7-10 days after infection and then started to decline. Pathological observations demonstrated various degree lesions, bleeding and necrosis in the lungs of the infected piglets. CONCLUSIONS: These results clearly indicated that HP-PRRSV TJ strain infection would activate host humoral immune response at the early period post infection and cause severe pathological damages on lungs and inhibit cellular immune response after infection.
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