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Pathological and immunological characteristics of piglets infected experimentally with a HP-PRRSV TJ strain.


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.

SUBMITTER: Li Z 

PROVIDER: S-EPMC5062860 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature

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Publications

Pathological and immunological characteristics of piglets infected experimentally with a HP-PRRSV TJ strain.

Li Zhenguang Z   He Yanliang Y   Xu Xiaoqin X   Leng Xue X   Li Shufen S   Wen Yongjun Y   Wang Fengxue F   Xia Mingqi M   Cheng Shipeng S   Wu Hua H  

BMC veterinary research 20161012 1


<h4>Background</h4>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).<h4>Results</h4>All piglets experimentally infected with a HP-PRRSV TJ strain virus developed typical clinical signs of PRRS. The percentages of CD3<sup>+</sup>, CD4<sup>+</sup>, and  ...[more]

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