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

Zhenguang Li,Hua Wu,Xiaoqin Xu,Fengxue Wang,Shipeng Cheng,Yanliang He,Shufen Li,Mingqi Xia,Yongjun Wen,Xue Leng

doi:10.1186/s12917-016-0854-x

Abstract

BackgroundPorcine 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).ResultsAll 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.ConclusionsThese 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.

Highlights

Porcine reproductive and respiratory syndrome (PRRS) remains a major threat to swine industry all over the world
Clinical signs observations post infection All piglets infected with HP-PRRS virus (PRRSV) TJ strain virus developed typical clinical signs of HP-PRRS, such as severe depression and anorexia, lameness and shivering, dyspnea, skin cyanosis and death
Four of five PRRSVinfected piglets died of acute respiratory disease

Summary

Introduction

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). Porcine reproductive and respiratory syndrome (PRRS) is characterized by reproductive failure in pregnant sows and respiratory distress in pigs of all ages [1]. PRRSV mainly replicates in alveolar macrophages in the lungs and lymphoid organs [4]. The virus is well- known to stay in lungs and lymphoid organs of infected pigs for a long time. Others had detected PRRSV in lymph organs up to 132 days when the piglets were infected in the uterus [6]. The mechanism of PRRSV persistence is not completely understood but is likely related to the emergence of viral variants which can escape host immune response [8]

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