猪萨佩罗病毒对仔猪的致病性

Pathogenicity of porcine sapelovirus to newborn piglets

猪萨佩罗病毒(PSV)是我国近年来新报道的仔猪腹泻病原,为深入了解PSV对仔猪腹泻的致病作用,本研究建立了PSV感染仔猪模型,通过对感染仔猪临床症状、剖检及组织病理学变化观察发现PSV能感染仔猪并导致发病,临床仔猪表现体温下降、出现腹泻症状,腹泻率可达80%,病死率20%。组织病理学观察肠道、肺脏及淋巴结病变明显,肠道绒毛受损,肺脏和淋巴结炎性细胞浸润。感染仔猪组织脏器病毒载量检测显示,病毒主要定植在肠道、肺脏和淋巴组织。荧光定量PCR对外周血中相关细胞因子水平检测,攻毒初期IL-1α、IL-6细胞因子上升明显,后期IL-2水平升高较快;抗病毒因子MX1水平持续上高,在14 d左右达到高峰。结果表明,PSV感染低日龄仔猪可引起腹泻,甚至死亡;病毒定植部位以肠道、肺脏及淋巴组织为主;感染后能诱导仔猪机体产生高水平细胞因子及抗病毒因子,攻毒仔猪体内先诱导产生TH2型体液免疫反应为主的抗炎性反应为主,后期以诱导TH1型促炎症反应的免疫应答为主。

Porcine sapelovirus(PSV)is a newly reported pathogen of piglet diarrhea in China in recent years.In order to understand the pathogenic effect of PSV on piglet diarrhea,a PSV-infected piglet model was established,and the clinical symptoms,autopsy and histopathological changes of infected piglets revealed that PSV can infect piglets and cause disease,with clinical piglets showing decreased body temperature,diarrheal symptoms,diarrhea rate of up to 80% and mortality rate of 20%.Histopathological observations of intestinal,pulmonary and lymph node lesions were evident,with damaged intestinal villi and infiltration of inflammatory cells in the lungs and lymph nodes.The viral load in tissues and organs of infected piglets showed that the viruses were mainly colonized in the intestine,lung and lymphatic tissues;the levels of IL-1α and IL-2 were detected by fluorescence quantitative PCR in peripheral blood,and the levels of IL-1α and IL-2 first decreased and then increased;the IL-6 cytokine first increased and then decreased;the anti-viral factor MX1 was significantly increased.It was concluded that PSV infection of young piglets could cause diarrhea and death,and virus colonization sites were mainly in the intestine,lung and lymphatic tissues,which could induce high levels of cytokines and antiviral factors in the piglet organism after infection.The anti-inflammatory response in the infected piglets was first induced to produce a TH2 type humoral immune response mainly,and later the immune response induced was mainly the TH1 type pro-inflammatory response.