Comparative pathogenesis of infection of pigs with hepatitis E viruses recovered from a pig and a human
Comparative pathogenesis of infection of pigs with hepatitis E viruses recovered from a pig and a human
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DOI：
10.1128/jcm.39.3.918-923.2001
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发表时间：
2001-03-01
影响因子：
9.4
通讯作者：
Meng, XJ
中科院分区：
文献类型：
--
作者：
Halbur, PG;Kasorndorkbua, C;Meng, XJ
用猪源戊型肝炎病毒（KEV）和人源戊型肝炎病毒（KEV）分别接种无特异病原的猪，研究两种病毒在猪体内的相对致病性。将54头猪随机分为3组。第1组中的17头猪作为未接种的对照，第2组中的18头猪静脉接种从美国猪中回收的猪HEV，第3组中的19头猪静脉接种从美国肝炎患者中回收的US-2人HEV株。在接种后3、7、14、20、27或55天（DPI）对每组2 - 4头猪进行尸检。在三个组的任何猪中均未发现临床疾病或肝酶或胆红素升高的证据。在两个HEV接种组中均观察到肝和肠系膜淋巴结肿大。在第1至3组中，分别在9/17、15/18和16/19头猪中观察到多灶性淋巴浆细胞性肝炎。第1至3组中分别在5/17、10/18和13/19头猪中观察到局灶性肝细胞坏死。第1组猪的肝炎病变非常轻微，第2组猪为轻度至中度，第3组猪为中度至重度。在接种人HEV的组中，肝脏炎症和肝细胞坏死的严重程度在20 DPI时达到峰值，并且在55 DPI时仍为中度严重。在猪-HEV接种的猪中，到55 DPI时肝炎病变不存在或几乎消退。所有接种HEV的猪血清转化为抗HEV免疫球蛋白G。用逆转录酶FCR法在3~27 DPI的两个MEV接种组的猪粪便、肝组织和胆汁中检测到HEV RNA。基于对显微镜病变的评价，US-2株人HEV在猪中诱导的肝病变比猪HEV更严重和持久。猪肝脏或来自HEV感染猪肝脏的细胞可能代表HEV从猪传播到人类异种移植受体的风险。由于戊型肝炎病毒是在受感染猪的粪便中排出的，因此接触受感染猪的粪便代表了戊型肝炎病毒传播的风险，猪应被视为戊型肝炎病毒的储存库。
Specific-pathogen-free pigs were inoculated with one of two hepatitis E viruses (KEV) tone recovered from a pig and the other from a human) to study the relative pathogenesis of the two viruses in swine. Fifty-four pigs were randomly assigned to three groups. Seventeen pigs in group 1 served as uninoculated controls, 18 pigs in group 2 were intravenously inoculated with the swine HEV recovered from a pig in the United States, and 19 pigs in group 3 were intravenously inoculated with the US-2 strain of human HEV recovered from a hepatitis patient in the United States. Two to four pigs from each group were necropsied at 3, 7, 14, 20, 27, or 55 days postinoculation (DPI). Evidence of clinical disease or elevation of liver enzymes or bilirubin was not found in pigs from any of the three groups. Enlarged hepatic and mesenteric lymph nodes were observed in both HEV-inoculated groups. Multifocal lymphoplasmacytic hepatitis was observed in 9 of 17, 15 of 18, and 16 of 19 pigs in groups 1 to 3, respectively. Focal hepatocellular necrosis was observed in 5 of 17, 10 of 18, and 13 of 19 pigs in groups 1 to 3, respectively. Hepatitis lesions were very mild in group 1 pigs, mild to moderate in group 2 pigs, and moderate to severe in group 3 pigs. Hepatic inflammation and hepatocellular necrosis peaked in severity at 20 DPI and were still moderately severe at 55 DPI in the group inoculated with human HEV. Hepatitis lesions were absent or nearly resolved by 55 DPI in the swine-HEV-inoculated pigs. All HEV-inoculated pigs seroconverted to anti-HEV immunoglobulin G. HEV RNA was detected by reverse transcriptase FCR in feces, fiver tissue, and bile of pigs in both MEV-inoculated groups from 3 to 27 DPI. Based on evaluation of microscopic lesions, the US-2 strain of human HEV induced more severe and persistent hepatic lesions in pigs than did swine HEV. Pig livers or cells from the livers of HEV-infected pigs may represent a risk for transmission of HEV from pigs to human xenograft recipients. Since HEV was shed in the feces of infected pigs, exposure to feces from infected pigs represents a risk for transmission of HEV, and pigs should be considered a reservoir for HEV.