Halbur P G, Kasorndorkbua C, Gilbert C, Guenette D, Potters M B, Purcell R H, Emerson S U, Toth T E, Meng X J
Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa 50011, USA.
J Clin Microbiol. 2001 Mar;39(3):918-23. doi: 10.1128/JCM.39.3.918-923.2001.
Specific-pathogen-free pigs were inoculated with one of two hepatitis E viruses (HEV) (one 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 PCR in feces, liver tissue, and bile of pigs in both HEV-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.
将无特定病原体猪接种两种戊型肝炎病毒（HEV）之一（一种从猪身上分离得到，另一种从人身上分离得到），以研究这两种病毒在猪体内的相对致病机制。54头猪被随机分为三组。第1组17头猪作为未接种对照，第2组18头猪静脉接种从美国一头猪身上分离得到的猪源HEV，第3组19头猪静脉接种从美国一名肝炎患者身上分离得到的人源HEV US - 2株。在接种后3、7、14、20、27或55天（dpi），每组处死2至4头猪。在三组中的任何一组猪中均未发现临床疾病证据或肝酶或胆红素升高。在两个接种HEV的组中均观察到肝和肠系膜淋巴结肿大。在第1至3组中，分别有17头猪中的9头、18头猪中的15头和19头猪中的16头观察到多灶性淋巴浆细胞性肝炎。在第1至3组中，分别有17头猪中的5头、18头猪中的10头和19头猪中的13头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。接种人源HEV组的肝脏炎症和肝细胞坏死在20 dpi时严重程度达到峰值，在55 dpi时仍为中度严重。在接种猪源HEV的猪中，肝炎病变在55 dpi时消失或几乎消退。所有接种HEV的猪均血清转化为抗HEV免疫球蛋白G。在接种HEV的两组猪中，从3至27 dpi，在粪便、肝脏组织和胆汁中通过逆转录酶PCR检测到HEV RNA。基于微观病变评估，人源HEV US - 2株在猪体内诱导的肝脏病变比猪源HEV更严重且持续时间更长。来自HEV感染猪的猪肝或肝细胞可能对HEV从猪传播给人类异种移植受者构成风险。由于HEV在感染猪的粪便中排出，接触感染猪的粪便代表HEV传播的风险，并且猪应被视为HEV的储存宿主。
