Fultz P N, Shadduck J A, Kang C Y, Streilein J W
Infect Immun. 1981 Nov;34(2):540-9. doi: 10.1128/iai.34.2.540-549.1981.
Susceptibility of Syrian hamsters of the inbred LSH and MHA strains to injection of as few as 10 plaque-forming units of vesicular stomatitis virus (VSV) was shown to occur only after intraperitoneal and intrapleural injection and not after injection of VSV intravenously, intranasally, or in the footpads. Despite the fact that fewer LSH hamsters died when VSV was injected via the latter routes, the histopathology of the VSV-induced disease at early times after infection was identical irrespective of the route of virus administration. Histological examination of tissues at various times after administration of VSV by the various routes revealed that VSV exhibited tropism for lymphoreticular tissue, with the greatest amount of necrosis in the splenic periarteriolar lymphoid sheath. A similar pattern also was observed in VSV-infected tissues from genetically resistant UT1 hamsters. Infectivity titrations of various tissues at different times after intraperitoneal injection of VSV revealed that resistant UT1 hamsters began to clear virus from tissues between 40 and 48 h postinfection, whereas virus titers remained high in susceptible animals. Resistance of UT1 hamsters appeared to require an intact spleen since survival of splenectomized animals was less than that of sham-splenectomized UT1 controls. Sublethal whole-body irradiation was also able to reduce resistance of UT1 hamsters (survival was reduced from 100 to 50%). Bone marrow cells from resistant (UT1 X LSH) F1 females were transferred into lethally irradiated susceptible LSH hamsters, and hematopoietic chimeras were produced. After intraperitoneal injection of 100 plaque-forming units of VSV, all of the female chimeras survived, but only 33% of male chimeras survived. These data indicate that resistance to VSV in Syrian hamsters is mediated, at least partially, by cells of hematopoietic origin.
近交系LSH和MHA叙利亚仓鼠对低至10个空斑形成单位水泡性口炎病毒（VSV）注射的易感性仅在腹腔内和胸膜内注射后出现，而静脉内、鼻内或足垫注射VSV后则不会出现。尽管通过后几种途径注射VSV时死亡的LSH仓鼠较少，但感染后早期VSV诱导疾病的组织病理学与病毒给药途径无关。通过各种途径给予VSV后不同时间对组织进行组织学检查发现，VSV对淋巴网状组织具有嗜性，脾动脉周围淋巴鞘中的坏死量最大。在基因抗性UT1仓鼠的VSV感染组织中也观察到类似模式。腹腔注射VSV后不同时间对各种组织进行感染性滴定显示，抗性UT1仓鼠在感染后40至48小时开始从组织中清除病毒，而易感动物的病毒滴度仍保持较高水平。UT1仓鼠的抗性似乎需要完整的脾脏，因为脾切除动物的存活率低于假脾切除的UT1对照。亚致死剂量的全身照射也能够降低UT1仓鼠的抗性（存活率从100%降至50%）。将抗性（UT1×LSH）F1雌性的骨髓细胞转移到经致死性照射的易感LSH仓鼠中，产生了造血嵌合体。腹腔注射100个空斑形成单位的VSV后，所有雌性嵌合体均存活，但只有33%的雄性嵌合体存活。这些数据表明，叙利亚仓鼠对VSV的抗性至少部分由造血来源的细胞介导。
