Teo H K, Price P, Papadimitriou J M
Department of Microbiology, University of Western Australia, Nedlands.
Int J Exp Pathol. 1991 Feb;72(1):67-82.
BALB/c and CBA mice maintained on low (4%) or normal (18%) protein diets for 2 weeks after weaning were infected with a sublethal dose of murine cytomegalovirus, adjusted in proportion to body weight. Viral replication, histopathological changes and humoral responses to the virus were compared between the dietary groups 2-42 days post infection (p.i.). Higher numbers of viral antigen-positive cells and/or more prominent tissue necrosis were noted in the livers, spleens, hearts, adrenal glands, kidneys and bone marrows of infected protein-deficient mice. These mice also showed a delayed onset of leucocytic exudation in their livers and salivary glands, relative to infected mice on the normal diet. Second peaks of viral replication were detected by plaque assays in livers and spleens from protein-deficient mice and in livers from normal mice 12-18 days p.i., but few antigen-positive cells and no tissue necrosis were observed. Virus also persisted at higher titres in the salivary glands from protein-deficient mice. Although cellular immunity may be defective in these mice, humoral IgG and IgM responses to the virus were not inhibited. The influence of genetic factors on the pathogenesis of murine cytomegalovirus disease in protein-deficient mice is discussed.
断奶后以低蛋白（4%）或正常蛋白（18%）饮食维持2周的BALB/c和CBA小鼠，用与体重成比例调整的亚致死剂量鼠巨细胞病毒感染。在感染后（p.i.）2 - 42天比较各饮食组之间的病毒复制、组织病理学变化以及对该病毒的体液反应。在感染的蛋白质缺乏小鼠的肝脏、脾脏、心脏、肾上腺、肾脏和骨髓中，观察到更多数量的病毒抗原阳性细胞和/或更明显的组织坏死。相对于正常饮食的感染小鼠，这些小鼠肝脏和唾液腺中白细胞渗出的起始也延迟。通过噬斑测定在蛋白质缺乏小鼠的肝脏和脾脏以及正常小鼠肝脏中于感染后12 - 18天检测到病毒复制的第二个峰值，但观察到很少的抗原阳性细胞且无组织坏死。病毒在蛋白质缺乏小鼠的唾液腺中也以更高滴度持续存在。尽管这些小鼠的细胞免疫可能存在缺陷，但对该病毒的体液IgG和IgM反应未受抑制。讨论了遗传因素对蛋白质缺乏小鼠中鼠巨细胞病毒病发病机制的影响。
