Pathogenesis of cytomegalovirus infection. Distribution of viral products, immune complexes and autoimmunity during latent murine infection.
Pathogenesis of cytomegalovirus infection. Distribution of viral products, immune complexes and autoimmunity during latent murine infection.
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巨细胞病毒感染的发病机制。
DOI：
10.1099/0022-1317-33-2-267
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
M. Oldstone
中科院分区：
文献类型：
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作者：
L. Olding;D. Kingsbury;M. Oldstone
在对子宫内或出生时感染鼠巨细胞病毒（MCMV）的小鼠的病毒潜伏、重新激活和由此产生的组织损伤机制进行研究时，我们发现了三种不同的病理组的发生。在第一组中，小鼠在接触病毒后 4 周内死亡，并在身体多个组织和器官中显示出 MCMV 造成的组织损伤的证据。第二组由初次感染后幸存的小鼠组成，其中少数（约 25%）释放病毒（慢性感染）。第三组（约 75%）由无法检测到病毒脱落（潜伏感染）的小鼠组成。后一组的研究表明，通过共培养技术或通过细胞DNA-MCMV DNA杂交，在脑、胸腺、肝脏、肾脏、尿液或血清中未检测到病毒。相比之下，通过与同种异体而非同基因饲养细胞共培养，可以从脾细胞中激活病毒，并且检测到的 MCMV-DNA 数量相当于每 100 个脾细胞 3 至 4 个病毒基因组。在潜伏感染和慢性感染的小鼠中，在所有研究的品系中，都有病毒-抗病毒免疫复合物沉积在肾小球中的证据。研究的六种感染菌株（C57 Br/cdJ）中只有一种表现出自身免疫性疾病的表现，并形成针对核抗原、DNA 和可溶性核蛋白的抗体。
During studies on the mechanisms of virus latency, reactivation and resultant tissue injury in mice infected with murine cytomegalovirus (MCMV) in utero or at birth, we found the occurrence of three distinct pathological groups. In the first group, mice died within 4 weeks of exposure to virus and showed evidence of tissue injury due to MCMV in multiple tissues and organs of the body. The second group consisted of mice which survived the initial infection and was composed of a minority (about 25%) which shed virus (chronically infected). The third group (about 75%) consisted of mice in which shedding of virus could not be detected (latently infected). Study of the latter group indicated that virus was not detected in brain, thymus, liver, kidneys, urine or serum by co-cultivation techniques or by cellular DNA-MCMV DNA hybridization. In contrast, virus could be activated from spleen cells by co-cultivation with allogenic but not syngeneic feeder cells and MCMV-DNA was detected in amounts equivalent to 3 to 4 virus genomes per 100 spleen cells. In both the latently infected and chronically infected mice, in all strains studied evidence of virus-antivirus immune complex deposits in the renal glomeruli occurred. Only one of the six infected strains (C57 Br/cdJ) studied showed manifestations of autoimmune disease with the formation of antibodies to nuclear antigens, DNA and soluble nucleoprotein.