Mutter W, Reddehase M J, Busch F W, Bühring H J, Koszinowski U H
Federal Research Centre for Virus Diseases of Animals, Tübingen, Federal Republic of Germany.
J Exp Med. 1988 May 1;167(5):1645-58. doi: 10.1084/jem.167.5.1645.
We have shown in a murine model system for cytomegalovirus (CMV) disease in the immunocompromised host that CMV infection interferes with the earliest detectable step in hemopoiesis, the generation of the stem cell CFU-S-I, and thereby prevents the autoreconstitution of bone marrow after sublethal irradiation. The antihemopoietic effect could not be ascribed to a direct infection of stem cells. The failure in hemopoiesis was prevented by adoptive transfer of antiviral CD8+ T lymphocytes and could be overcome by syngeneic bone marrow transplantation. CD8+ T lymphocytes and bone marrow cells both mediated survival, although only CD8+ T lymphocytes were able to limit virus multiplication in host tissues. We concluded that not the cytopathic effect of virus replication in host tissues, but the failure in hemopoiesis, is the primary cause of death in murine CMV disease.
我们在免疫功能低下宿主的巨细胞病毒(CMV)疾病小鼠模型系统中表明,CMV感染会干扰造血过程中最早可检测到的步骤,即干细胞CFU-S-I的生成,从而阻止亚致死剂量照射后骨髓的自身重建。抗造血作用不能归因于干细胞的直接感染。抗病毒CD8 + T淋巴细胞的过继转移可预防造血功能衰竭,同基因骨髓移植可克服这一问题。CD8 + T淋巴细胞和骨髓细胞都介导了存活,尽管只有CD8 + T淋巴细胞能够限制病毒在宿主组织中的增殖。我们得出结论,小鼠CMV疾病死亡的主要原因不是病毒在宿主组织中复制的细胞病变效应,而是造血功能衰竭。