Narayan O, Zink M C, Gorrell M, McEntee M, Sharma D, Adams R
Division of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
J Rheumatol Suppl. 1992 Jan;32:25-32; discussion 32-4.
Retroviral arthritis in sheep and goats depends on persistent infection in the animals. Virus is latent in macrophage precursor cells and viral replication is initiated when these cells are induced to differentiate. Antiviral antibodies and cytokines modulate the efficiency of viral gene product expression. Specific cytokines induced during replication of the lentivirus in mononuclear cells are also responsible for directing infected cells from peripheral blood through the vascular endothelium to particular tissues. Cytokines induced by other infectious agents such as bacteria, mycoplasma or protozoa, may also contribute to this chemotactic process. Once in the tissue, macrophages interact with lymphocytes to induce an inflammatory cascade with further production of cytokines which enhances expression of class II major histocompatibility complex antigens and proliferation of B and CD8 lymphocytes. In addition, immune complexes between viral glycoproteins and immunoglobulins are produced locally and probably lead to further enhancement of pathological changes in the tissues.
绵羊和山羊的逆转录病毒关节炎取决于动物体内的持续感染。病毒潜伏在巨噬细胞前体细胞中，当这些细胞被诱导分化时，病毒复制就会开始。抗病毒抗体和细胞因子调节病毒基因产物表达的效率。慢病毒在单核细胞复制过程中诱导产生的特定细胞因子，也负责将外周血中的感染细胞通过血管内皮引导至特定组织。由其他感染因子如细菌、支原体或原生动物诱导产生的细胞因子，也可能参与这一趋化过程。一旦进入组织，巨噬细胞与淋巴细胞相互作用，引发炎症级联反应，进一步产生细胞因子，从而增强II类主要组织相容性复合体抗原的表达以及B淋巴细胞和CD8淋巴细胞的增殖。此外，病毒糖蛋白与免疫球蛋白之间的免疫复合物在局部产生，可能会进一步加剧组织中的病理变化。
