Tornquist S J, Oaks J L, Crawford T B
Department of Veterinary Microbiology and Pathology, Washington State University, Pullman 99164-7040, USA.
J Gen Virol. 1997 Oct;78 ( Pt 10):2541-8. doi: 10.1099/0022-1317-78-10-2541.
Thrombocytopenia is a common finding in infection with equine infectious anaemia virus (EIAV), a lentivirus with some homology to human immunodeficiency virus (HIV). The thrombocytopenia of EIA, like that in some HIV patients, appears to have a multifactorial pathogenesis. To investigate the decreased platelet production seen in experimental EIA, the levels of three potential negative regulators of platelet production--tumour necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta) and interferon-alpha (IFN-alpha)--were measured in serum and bone marrow of six severe combined immunodeficient (SCID) foals and ten immunocompetent EIAV-infected foals. Levels of cytokines in pre-infection foal sera and bone marrow were compared with levels observed during clinical EIA. Mean serum levels of TNF-alpha and IFN-alpha were significantly higher (P < 0.05) on days -4 to 0 of thrombocytopenia than before infection. Serum TGF-beta was significantly elevated on all days except day -1 of thrombocytopenia. Bone marrow TNF-alpha levels were significantly increased in infected foals just before clinical thrombocytopenia. TGF-beta activity was not different in pre-infection and pre-thrombocytopenia bone marrows, but levels of TGF-beta protein as determined by immunohistochemical staining were significantly higher in pre-thrombocytopenia bone marrow. IFN-alpha activity in bone marrow increased just before thrombocytopenia, but the difference was not significant at P < 0.05. Serum TNF-alpha levels were 2-2.5 times higher in SCID foals on three of the days prior to thrombocytopenia than in immunocompetent foals. No significant differences were found between the levels in SCID and immunocompetent foals of serum and bone marrow TGF-beta or IFN-alpha at any of the times examined.
血小板减少症是感染马传染性贫血病毒（EIAV）时的常见表现，EIAV是一种与人类免疫缺陷病毒（HIV）有一定同源性的慢病毒。EIA的血小板减少症与一些HIV患者的情况类似，似乎具有多因素发病机制。为了研究实验性EIA中血小板生成减少的情况，在6只严重联合免疫缺陷（SCID）马驹和10只具有免疫能力的EIAV感染马驹的血清和骨髓中，检测了三种潜在的血小板生成负调节因子——肿瘤坏死因子-α（TNF-α）、转化生长因子-β（TGF-β）和干扰素-α（IFN-α）的水平。将感染前马驹血清和骨髓中的细胞因子水平与临床EIA期间观察到的水平进行比较。在血小板减少症的第-4天至第0天，TNF-α和IFN-α的平均血清水平显著高于感染前（P<0.05）。除血小板减少症第-1天外，血清TGF-β在所有天数均显著升高。在临床血小板减少症出现前，感染马驹的骨髓TNF-α水平显著升高。感染前和血小板减少症前骨髓中的TGF-β活性没有差异，但通过免疫组织化学染色测定的TGF-β蛋白水平在血小板减少症前骨髓中显著更高。骨髓中的IFN-α活性在血小板减少症出现前增加，但差异在P<0.05时不显著。在血小板减少症前的三天中，SCID马驹的血清TNF-α水平比具有免疫能力的马驹高2至2.5倍。在任何检测时间，SCID马驹和具有免疫能力的马驹的血清和骨髓TGF-β或IFN-α水平均未发现显著差异。
