Russell K E, Perkins P C, Hoffman M R, Miller R T, Walker K M, Fuller F J, Sellon D C
College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.
Virology. 1999 Jun 20;259(1):7-19. doi: 10.1006/viro.1999.9737.
Thrombocytopenia is a consistent finding and one of the earliest hematological abnormalities in horses acutely infected with equine infectious anemia virus (EIAV), a lentivirus closely related to human immunodeficiency virus. Multifactorial mechanisms, including immune-mediated platelet destruction and impaired platelet production, are implicated in the pathogenesis of EIAV-associated thrombocytopenia. This study was undertaken to investigate whether regenerative thrombopoiesis and platelet destruction occurred in ponies acutely infected with EIAV. Circulating large, immature platelets were increased in ponies acutely infected with EIAV late in the infection when platelet count was at a nadir. Morphometric analysis of bone marrow from acutely infected ponies revealed significant increased in megakaryocyte area and megakaryocyte nuclear area. A trend toward increased numbers of megakaryocytes was also observed. Platelets from acutely infected ponies had increased surface-bound fibrinogen and ultrastructural changes consistent with in vivo platelet activation. Platelets also had hypofunctional aggregation responses to three agonists in vitro. We conclude that thrombocytopenia in ponies acutely infected with EIAV is regenerative and suggest that bone marrow platelet production is not severely compromised in these ponies. Our findings reveal that in vivo platelet activation occurs in ponies acutely infected with EIAV, and as a result platelets are hypofunctional in vitro. Activation of platelets in vivo may cause platelet degranulation or formation of platelet aggregates, which would result in removal of these damages platelets from circulation. This may represent a form of nonimmune-mediated platelet destruction in ponies acutely infected with EIAV.
血小板减少是感染马传染性贫血病毒（EIAV）的急性感染马的常见表现，也是最早出现的血液学异常之一。EIAV是一种与人类免疫缺陷病毒密切相关的慢病毒。包括免疫介导的血小板破坏和血小板生成受损在内的多因素机制与EIAV相关血小板减少的发病机制有关。本研究旨在调查急性感染EIAV的小马是否发生再生性血小板生成和血小板破坏。在感染后期血小板计数处于最低点时，急性感染EIAV的小马循环中的大的未成熟血小板数量增加。对急性感染小马的骨髓进行形态计量分析显示，巨核细胞面积和巨核细胞核面积显著增加。还观察到巨核细胞数量有增加的趋势。急性感染小马的血小板表面结合的纤维蛋白原增加，超微结构变化与体内血小板活化一致。血小板在体外对三种激动剂的聚集反应功能减退。我们得出结论，急性感染EIAV的小马的血小板减少是再生性的，表明这些小马的骨髓血小板生成没有受到严重损害。我们的研究结果表明，急性感染EIAV的小马体内发生血小板活化，结果导致血小板在体外功能减退。体内血小板活化可能导致血小板脱颗粒或形成血小板聚集体，这将导致这些受损血小板从循环中清除。这可能代表急性感染EIAV的小马非免疫介导的血小板破坏形式。
