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猪繁殖与呼吸综合征病毒感染骨髓:病变与发病机制。

Porcine reproductive and respiratory syndrome virus infection of bone marrow: Lesions and pathogenesis.

机构信息

State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China; Department of Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, USA.

State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China.

出版信息

Virus Res. 2019 May;265:20-29. doi: 10.1016/j.virusres.2019.02.019. Epub 2019 Mar 1.

DOI:10.1016/j.virusres.2019.02.019
PMID:30831176
Abstract

Red bone marrow is physiologically unique in that it is both the major hematopoietic organ and a primary lymphoid organ. Porcine reproductive and respiratory syndrome virus (PRRSV) affects normal bone marrow functions. The cumulative effect of PRRSV infection is acute bone marrow failure, i.e., hypoplasia characterized by the absence of normal myeloid and erythroid precursors and increased red bone marrow M:E ratios. The measurable clinical consequence of PRRSV infection on normal red bone marrow functions is a reduction in the number of cells emigrating to the peripheral blood resulting in leucopenia, anemia, and thrombocytopenia. These observations may be explained by the fact that bone marrow-derived mononuclear cells, i.e., imDCs, mDCs, monocytes, macrophages, and myeloid precursor cells are susceptible to PRRSV. Apoptosis in bone marrow-derived cells occurs both as a direct consequence of infection and indirectly via a bystander effect. Immunologically, PRRSV-susceptible mononuclear cells are the first line of defense against microbial infection and responsible for antigen recognition, processing, and presentation to T and B cells; a critical step in the initiation and development of an effective adaptive immune. Thus, impairment of normal immune function renders the host less able to resist and/or eliminate secondary infectious agents and partially explains the synergy between PRRSV and bacterial and viral co-infections.

摘要

红骨髓在生理学上是独一无二的,它既是主要的造血器官,也是主要的淋巴器官。猪繁殖与呼吸综合征病毒(PRRSV)会影响正常的骨髓功能。PRRSV 感染的累积效应是急性骨髓衰竭,即表现为正常髓系和红系前体缺失以及红骨髓 M:E 比值增加的骨髓发育不良。PRRSV 感染对正常红骨髓功能的可测量临床后果是向外周血迁移的细胞数量减少,导致白细胞减少、贫血和血小板减少。这些观察结果可能是由于骨髓来源的单核细胞,即未成熟树突状细胞(imDCs)、成熟树突状细胞(mDCs)、单核细胞、巨噬细胞和髓系前体细胞易受 PRRSV 感染所致。骨髓来源细胞的凋亡既可以是感染的直接后果,也可以通过旁观者效应间接发生。从免疫学角度来看,PRRSV 易感单核细胞是抵御微生物感染的第一道防线,负责抗原识别、加工和呈递给 T 细胞和 B 细胞;这是启动和发展有效适应性免疫的关键步骤。因此,正常免疫功能的损害使宿主更难以抵抗和/或消除继发性感染因子,并部分解释了 PRRSV 与细菌和病毒合并感染的协同作用。

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