Gómez-Villamandos J C, Bautista M J, Carrasco L, Caballero M J, Hervás J, Villeda C J, Wilkinson P J, Sierra M A
Departamento Anatomía y Anatomía Patológica, Facultad de Veterinaria, Universidad de Córdoba, Spain.
Vet Pathol. 1997 Mar;34(2):97-107. doi: 10.1177/030098589703400202.
The effects of African swine fever (ASF) virus infection on bone marrow hematopoiesis and microenvironment were determined by studying the sequential development of ultrastructural lesions of bone marrow and blood cell changes. Eight pigs (two pigs/infected group) were inoculated by intramuscular route with 10(5) 50% hemadsorbing doses (HAD50) of the Malawi'83 ASF virus isolate. Two uninfected pigs were used as controls. Ultrastructural changes developed by day 3 postinoculation (PI), persisted through day 7 PI, and were characterized by activation of macrophages. From day 5 PI, viral replication was observed in monocytes/macrophages, reticular cells, immature neutrophils, and promonocytes. Also viral replication was detected in megakaryocytes, endothelial cells, and pericytes at day 7 PI. Vascular alterations consisted of activation of sinusoidal endothelial cells, intravascular coagulation, and fibrin strands interspersed among microenvironment and hematopoietic cells. No significant changes were observed in total white blood cells counts, percentage of monocytes, and platelet counts; however, severe lymphopenia and neutrophilia were detected from day 3 PI. Results of this experiment indicate that there is increased hematopoiesis in bone marrow during acute ASF, coinciding with macrophage activation. Neither vascular changes nor viral replication in different bone marrow cell populations gave rise to impaired bone marrow function. Increased hematopoiesis would exert a positive influence by preventing the early onset of thrombocytopenia and would exert a negative influence by stimulating the spread of the virus via neutrophils. Increased hematopoiesis would be unable to compensate for the lymphopenia.
通过研究骨髓超微结构病变的连续发展和血细胞变化，确定非洲猪瘟（ASF）病毒感染对骨髓造血和微环境的影响。八头猪（每组两头感染猪）通过肌肉注射途径接种10(5) 50%血细胞吸附剂量（HAD50）的马拉维83株ASF病毒分离株。两头未感染的猪用作对照。接种后第3天出现超微结构变化，持续至接种后第7天，其特征为巨噬细胞活化。从接种后第5天起，在单核细胞/巨噬细胞、网状细胞、未成熟中性粒细胞和原单核细胞中观察到病毒复制。在接种后第7天，巨核细胞、内皮细胞和周细胞中也检测到病毒复制。血管改变包括窦状内皮细胞活化、血管内凝血以及散布在微环境和造血细胞之间的纤维蛋白丝。全白细胞计数、单核细胞百分比和血小板计数未观察到显著变化；然而，从接种后第3天起检测到严重淋巴细胞减少和中性粒细胞增多。本实验结果表明，急性ASF期间骨髓造血增加，与巨噬细胞活化同时发生。不同骨髓细胞群体中的血管变化和病毒复制均未导致骨髓功能受损。造血增加会通过预防血小板减少的早期发作产生积极影响，同时会通过刺激病毒经中性粒细胞传播产生消极影响。造血增加无法弥补淋巴细胞减少。
