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Veterinary Pathology, Vol 34, Issue 2 97-107, Copyright © 1997 by American College of Veterinary Pathologists

ARTICLES

African swine fever virus infection of bone marrow: lesions and pathogenesis

J. C. Gomez-Villamandos, M. J. Bautista, L. Carrasco, M. J. Caballero, J. Hervas, C. J. Villeda, P. J. Wilkinson and M. A. Sierra
Departamento Anatomia y Anatomia Patologica, Facultad de Veterinaria, Universidad de Cordoba, Spain.

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.
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C. Rodriguez-Carino and J. Segales
Ultrastructural Findings in Lymph Nodes from Pigs Suffering from Naturally Occurring Postweaning Multisystemic Wasting Syndrome
Vet. Pathol., July 1, 2009; 46(4): 729 - 735.
[Abstract] [Full Text] [PDF]


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