Why the study?
Does equine infectious anemia virus infection alter bone marrow megakaryocyte density and size in normal and SCID foals?
Does equine infectious anemia virus infection alter bone marrow megakaryocyte density and size in normal and SCID foals?
The lack of compensatory megakaryocytopoiesis in both SCID and normal foals suggests that altered platelet production, independent of immune-specific responses, plays a role in EIAV-induced thrombocytopenia.
Findings do not support compensatory megakaryocytopoiesis in EIAV thrombocytopenia; leaves open non-immune mechanisms in equine models.
Morphometric evaluation of bone marrow core biopsies was used to determine megakaryocyte (MK) numbers and MK size in nine foals with equine infectious anemia virus (EIAV)-induced thrombocytopenia. Both immunocompetent normal foals and foals with severe combined immunodeficiency (SCID) were used. Platelet counts were made three times weekly following viral infection. Bone marrow core biopsies were taken from the ilium of each foal prior to experimental infection, immediately after the onset of thrombocytopenia, and at necropsy. All foals developed thrombocytopenia by 23 days postinfection. The bone marrow MK density did not change in response to the thrombocytopenia. MK area did not change significantly; however, the MK nuclear area at necropsy was significantly higher than that preinfection. The presence of thrombocytopenia in the SCID foals showed that immune-specific responses were not required for the production of EIAV-induced thrombocytopenia. Furthermore, the lack of a compensatory megakaryocytopoiesis in both SCID and normal foals was consistent with the theory that altered platelet production plays a role in the development of this thrombocytopenia.
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Wardrop et al. (1996) studied this question.
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