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Abstract
The pathogenesis of cytomegalovirus-induced thrombocytopenia in neonatal cytomegalic
inclusion disease is obscure, and the phenomenon has not previously been described
in cytomegalovirus infections of other species. In these studies, 4-week-old HA-ICR
female mice were infected intraperitoneally with 105.0 plaque-forming units of murine cytomegalovirus (MCMV) and their hemograms were serially
determined over the succeeding 14 days. Mice infected similarly were killed on appropriate
days for histopathologic and fluorescent microscopic study of their spleens. Significant
thrombocytopenia occurred uniformly on the fourth day of infection. This was correlated
with distinctive histopathologic changes in megakaryocytes which included cytoplasmic
and intranuclear vacuolization, and appearance of markedly basophilic megakaryocytes
in large number suggesting increased turnover. Direct immunofluorescent staining for
MCMV antigen in the spleen, using hyperimmune anti-MCMV serum, revealed positive megakaryocytic
fluorescence. The pathologic alterations in the bone marrow gradually reverted to
normal between Days 7 and 14, concomitant with a return toward normal control levels
of circulating platelets. Decreased platelet production due to megakaryocytic infection
by MCMV is suggested as the mechanism of the observed thrombocytopenia. The MCMV model
appears useful for the further exploration of pathogenetic mechanisms of virus-induced
thrombocytopenia.
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Article info
Publication history
Accepted:
September 29,
1972
Received:
March 21,
1972
Footnotes
☆Supported by United States Public Health Service Research Grants AI-09095 and AM-11879.
☆☆Presented in part before the Society for Pediatric Research, Atlantic City, May, 1971.
Identification
Copyright
© 1973 Published by Elsevier Inc.
