
Dengue 2 virus inhibits in vitro megakaryocytic colony formation and induces apoptosis in thrombopoietin‐inducible megakaryocytic differentiation from cord blood CD34+ cells
Author(s) -
Basu Atanu,
Jain Preksha,
Gangodkar Shobha V.,
Shetty Shrimati,
Ghosh Kanjaksha
Publication year - 2008
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2008.00399.x
Subject(s) - thrombopoietin , biology , dengue virus , virology , dengue fever , megakaryocyte , flavivirus , cord blood , virus , progenitor cell , immunology , stem cell , haematopoiesis , microbiology and biotechnology
Thrombocytopenia is frequently associated with dengue virus infection in humans. Although antiplatelet immunopathogenic processes have been implicated in the origin of dengue‐associated thrombocytopenia, the effect of dengue viruses on megakaryocyte differentiation remains incompletely understood. In this study, we examined the effect of human dengue 2 virus isolates on the in vitro growth and differentiation of thrombopoietin‐induced megakaryopoiesis of cord blood CD34+ cells. Dengue 2 viruses, but not Japanese encephalitis virus, showed a dose‐dependent inhibition of CFU‐Mk. Viral antigens could be detected by an immunohistochemical technique in 3–5% of the early megakaryocytic progenitors by the 5th postexposure day in liquid cultures with cell loss, increased annexin V binding and active caspase‐3 expression. In summary, dengue 2 viruses can inhibit in vitro megakaryopoiesis, as well as infect and induce apoptotic cell death in a subpopulation of early megakaryocytic progenitors. These events might contribute towards the origin of thrombocytopenia in dengue disease.