Goldthorpe SC, Conway MJ. New insight on dengue virus-induced thrombocytopenia. Virulence. 2017;8:1492–1493
http://dx.doi.org/10.1080/21505594.2017.1368943
The article gives reference 13 instead of 12 at three places in the fourth paragraph. The correct numbering is as follows (changes in bold):
In the current study, Lin et al. (2017) suggest that DENV-envelope protein domain III (DENV-EIII) is sufficient to suppress differentiation of megakaryocytes to thrombocytes and that replication within hematopoietic precursors is not required.12 The investigators hypothesized that engagement of DENV-EIII with the cell surface would be sufficient to perturb cell signaling and the differentiation of the thrombocyte progenitors.12 Previous research has shown that DENV antigens are present on the surface of thrombocytes and that virions can enter into these cells through engagement with DC-SIGN.4,9 To test their hypothesis, the investigators confirmed that DENV-EIII could bind to megakaryocytes, and then administered DENV-EIII to a mouse model and progenitor cells from both murine bone marrow and human cord blood. Treatment with DENV-EIII reduced megakaryocyte numbers in each of these model systems.12 In order to understand how DENV-EIII suppressed megakaryopoiesis, megakaryocytic differentiation was performed using human cord blood-derived CD34+ cells. Cells treated with DENV-EIII had altered autophagy profiles and increased markers associated with apoptosis.12 Previous studies have demonstrated that altered autophagy profiles can lead to cell death of megakaryocytes.13 These data suggest that DENV-EIII alone can modulate autophagy and induce apoptosis in progenitor and mature megakaryocytes.
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