Suppressive effect of dengue virus envelope protein domain III on megakaryopoiesis

Guan Ling Lin, Hsin Hou Chang, Te Sheng Lien, Po Kong Chen, Hao Chan, Mei Tzu Su, Chi Yuan Liao, Der Shan Sun

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Dengue virus (DENV) infection can cause severe, life-threatening events, and no specific treatments of DENV infection are currently approved. Although thrombocytopenia is frequently observed in dengue patients, its pathogenesis is still not fully understood. Previous studies have suggested that DENV-induced thrombocytopenia occurs through viral-replication-mediated megakaryopoiesis inhibition in the bone marrow; however, the exact mechanism for megakaryopoiesis suppression remains elusive. In this study, a reductionist approach was applied, in which C57B/6J mice were inoculated with recombinant DENV-envelope protein domain III (DENV-EIII) instead of the full viral particle. Our results demonstrated that DENV-EIII-suppressed megakaryopoiesis is similar to those observed with DENV infection. Furthermore, in agreement with our in vivo analyses, DENV-EIII sufficiently suppressed the megakaryopoiesis of progenitor cells from murine bone marrow and human cord blood in vitro. Additional analyses suggested that autophagy impairment and apoptosis are involved in DENV-EIII-mediated suppression of megakaryopoiesis. These data suggest that, even without viral replication, the binding of DENV-EIII to the cell surface is sufficient to suppress megakaryopoiesis.

Original languageEnglish
Pages (from-to)1719-1731
Number of pages13
JournalVirulence
Volume8
Issue number8
DOIs
Publication statusPublished - 2017 Nov 17
Externally publishedYes

Keywords

  • apoptosis
  • autophagy
  • dengue virus
  • envelop protein domain III
  • megakaryocytic differentiation
  • megakaryopoiesis
  • thrombocytopenia

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

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