Model of dengue-mediated platelet IL-1β synthesis and release. (A) Model proposes that platelets in healthy state have relatively modest levels of the components of the inflammasome and caspase 1 activity, and limited messenger RNA (mRNA) translation into protein. The low level of translation may be due to microRNA (miRNA) inhibition of translation and/or low mRNA levels. (B) DV induces in vivo platelet translation of mRNA into IL-1β. DV mediates inflammasome-mediated caspase 1 activation, enabling processing into active IL-1β with subsequent release into MVs for systemic transport. Activated platelets also release RNA in vesicles. Because DV replication involves silencing host miRNA production, megakaryocytes may deliver less miRNA for inhibiting platelet mRNA translation, or DV could compete with endogenous miRNAs. In addition, DV may induce increased megakaryocyte delivery of IL-1β mRNA to the platelet. Dashed lines indicate the uncertainty of the early events in the model.

Model of dengue-mediated platelet IL-1β synthesis and release. (A) Model proposes that platelets in healthy state have relatively modest levels of the components of the inflammasome and caspase 1 activity, and limited messenger RNA (mRNA) translation into protein. The low level of translation may be due to microRNA (miRNA) inhibition of translation and/or low mRNA levels. (B) DV induces in vivo platelet translation of mRNA into IL-1β. DV mediates inflammasome-mediated caspase 1 activation, enabling processing into active IL-1β with subsequent release into MVs for systemic transport. Activated platelets also release RNA in vesicles. Because DV replication involves silencing host miRNA production, megakaryocytes may deliver less miRNA for inhibiting platelet mRNA translation, or DV could compete with endogenous miRNAs. In addition, DV may induce increased megakaryocyte delivery of IL-1β mRNA to the platelet. Dashed lines indicate the uncertainty of the early events in the model.

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