Platelet-like particles released from Ebola virus-infected megakaryocytic cells behave like virus-like particles

Ebola virus (EBOV) is likely a zoonotic and re-emerging virus that causes severe outbreaks of Ebola virus disease. The virus spreads to various tissues during the late stage of infection and has been detected in immune-privileged sites of survivors. However, the mechanism of how EBOV disseminates throughout the body is not completely elucidated. In this study, by using a biologically contained EBOVΔVP30 system, we demonstrate that a megakaryocytic-like MEG-01 cell line that stably expresses VP30 (MEG-01 VP30 cells) is susceptible to EBOVΔVP30 infection and that MEG-01 VP30 cells exposed to EBOVΔVP30 produce platelet-like particles (PLPs) that contain EBOV proteins and viral genetic material. We further found that the viral envelope glycoprotein is expressed on the surface of the produced PLPs and contributes to PLP internalization into recipient cells. In addition, viral mRNA and genome RNA are actively synthesized in these PLPs, which may lead to progeny EBOV production from recipient cells that internalize the PLPs. Taken together, our data provide new insights into the potential role of platelets in the widespread dissemination of EBOV and the pathogenesis of Ebola virus disease.

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Publication Details

Journal
PLoS Pathogens
Published
2026-02-23
DOI
https://doi.org/10.1371/journal.ppat.1013985
Primary Topic
Viral Infections and Outbreaks Research
Type
article
Field-Weighted Citation Impact
0.00

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article

Platelet-like particles released from Ebola virus-infected megakaryocytic cells behave like virus-like particles

Makoto Kuroda
PLoS Pathogens
Viral Infections and Outbreaks Research
article

Platelet-like particles released from Ebola virus-infected megakaryocytic cells behave like virus-like particles

Makoto Kuroda
article en

Abstract

Ebola virus (EBOV) is likely a zoonotic and re-emerging virus that causes severe outbreaks of Ebola virus disease. The virus spreads to various tissues during the late stage of infection and has been detected in immune-privileged sites of survivors. However, the mechanism of how EBOV disseminates throughout the body is not completely elucidated. In this study, by using a biologically contained EBOVΔVP30 system, we demonstrate that a megakaryocytic-like MEG-01 cell line that stably expresses VP30 (MEG-01 VP30 cells) is susceptible to EBOVΔVP30 infection and that MEG-01 VP30 cells exposed to EBOVΔVP30 produce platelet-like particles (PLPs) that contain EBOV proteins and viral genetic material. We further found that the viral envelope glycoprotein is expressed on the surface of the produced PLPs and contributes to PLP internalization into recipient cells. In addition, viral mRNA and genome RNA are actively synthesized in these PLPs, which may lead to progeny EBOV production from recipient cells that internalize the PLPs. Taken together, our data provide new insights into the potential role of platelets in the widespread dissemination of EBOV and the pathogenesis of Ebola virus disease.

PLoS PathogensVol. 22(2)
University of Wisconsin–Madison (US)
Office of the Vice Chancellor for Research, University of Illinois at Chicago
Openalex Percentile: Top 45%
Viral Infections and Outbreaks Research
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