Plasma lipidome reveals critical illness and recovery from human Ebola virus disease

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  • J. E. Kyle
    Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352;
  • K. E. Burnum-Johnson
    Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352;
  • J. P. Wendler
    Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352;
  • A. J. Eisfeld
    Department of Pathobiological Sciences, University of Wisconsin–Madison, Madison, WI 53711;
  • Peter J. Halfmann
    Department of Pathobiological Sciences, University of Wisconsin–Madison, Madison, WI 53711;
  • Tokiko Watanabe
    Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 108-8639 Tokyo, Japan;
  • Foday Sahr
    34th Regimental Military Hospital at Wilberforce, Freetown, Sierra Leone;
  • R. D. Smith
    Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352;
  • Y. Kawaoka
    Department of Pathobiological Sciences, University of Wisconsin–Madison, Madison, WI 53711;
  • K. M. Waters
    Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352;
  • T. O. Metz
    Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352;

説明

<jats:p>Ebola virus disease (EVD) often leads to severe and fatal outcomes in humans with early supportive care increasing the chances of survival. Profiling the human plasma lipidome provides insight into critical illness as well as diseased states, as lipids have essential roles as membrane structural components, signaling molecules, and energy sources. Here we show that the plasma lipidomes of EVD survivors and fatalities from Sierra Leone, infected during the 2014–2016 Ebola virus outbreak, were profoundly altered. Focusing on how lipids are associated in human plasma, while factoring in the state of critical illness, we found that lipidome changes were related to EVD outcome and could identify states of disease and recovery. Specific changes in the lipidome suggested contributions from extracellular vesicles, viremia, liver dysfunction, apoptosis, autophagy, and general critical illness, and we identified possible targets for therapies enhancing EVD survival.</jats:p>

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