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      Treating the Host Response to Ebola Virus Disease with Generic Statins and Angiotensin Receptor Blockers

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          ABSTRACT

          Treatments targeting the Ebola virus may eventually be shown to work, but they will not have an impact on overall Ebola mortality in West Africa. Endothelial dysfunction is responsible for the fluid and electrolyte imbalances seen in Ebola patients. Because inexpensive generic statins and angiotensin receptor blockers restore endothelial barrier integrity, they can be used to treat the host response in these patients. In Sierra Leone, approximately 100 Ebola patients were treated with this combination, and reports indicate that survival was greatly improved.

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          Endothelial barrier dysfunction in septic shock.

          S M Opal, T van der Poll (2015)
          The endothelium provides an essential and selective membrane barrier that regulates the movement of water, solutes, gases, macromolecules and the cellular elements of the blood from the tissue compartment in health and disease. Its structure and continuous function is essential for life for all vertebrate organisms. Recent evidence indicates that the endothelial surface does not have a passive role in systemic inflammatory states such as septic shock. In fact, endothelial cells are in dynamic equilibrium with a myriad of inflammatory mediators and elements of the innate immune and coagulation systems to orchestrate the host response in sepsis. The barrier function of the endothelial surface is almost uniformly impaired in septic shock, and it is likely that this contributes to adverse outcomes. In this review, we will highlight recent advances in the understanding of the signalling events that regulate endothelial function and molecular events that induce endothelial dysfunction in sepsis. Endothelial barrier repair strategies as a treatment for sepsis include modulation of C5a, high-mobility group box 1 and VEGF receptor 2; stimulation of angiopoietin-1, sphingosine 1 phosphate receptor 1 and Slit; and a number of other innovative approaches.
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            Host genetic diversity enables Ebola hemorrhagic fever pathogenesis and resistance.

            Martin Ferris, Atsushi Okumura, Heinz Feldmann … (2014)
            Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation nor death from shock, thus restricting pathogenesis studies to nonhuman primates. Here we show that mice from the Collaborative Cross panel of recombinant inbred mice exhibit distinct disease phenotypes after mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, probably mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever. Copyright © 2014, American Association for the Advancement of Science.
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              Clinical care of two patients with Ebola virus disease in the United States.

              G Marshall Lyon, Aneesh Mehta, Jay B Varkey … (2014)
              West Africa is currently experiencing the largest outbreak of Ebola virus disease (EVD) in history. Two patients with EVD were transferred from Liberia to our hospital in the United States for ongoing care. Malaria had also been diagnosed in one patient, who was treated for it early in the course of EVD. The two patients had substantial intravascular volume depletion and marked electrolyte abnormalities. We undertook aggressive supportive measures of hydration (typically, 3 to 5 liters of intravenous fluids per day early in the course of care) and electrolyte correction. As the patients' condition improved clinically, there was a concomitant decline in the amount of virus detected in plasma.
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                Author and article information

                Journal
                Journal ID (nlm-ta): mBio
                Journal ID (iso-abbrev): MBio
                Journal ID (hwp): mbio
                Journal ID (pmc): mbio
                Journal ID (publisher-id): mBio
                Title: mBio
                Publisher: American Society of Microbiology (1752 N St., N.W., Washington, DC )
                ISSN (Electronic): 2150-7511
                Publication date (Electronic): 23 June 2015
                Publication date Collection: May-Jun 2015
                Volume: 6
                Issue: 3
                Electronic Location Identifier: e00716-15
                Affiliations
                [ a ]Retired Physician, Sergy Haut, France
                [ b ]University of Illinois College of Medicine, Chicago, Illinois, USA
                [ c ]Practicing Physician, Trondheim, Norway
                [ d ]Alpert Medical School, Brown University, Providence, Rhode Island, USA
                Author notes
                Address correspondence to David S. Fedson, dfedson@ 123456wanadoo.fr .
                Article
                Publisher ID: mBio00716-15
                DOI: 10.1128/mBio.00716-15
                PMC ID: 4479704
                PubMed ID: 26106080
                SO-VID: 13fa7a87-77d4-4aaa-bdda-419d8cec0f30
                Copyright © Copyright © 2015 Fedson et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license, which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Page count
                supplementary-material: 0, Figures: 0, Tables: 0, Equations: 0, References: 25, Pages: 4, Words: 4093
                Categories
                Subject: Opinion/Hypothesis
                Custom metadata
                cover-date May/June 2015

                ScienceOpen disciplines: Life sciences
                Data availability:
                ScienceOpen disciplines: Life sciences

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