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Vascular Disease and Thrombosis in SARS-CoV-2-Infected Rhesus Macaques.

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Affiliations

  • 1. Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
      Authors
    • Aid M 1
    • Vidal SJ 1
    • Chandrashekar A 1
    • Patel S 1
    • Stephenson K 1
    (5 authors)
  • 2. Oregon Health & Sciences University, Beaverton, OR 97006, USA.
      Authors
    • Busman-Sahay K 2
    • Bondoc S 2
    • Starke C 2
    • Terry M 2
    • Estes JD 2
    (5 authors)
  • 3. Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
      Authors
    • Maliga Z 3
    • Jacobson CA 3
    • Sorger PK 3
    (3 authors)
  • 4. Tufts University Cummings School of Veterinary Medicine, North Grafton, MA 01536, USA.
      Authors
    • Wrijil L 4
    • Ducat S 4
    (2 authors)
  • 5. Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
      Authors
    • Brook OR 5
    (1 author)
    • Show all (13)

ORCIDs linked to this article

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Cell, 09 Oct 2020, 183(5):1354-1366.e13
https://doi.org/10.1016/j.cell.2020.10.005 PMID: 33065030 PMCID: PMC7546181

This article is in the Europe PMC Open access subset. Refer to the copyright information in the article for licensing details.
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Abstract 

The COVID-19 pandemic has led to extensive morbidity and mortality throughout the world. Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details underlying these processes remain to be determined. In this study, we demonstrate endothelial disruption and vascular thrombosis in histopathologic sections of lungs from both humans and rhesus macaques infected with SARS-CoV-2. To define key molecular pathways associated with SARS-CoV-2 pathogenesis in macaques, we performed transcriptomic analyses of bronchoalveolar lavage and peripheral blood and proteomic analyses of serum. We observed macrophage infiltrates in lung and upregulation of macrophage, complement, platelet activation, thrombosis, and proinflammatory markers, including C-reactive protein, MX1, IL-6, IL-1, IL-8, TNFα, and NF-κB. These results suggest a model in which critical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2-induced vascular disease. Our findings suggest potential therapeutic targets for COVID-19.

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Read article at publisher's site: https://doi.org/10.1016/j.cell.2020.10.005

Read article for free, from open access legal sources, via Unpaywall: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7546181Unpaywall

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    Funding 

    Funders who supported this work.

    NCI NIH HHS (2)

    • Grant ID: U54 CA225088

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    • Grant ID: U01 CA260476

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    NIAID NIH HHS (8)

    • Grant ID: R01 AI149670

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    • Grant ID: UM1 AI126603

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    • Grant ID: R01 AI129797

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    • Grant ID: T32 AI007387

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    • Grant ID: U24 AI118672

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    • Grant ID: UM1 AI124377

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    • Grant ID: K08 AI135098

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    • Grant ID: U19 AI128751

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    NIH HHS (5)

    • Grant ID: P51 OD011132

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    • Grant ID: R01 OD024917

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    • Grant ID: S10 OD025002

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    • Grant ID: P51 OD011092

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    • Grant ID: S10 OD026799

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    NIH Office of the Director

      National Cancer Institute

        National Institute of Allergy and Infectious Diseases

          Ragon Institute of MGH, MIT and Harvard

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