Vascular Disease and Thrombosis in SARS-CoV-2-Infected Rhesus Macaques
Open accessAbstract
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.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Ineffective IFN innate immunity is strongly associated with failure to control primary SARS-CoV-2 infection and high risk of fatal COVID-19, accompanied by innate cell immunopathology and elevated CXCL10, IL-6, and IL-8.
“Ineffective IFN innate immunity has been strongly associated with failure to control a primary SARS-CoV-2 infection and a high risk of fatal COVID-19, accompanied by innate cell immunopathology and a plasma cytokine signature of elevated CXCL10, interleukin (IL)-6, and IL-8 in many studies (Aid et al., 2020; Kuri-Cervantes et al., 2020; Li et al., 2020b; Lucas et al., 2020; Radermecker et al., 202”
From Adaptive immunity to SARS-CoV-2 and COVID-19 (2021) · cites this paper as Aid et al., 2020
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 55 · Cited by 215
- Authors
- Aid, M., Busman-Sahay, K., Vidal, S. J., Maliga, Z., Bondoc, S., Starke, C., Terry, M., Jacobson, C. A., Wrijil, L., Ducat, S., Brook, O. R., Miller, A. D., Porto, M., Pellegrini, K. L., Pino, M., Hoang, T. N., Chandrashekar, A., Patel, S., Stephenson, K., Bosinger, S. E., Andersen, H., Lewis, M. G., Hecht, J. L., Sorger, P. K., Martinot, A. J., Estes, J. D., & Barouch, D. H.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Harvard University (US)
- Oregon Health & Science University (US)
- Tufts University (US)
- Cornell University (US)
- Bioqual (US)
- Emory University (US)
- Corresponding author
- Barouch, Dan H.
- ORCID
- Vidal, Samuel J.
- Maliga, Zoltan
- Bondoc, Stephen
- Starke, Carly
- Terry, Margaret
- Jacobson, Connor A.
- Wrijil, Linda
- Ducat, Sarah
- Brook, Olga R.
- Miller, Andrew D.
- Porto, Maciel
- Pellegrini, Kathryn L.
- Hoang, Timothy N.
- Chandrashekar, Abishek
- Patel, Shivani
- Stephenson, Kathryn
- Bosinger, Steven E.
- Lewis, Mark G.
- Hecht, Jonathan L.
- Sorger, Peter K.
- Martinot, Amanda J.
- Estes, Jacob D.
- Barouch, Dan H.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 183
- Issue
- 5
- Pages
- 1354-1366.e13
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC7546181
- OpenAlex
- W3092357584
- Cited by
- 215
- References
- 55
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 15 · 2023: 35 · 2022: 62 · 2021: 77 · 2020: 12
- FWCI
- 6.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ImmPort
- Funders
- NIH Office of the Director
- National Cancer Institute
- National Institute of Allergy and Infectious Diseases
- Ragon Institute of MGH, MIT and Harvard
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Keywords
- SARS-CoV-2, COVID-19 pandemic, thrombosis, vascular disease, endothelial disruption, rhesus monkeys, lung histopathology, macrophage infiltration, inflammation, complement system, platelet activation, inflammatory cytokines, NF-κB, therapeutic target
- MeSH terms
- COVID-19, SARS-CoV-2, Aged, 80 and over, Animals, C-Reactive Protein, Complement Activation, Female, Humans, Inflammation, Lung, Macaca mulatta, Macrophages, Male, Thrombosis, Vascular Diseases, Platelet Activation, Cytokines, Bronchoalveolar Lavage, Transcriptome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
