Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection.
<h4>Background</h4>Coronavirus disease 2019 (COVID-19) is associated with endothelial activation and coagulopathy, which may be related to pre-existing or infection-induced pro-thrombotic autoantibodies such as those targeting angiotensin II type I receptor (AT1R-Ab).<h4>Methods<...
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Public Library of Science (PLoS)
2021
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oai:doaj.org-article:3a7ec7eb35a945a696892947a1be46f42021-12-02T20:16:20ZAngiotensin II receptor I auto-antibodies following SARS-CoV-2 infection.1932-620310.1371/journal.pone.0259902https://doaj.org/article/3a7ec7eb35a945a696892947a1be46f42021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0259902https://doaj.org/toc/1932-6203<h4>Background</h4>Coronavirus disease 2019 (COVID-19) is associated with endothelial activation and coagulopathy, which may be related to pre-existing or infection-induced pro-thrombotic autoantibodies such as those targeting angiotensin II type I receptor (AT1R-Ab).<h4>Methods</h4>We compared prevalence and levels of AT1R-Ab in COVID-19 cases with mild or severe disease to age and sex matched negative controls utilizing multivariate logistic and quantile regression adjusted for comorbidities including hypertension, diabetes, and heart disease.<h4>Results</h4>There were trends toward increased prevalence (50% vs. 33%, p = 0.1) and level of AT1R-Ab (median 9.8 vs. 6.1 U/mL, p = 0.06) in all cases versus controls. When considered by COVID-19 disease severity, there was a trend toward increased prevalence of AT1R-Ab (55% vs. 31%, p = 0.07), as well as significantly higher AT1R-Ab levels (median 10.7 vs. 5.9 U/mL, p = 0.03) amongst individuals with mild COVID-19 versus matched controls. In contrast, the prevalence (42% vs. 37%, p = 0.9) and level (both medians 6.7 U/mL, p = 0.9) of AT1R-Ab amongst those with severe COVID-19 did not differ from matched controls.<h4>Conclusions</h4>These findings support an association between COVID-19 and AT1R-Ab, emphasizing that vascular pathology may be present in individuals with mild COVID-19 as well as those with severe disease.Yonghou JiangFergal DuffyJennifer HadlockAndrew RaappanaSheila StyrchakIngrid BeckFred D MastLeslie R MillerWilliam ChourJohn HouckBlair ArmisteadVenkata R DuvvuriWinnie YeungMicaela HaglundJackson WallnerJulie A WallickSamantha HardyAlyssa OldroydDaisy KoAna GervassiKim M MurrayHenry KaplanJohn D AitchisonJames R HeathD Noah SatherJason D GoldmanLisa FrenkelWhitney E HarringtonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 11, p e0259902 (2021) |
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Medicine R Science Q Yonghou Jiang Fergal Duffy Jennifer Hadlock Andrew Raappana Sheila Styrchak Ingrid Beck Fred D Mast Leslie R Miller William Chour John Houck Blair Armistead Venkata R Duvvuri Winnie Yeung Micaela Haglund Jackson Wallner Julie A Wallick Samantha Hardy Alyssa Oldroyd Daisy Ko Ana Gervassi Kim M Murray Henry Kaplan John D Aitchison James R Heath D Noah Sather Jason D Goldman Lisa Frenkel Whitney E Harrington Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection. |
description |
<h4>Background</h4>Coronavirus disease 2019 (COVID-19) is associated with endothelial activation and coagulopathy, which may be related to pre-existing or infection-induced pro-thrombotic autoantibodies such as those targeting angiotensin II type I receptor (AT1R-Ab).<h4>Methods</h4>We compared prevalence and levels of AT1R-Ab in COVID-19 cases with mild or severe disease to age and sex matched negative controls utilizing multivariate logistic and quantile regression adjusted for comorbidities including hypertension, diabetes, and heart disease.<h4>Results</h4>There were trends toward increased prevalence (50% vs. 33%, p = 0.1) and level of AT1R-Ab (median 9.8 vs. 6.1 U/mL, p = 0.06) in all cases versus controls. When considered by COVID-19 disease severity, there was a trend toward increased prevalence of AT1R-Ab (55% vs. 31%, p = 0.07), as well as significantly higher AT1R-Ab levels (median 10.7 vs. 5.9 U/mL, p = 0.03) amongst individuals with mild COVID-19 versus matched controls. In contrast, the prevalence (42% vs. 37%, p = 0.9) and level (both medians 6.7 U/mL, p = 0.9) of AT1R-Ab amongst those with severe COVID-19 did not differ from matched controls.<h4>Conclusions</h4>These findings support an association between COVID-19 and AT1R-Ab, emphasizing that vascular pathology may be present in individuals with mild COVID-19 as well as those with severe disease. |
format |
article |
author |
Yonghou Jiang Fergal Duffy Jennifer Hadlock Andrew Raappana Sheila Styrchak Ingrid Beck Fred D Mast Leslie R Miller William Chour John Houck Blair Armistead Venkata R Duvvuri Winnie Yeung Micaela Haglund Jackson Wallner Julie A Wallick Samantha Hardy Alyssa Oldroyd Daisy Ko Ana Gervassi Kim M Murray Henry Kaplan John D Aitchison James R Heath D Noah Sather Jason D Goldman Lisa Frenkel Whitney E Harrington |
author_facet |
Yonghou Jiang Fergal Duffy Jennifer Hadlock Andrew Raappana Sheila Styrchak Ingrid Beck Fred D Mast Leslie R Miller William Chour John Houck Blair Armistead Venkata R Duvvuri Winnie Yeung Micaela Haglund Jackson Wallner Julie A Wallick Samantha Hardy Alyssa Oldroyd Daisy Ko Ana Gervassi Kim M Murray Henry Kaplan John D Aitchison James R Heath D Noah Sather Jason D Goldman Lisa Frenkel Whitney E Harrington |
author_sort |
Yonghou Jiang |
title |
Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection. |
title_short |
Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection. |
title_full |
Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection. |
title_fullStr |
Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection. |
title_full_unstemmed |
Angiotensin II receptor I auto-antibodies following SARS-CoV-2 infection. |
title_sort |
angiotensin ii receptor i auto-antibodies following sars-cov-2 infection. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2021 |
url |
https://doaj.org/article/3a7ec7eb35a945a696892947a1be46f4 |
work_keys_str_mv |
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