Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis

Inflammatory responses to the novel coronavirus SARS-CoV-2, which causes COVID-19, range from asymptomatic to severe. Here we present a follow-up analysis of a longitudinal study characterizing COVID-19 immune responses from a father and son with distinctly different clinical courses. The father req...

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Main Authors: Melissa A. Hausburg, Kaysie L. Banton, Michael Roshon, David Bar-Or
Format: Article
Language:English
Published: Elsevier 2021-01-01
Series:Heliyon
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2405844020327195
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author Melissa A. Hausburg
Kaysie L. Banton
Michael Roshon
David Bar-Or
author_facet Melissa A. Hausburg
Kaysie L. Banton
Michael Roshon
David Bar-Or
author_sort Melissa A. Hausburg
collection DOAJ
description Inflammatory responses to the novel coronavirus SARS-CoV-2, which causes COVID-19, range from asymptomatic to severe. Here we present a follow-up analysis of a longitudinal study characterizing COVID-19 immune responses from a father and son with distinctly different clinical courses. The father required a lengthy hospital stay for severe symptoms, whereas his son had mild symptoms and no fever yet tested positive for SARS-CoV-2 for 29 days. Father and son, as well as another unrelated COVID-19 patient, displayed a robust increase of SERPING1, the transcript encoding C1 esterase inhibitor (C1–INH). We further bolstered this finding by incorporating a serum proteomics dataset and found that serum C1–INH was consistently increased in COVID-19 patients. C1–INH is a central regulator of the contact and complement systems, potentially linking COVID-19 to complement hyperactivation, fibrin clot formation, and immune depression. Furthermore, despite distinct clinical cases, significant parallels were observed in transcripts involved in interferon and B cell signaling. As symptoms were resolving, widespread decreases were seen in immune-related transcripts to levels below those of healthy controls. Our study provides insight into the immune responses of likely millions of people with extremely mild symptoms who may not be aware of their infection with SARS-CoV-2 and implies a potential for long-lasting consequences that could contribute to reinfection risk.
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spelling doaj.art-c8c8183d49064e7583747ca23865f4aa2022-12-21T22:41:33ZengElsevierHeliyon2405-84402021-01-0171e05877Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysisMelissa A. Hausburg0Kaysie L. Banton1Michael Roshon2David Bar-Or3Trauma Research Department, Swedish Medical Center, Englewood, CO, USA; Trauma Research Department, St. Anthony Hospital, Lakewood, CO, USA; Trauma Research Department, Penrose Hospital, Colorado Springs, CO, USA; Emergency Room Department, Penrose Hospital, Colorado Springs, CO, USATrauma Research Department, Swedish Medical Center, Englewood, CO, USAEmergency Room Department, Penrose Hospital, Colorado Springs, CO, USATrauma Research Department, Swedish Medical Center, Englewood, CO, USA; Trauma Research Department, St. Anthony Hospital, Lakewood, CO, USA; Trauma Research Department, Penrose Hospital, Colorado Springs, CO, USA; Emergency Room Department, Penrose Hospital, Colorado Springs, CO, USA; Department of Molecular Biology, Rocky Vista University, Parker, CO, USA; Corresponding author.Inflammatory responses to the novel coronavirus SARS-CoV-2, which causes COVID-19, range from asymptomatic to severe. Here we present a follow-up analysis of a longitudinal study characterizing COVID-19 immune responses from a father and son with distinctly different clinical courses. The father required a lengthy hospital stay for severe symptoms, whereas his son had mild symptoms and no fever yet tested positive for SARS-CoV-2 for 29 days. Father and son, as well as another unrelated COVID-19 patient, displayed a robust increase of SERPING1, the transcript encoding C1 esterase inhibitor (C1–INH). We further bolstered this finding by incorporating a serum proteomics dataset and found that serum C1–INH was consistently increased in COVID-19 patients. C1–INH is a central regulator of the contact and complement systems, potentially linking COVID-19 to complement hyperactivation, fibrin clot formation, and immune depression. Furthermore, despite distinct clinical cases, significant parallels were observed in transcripts involved in interferon and B cell signaling. As symptoms were resolving, widespread decreases were seen in immune-related transcripts to levels below those of healthy controls. Our study provides insight into the immune responses of likely millions of people with extremely mild symptoms who may not be aware of their infection with SARS-CoV-2 and implies a potential for long-lasting consequences that could contribute to reinfection risk.http://www.sciencedirect.com/science/article/pii/S2405844020327195SARS-CoV-2COVID-19SERPING1ComplementB cellInterferon
spellingShingle Melissa A. Hausburg
Kaysie L. Banton
Michael Roshon
David Bar-Or
Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis
Heliyon
SARS-CoV-2
COVID-19
SERPING1
Complement
B cell
Interferon
title Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis
title_full Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis
title_fullStr Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis
title_full_unstemmed Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis
title_short Clinically distinct COVID-19 cases share notably similar immune response progression: A follow-up analysis
title_sort clinically distinct covid 19 cases share notably similar immune response progression a follow up analysis
topic SARS-CoV-2
COVID-19
SERPING1
Complement
B cell
Interferon
url http://www.sciencedirect.com/science/article/pii/S2405844020327195
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AT michaelroshon clinicallydistinctcovid19casessharenotablysimilarimmuneresponseprogressionafollowupanalysis
AT davidbaror clinicallydistinctcovid19casessharenotablysimilarimmuneresponseprogressionafollowupanalysis