Humoral SARS-CoV-2 Immune Response in COVID-19 Recovered Vaccinated and Unvaccinated Individuals Related to Post-COVID-Syndrome.
anti-SARS-CoV-2 antibodies
antibody dynamics
antibody kinetics
longitudinal assessment
post-COVID syndrome
post-vaccination boosting
serological immune response
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
06 02 2023
06 02 2023
Historique:
received:
20
12
2022
revised:
01
02
2023
accepted:
03
02
2023
entrez:
28
2
2023
pubmed:
1
3
2023
medline:
3
3
2023
Statut:
epublish
Résumé
The duration of anti-SARS-CoV-2-antibody detectability up to 12 months was examined in individuals after either single convalescence or convalescence and vaccination. Moreover, variables that might influence an anti-RBD/S1 antibody decline and the existence of a post-COVID-syndrome (PCS) were addressed. Forty-nine SARS-CoV-2-qRT-PCR-confirmed participants completed a 12-month examination of anti-SARS-CoV-2-antibody levels and PCS-associated long-term sequelae. Overall, 324 samples were collected. Cell-free DNA (cfDNA) was isolated and quantified from EDTA-plasma. As cfDNA is released into the bloodstream from dying cells, it might provide information on organ damage in the late recovery of COIVD-19. Therefore, we evaluated cfDNA concentrations as a biomarker for a PCS. In the context of antibody dynamics, a random forest-based logistic regression with antibody decline as the target was performed and internally validated. The mean percentage dynamic related to the maximum measured value was 96 (±38)% for anti-RBD/S1 antibodies and 30 (±26)% for anti-N antibodies. Anti-RBD/S1 antibodies decreased in 37%, whereas anti-SARS-CoV-2-anti-N antibodies decreased in 86% of the subjects. Clinical anti-RBD/S1 antibody decline prediction models, including vascular and other diseases, were cross-validated (highest AUC 0.74). Long-term follow-up revealed no significant reduction in PCS prevalence but an increase in cognitive impairment, with no indication for cfDNA as a marker for a PCS. Long-term anti-RBD/S1-antibody positivity was confirmed, and clinical parameters associated with declining titers were presented. A fulminant decrease in anti-SARS-CoV-2-anti-N antibodies was observed (mean change to maximum value 30 (±26)%). Anti-RBD/S1 antibody titers of SARS-CoV-2 recovered subjects boosted with a vaccine exceeded the maximum values measured after single infection by 235 ± 382-fold, with no influence on preexisting PCS. PCS long-term prevalence was 38.6%, with an increase in cognitive impairment compromising the quality of life. Quantified cfDNA measured in the early post-COVID-19 phase might not be an effective marker for PCS identification.
Sections du résumé
BACKGROUND
The duration of anti-SARS-CoV-2-antibody detectability up to 12 months was examined in individuals after either single convalescence or convalescence and vaccination. Moreover, variables that might influence an anti-RBD/S1 antibody decline and the existence of a post-COVID-syndrome (PCS) were addressed.
METHODS
Forty-nine SARS-CoV-2-qRT-PCR-confirmed participants completed a 12-month examination of anti-SARS-CoV-2-antibody levels and PCS-associated long-term sequelae. Overall, 324 samples were collected. Cell-free DNA (cfDNA) was isolated and quantified from EDTA-plasma. As cfDNA is released into the bloodstream from dying cells, it might provide information on organ damage in the late recovery of COIVD-19. Therefore, we evaluated cfDNA concentrations as a biomarker for a PCS. In the context of antibody dynamics, a random forest-based logistic regression with antibody decline as the target was performed and internally validated.
RESULTS
The mean percentage dynamic related to the maximum measured value was 96 (±38)% for anti-RBD/S1 antibodies and 30 (±26)% for anti-N antibodies. Anti-RBD/S1 antibodies decreased in 37%, whereas anti-SARS-CoV-2-anti-N antibodies decreased in 86% of the subjects. Clinical anti-RBD/S1 antibody decline prediction models, including vascular and other diseases, were cross-validated (highest AUC 0.74). Long-term follow-up revealed no significant reduction in PCS prevalence but an increase in cognitive impairment, with no indication for cfDNA as a marker for a PCS.
CONCLUSION
Long-term anti-RBD/S1-antibody positivity was confirmed, and clinical parameters associated with declining titers were presented. A fulminant decrease in anti-SARS-CoV-2-anti-N antibodies was observed (mean change to maximum value 30 (±26)%). Anti-RBD/S1 antibody titers of SARS-CoV-2 recovered subjects boosted with a vaccine exceeded the maximum values measured after single infection by 235 ± 382-fold, with no influence on preexisting PCS. PCS long-term prevalence was 38.6%, with an increase in cognitive impairment compromising the quality of life. Quantified cfDNA measured in the early post-COVID-19 phase might not be an effective marker for PCS identification.
Identifiants
pubmed: 36851668
pii: v15020454
doi: 10.3390/v15020454
pmc: PMC9966735
pii:
doi:
Substances chimiques
Antibodies, Viral
0
Cell-Free Nucleic Acids
0
COVID-19 Vaccines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Références
J Med Virol. 2021 Dec;93(12):6506-6511
pubmed: 34170519
Lancet Infect Dis. 2022 Apr;22(4):e102-e107
pubmed: 34951953
BMJ. 2022 May 18;377:e069676
pubmed: 35584816
J Neurol. 2022 Jan;269(1):44-46
pubmed: 34143277
Eur J Med Res. 2021 Sep 16;26(1):107
pubmed: 34530915
Sci Rep. 2021 Aug 3;11(1):15701
pubmed: 34344929
Nat Commun. 2021 Feb 19;12(1):1162
pubmed: 33608522
J Med Virol. 2021 Apr;93(4):2227-2233
pubmed: 33135795
Nature. 2020 Aug;584(7821):437-442
pubmed: 32555388
PLoS One. 2014 Feb 10;9(2):e87741
pubmed: 24520336
Crit Care. 2012 Aug 13;16(4):R151
pubmed: 22889177
Cell Rep Med. 2020 Jun 23;1(3):100040
pubmed: 32835303
Ann N Y Acad Sci. 2004 Jun;1022:232-8
pubmed: 15251966
Hautarzt. 2021 Feb;72(2):92-99
pubmed: 33462654
Transplantation. 2021 Jan 1;105(1):193-200
pubmed: 33141807
Eur J Phys Rehabil Med. 2020 Oct;56(5):642-651
pubmed: 32705860
N Engl J Med. 2020 Oct 29;383(18):1724-1734
pubmed: 32871063
J Med Virol. 2021 Dec;93(12):6566-6574
pubmed: 34255355
Innate Immun. 2021 Apr;27(3):240-250
pubmed: 33646058
J Infect. 2021 Mar;82(3):378-383
pubmed: 33450302
Eur Arch Otorhinolaryngol. 2021 Dec;278(12):4831-4837
pubmed: 33774737
Clin Chim Acta. 2020 Nov;510:746-750
pubmed: 32946795
Nat Med. 2020 Jun;26(6):845-848
pubmed: 32350462
Environ Sci Pollut Res Int. 2021 Jul;28(27):35584-35596
pubmed: 33674974
Viruses. 2021 Oct 05;13(10):
pubmed: 34696428
J Microbiol Biotechnol. 2020 Mar 28;30(3):313-324
pubmed: 32238757
Lancet Infect Dis. 2020 Sep;20(9):e245-e249
pubmed: 32687805
J Med Virol. 2021 Dec;93(12):6444-6446
pubmed: 34260066
Clin Infect Dis. 2021 Aug 2;73(3):e531-e539
pubmed: 32745196
Lancet Infect Dis. 2022 Jan;22(1):43-55
pubmed: 34480857
BMJ Open. 2021 Oct 1;11(10):e043790
pubmed: 34598979
Brief Bioinform. 2019 Mar 22;20(2):492-503
pubmed: 29045534
Int J Infect Dis. 2021 Jun;107:221-227
pubmed: 33932604
New Microbes New Infect. 2021 Sep;43:100926
pubmed: 34367645
Eur J Immunol. 2020 Dec;50(12):2025-2040
pubmed: 33084029
Clin Lab. 2016 Dec 1;62(12):2395-2404
pubmed: 28164563
BMC Med Genomics. 2020 Nov 23;13(1):178
pubmed: 33228632
Nat Med. 2022 Jul;28(7):1461-1467
pubmed: 35614233
Lancet Infect Dis. 2020 May;20(5):565-574
pubmed: 32213337
Emerg Infect Dis. 2020 Jul;26(7):1478-1488
pubmed: 32267220
J Infect Dis. 2021 May 28;223(10):1671-1676
pubmed: 33675366
Sci Immunol. 2020 Oct 8;5(52):
pubmed: 33033173