Dynamics of Anti-influenza Mucosal IgA Over a Season in a Cohort of Individuals Living or Working in a Long-term Care Facility.
influenza
mucosal immunity
surveillance
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
16 08 2023
16 08 2023
Historique:
received:
22
08
2022
accepted:
02
02
2023
medline:
17
8
2023
pubmed:
6
2
2023
entrez:
5
2
2023
Statut:
ppublish
Résumé
Serological surveys are used to ascertain influenza infection and immunity, but evidence for the utility of mucosal immunoglobulin A (IgA) as a correlate of infection or protection is limited. We performed influenza-like illness (ILI) surveillance on 220 individuals living or working in a retirement community in Gainesville, Florida from January to May 2018, and took pre- and postseason nasal samples of 11 individuals with polymerase chain reaction (PCR)-confirmed influenza infection and 60 randomly selected controls. Mucosal IgA against 10 strains of influenza was measured from nasal samples. Overall, 28.2% and 11.3% of individuals experienced a 2-fold and 4-fold rise, respectively, in mucosal IgA to at least 1 influenza strain. Individuals with PCR-confirmed influenza A had significantly lower levels of preseason IgA to influenza A. Influenza-associated respiratory illness was associated with a higher rise in mucosal IgA to influenza strains of the same subtype, and H3N2-associated respiratory illness was associated with a higher rise in mucosal IgA to other influenza A strains. By comparing individuals with and without influenza illness, we demonstrated that mucosal IgA is a correlate of influenza infection. There was evidence for cross-reactivity in mucosal IgA across influenza A subtypes.
Sections du résumé
BACKGROUND
Serological surveys are used to ascertain influenza infection and immunity, but evidence for the utility of mucosal immunoglobulin A (IgA) as a correlate of infection or protection is limited.
METHODS
We performed influenza-like illness (ILI) surveillance on 220 individuals living or working in a retirement community in Gainesville, Florida from January to May 2018, and took pre- and postseason nasal samples of 11 individuals with polymerase chain reaction (PCR)-confirmed influenza infection and 60 randomly selected controls. Mucosal IgA against 10 strains of influenza was measured from nasal samples.
RESULTS
Overall, 28.2% and 11.3% of individuals experienced a 2-fold and 4-fold rise, respectively, in mucosal IgA to at least 1 influenza strain. Individuals with PCR-confirmed influenza A had significantly lower levels of preseason IgA to influenza A. Influenza-associated respiratory illness was associated with a higher rise in mucosal IgA to influenza strains of the same subtype, and H3N2-associated respiratory illness was associated with a higher rise in mucosal IgA to other influenza A strains.
CONCLUSIONS
By comparing individuals with and without influenza illness, we demonstrated that mucosal IgA is a correlate of influenza infection. There was evidence for cross-reactivity in mucosal IgA across influenza A subtypes.
Identifiants
pubmed: 36740584
pii: 7026327
doi: 10.1093/infdis/jiad029
pmc: PMC10428196
doi:
Substances chimiques
Immunoglobulin A
0
Influenza Vaccines
0
Antibodies, Viral
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
383-390Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America.
Déclaration de conflit d'intérêts
Potential conflicts of interest. M. D. T. H. and D. A. T. C. report a contract from Merck (to the University of Florida) for research unrelated to this article. All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
Références
PLoS One. 2022 Feb 7;17(2):e0263419
pubmed: 35130308
Infect Immun. 1983 Aug;41(2):540-5
pubmed: 6874068
Vaccine. 2009 Aug 6;27(36):4953-60
pubmed: 19540952
PLoS Pathog. 2012;8(12):e1003061
pubmed: 23271967
PLoS Pathog. 2020 Jul 23;16(7):e1008635
pubmed: 32702069
Expert Rev Anti Infect Ther. 2011 Jun;9(6):669-83
pubmed: 21692672
Vaccine. 2012 Aug 31;30(40):5893-900
pubmed: 22835738
J Med Virol. 2004 Oct;74(2):328-35
pubmed: 15332283
Am J Epidemiol. 1971 Jun;93(6):480-6
pubmed: 5562720
Nat Commun. 2019 Apr 10;10(1):1660
pubmed: 30971703
MMWR Morb Mortal Wkly Rep. 2017 Jun 30;66(25):668-676
pubmed: 28662019
J Infect Dis. 2011 May 1;203(9):1309-15
pubmed: 21378375
Front Immunol. 2020 May 19;11:902
pubmed: 32508822
J Clin Microbiol. 1985 Aug;22(2):259-64
pubmed: 4031039
JAMA. 1969 Jan 20;207(3):520-4
pubmed: 5818213
Front Microbiol. 2017 May 17;8:900
pubmed: 28567036
J Clin Microbiol. 1986 Jul;24(1):157-60
pubmed: 3722363
J Immunol Methods. 2017 Oct;449:1-6
pubmed: 28647455
J Infect Dis. 2013 Mar 15;207(6):974-81
pubmed: 23307936
PLoS One. 2010 Aug 30;5(8):e12474
pubmed: 20814575
Nature. 2018 May;557(7707):719-723
pubmed: 29795354
Epidemiol Infect. 2015 Feb;143(3):540-9
pubmed: 24786933
JAMA. 1970 Feb 16;211(7):1157-61
pubmed: 5466966
Can J Infect Dis Med Microbiol. 2011 Spring;22(1):25-9
pubmed: 22379485
J Infect Dis. 2013 Jan 1;207(1):115-24
pubmed: 23087433
mBio. 2020 Jan 21;11(1):
pubmed: 31964741
J Immunol. 1970 Dec;105(6):1477-83
pubmed: 4320734
Nat Rev Immunol. 2019 Jun;19(6):383-397
pubmed: 30837674
Clin Vaccine Immunol. 2014 Aug;21(8):1054-60
pubmed: 24872516
Vaccine. 2009 Jun 8;27(28):3744-53
pubmed: 19464558
Vaccine. 2020 Dec 3;38(51):8161-8166
pubmed: 33162202
Influenza Other Respir Viruses. 2012 Nov;6(6):396-403
pubmed: 22226319
Hum Vaccin Immunother. 2013 Sep;9(9):1962-70
pubmed: 23896606
Elife. 2018 Aug 14;7:
pubmed: 30103854
J Infect. 2015 Feb;70(2):187-96
pubmed: 25224643
MMWR Morb Mortal Wkly Rep. 2018 Jun 08;67(22):634-642
pubmed: 29879098
Epidemiol Infect. 2016 Aug;144(11):2306-16
pubmed: 27018720