Evaluation of Humoral and Cellular Responses in SARS-CoV-2 mRNA Vaccinated Immunocompromised Patients.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2022
Historique:
received: 19 01 2022
accepted: 28 02 2022
entrez: 11 4 2022
pubmed: 12 4 2022
medline: 13 4 2022
Statut: epublish

Résumé

Immunocompromised patients are at increased risk of severe COVID-19 and impaired vaccine response. In this observational prospective study, we evaluated immunogenicity of the BNT162b2 mRNA vaccine in cohorts of primary or secondary immunocompromised patients. Five clinical groups of immunocompromised patients [primary immunodeficiency (PID) (n=57), people living with HIV (PLWH) (n=27), secondary immunocompromised patients with a broad variety of underlying rheumatologic (n=23) and homogeneous (multiple sclerosis) neurologic (n=53) conditions and chronic kidney disease (CKD) (n=39)] as well as a healthy control group (n=54) were included. Systemic humoral and cellular immune responses were evaluated by determination of anti-SARS-CoV-2 Spike antibodies using a TrimericS IgG assay (Diasorin) and through quantification of interferon gamma release in response to SARS-CoV-2 antigen with QuantiFERON SARS-CoV-2 assay (Qiagen), respectively. Responses were measured at pre-defined time-points after complete vaccination. All healthy controls, PLWH and CKD-patients had detectable antibodies 10 to 14 days (T2) and 3 months (T3) after administration of the second vaccination. In contrast, only 94.5% of the PID, 50.0% of the rheumatologic and 48.0% of neurologic patients developed antibodies at T2 and only 89.1% of the PID, 52.4% of the rheumatologic and 50.0% of neurologic patients developed antibodies at T3. At T3 no significant differences in cellular response between the healthy control group and the PLWH and CKD groups were found, while proportions of reactive subjects were lower in PID and rheumatologic patients and higher in neurologic patients. Humoral and cellular immune responses significantly correlated in the healthy control, PID, PLWH groups for all 3 antigens. Patients with acquired or inherited immune disorders may show variable immune responses to vaccination with the BNT162b2 mRNA vaccine against SARS-CoV-2. Whether humoral, cellular or both immune responses are delayed depends on the patient group, therapy and individual risk factors. These data may guide the counselling of patients with immune disorders regarding vaccination of SARS-CoV-2.

Sections du résumé

Background
Immunocompromised patients are at increased risk of severe COVID-19 and impaired vaccine response. In this observational prospective study, we evaluated immunogenicity of the BNT162b2 mRNA vaccine in cohorts of primary or secondary immunocompromised patients.
Methods
Five clinical groups of immunocompromised patients [primary immunodeficiency (PID) (n=57), people living with HIV (PLWH) (n=27), secondary immunocompromised patients with a broad variety of underlying rheumatologic (n=23) and homogeneous (multiple sclerosis) neurologic (n=53) conditions and chronic kidney disease (CKD) (n=39)] as well as a healthy control group (n=54) were included. Systemic humoral and cellular immune responses were evaluated by determination of anti-SARS-CoV-2 Spike antibodies using a TrimericS IgG assay (Diasorin) and through quantification of interferon gamma release in response to SARS-CoV-2 antigen with QuantiFERON SARS-CoV-2 assay (Qiagen), respectively. Responses were measured at pre-defined time-points after complete vaccination.
Results
All healthy controls, PLWH and CKD-patients had detectable antibodies 10 to 14 days (T2) and 3 months (T3) after administration of the second vaccination. In contrast, only 94.5% of the PID, 50.0% of the rheumatologic and 48.0% of neurologic patients developed antibodies at T2 and only 89.1% of the PID, 52.4% of the rheumatologic and 50.0% of neurologic patients developed antibodies at T3. At T3 no significant differences in cellular response between the healthy control group and the PLWH and CKD groups were found, while proportions of reactive subjects were lower in PID and rheumatologic patients and higher in neurologic patients. Humoral and cellular immune responses significantly correlated in the healthy control, PID, PLWH groups for all 3 antigens.
Conclusion
Patients with acquired or inherited immune disorders may show variable immune responses to vaccination with the BNT162b2 mRNA vaccine against SARS-CoV-2. Whether humoral, cellular or both immune responses are delayed depends on the patient group, therapy and individual risk factors. These data may guide the counselling of patients with immune disorders regarding vaccination of SARS-CoV-2.

Identifiants

pubmed: 35401575
doi: 10.3389/fimmu.2022.858399
pmc: PMC8988283
doi:

Substances chimiques

Antibodies, Viral 0
COVID-19 Vaccines 0
RNA, Messenger 0
Vaccines, Synthetic 0
mRNA Vaccines 0
BNT162 Vaccine N38TVC63NU

Types de publication

Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

858399

Informations de copyright

Copyright © 2022 Oyaert, De Scheerder, Van Herrewege, Laureys, Van Assche, Cambron, Naesens, Hoste, Claes, Haerynck, Kerre, Van Laecke, Van Biesen, Jacques, Verhasselt and Padalko.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Matthijs Oyaert (M)

Department of Laboratory Medicine, Ghent University Hospital, Ghent, Belgium.

Marie-Angélique De Scheerder (MA)

Department of General Internal Medicine, Ghent University Hospital, Ghent, Belgium.

Sophie Van Herrewege (S)

Department of General Internal Medicine, Ghent University Hospital, Ghent, Belgium.

Guy Laureys (G)

Department of Neurology, Ghent University Hospital, Ghent, Belgium.

Sofie Van Assche (S)

Department of Neurology, Ghent University Hospital, Ghent, Belgium.

Melissa Cambron (M)

Department of Neurology, Algemeen Ziekenhuis (AZ) Sint-Jan Brugge Oostende, Bruges, Belgium.

Leslie Naesens (L)

Department of Internal Medicine and Pediatrics, Ghent University Hospital, Ghent, Belgium.
Primary Immunodeficiency Research Lab, Ghent University, Ghent, Belgium.

Levi Hoste (L)

Department of Internal Medicine and Pediatrics, Ghent University Hospital, Ghent, Belgium.
Primary Immunodeficiency Research Lab, Ghent University, Ghent, Belgium.

Karlien Claes (K)

Department of Internal Medicine and Pediatrics, Ghent University Hospital, Ghent, Belgium.
Primary Immunodeficiency Research Lab, Ghent University, Ghent, Belgium.

Filomeen Haerynck (F)

Department of Internal Medicine and Pediatrics, Ghent University Hospital, Ghent, Belgium.
Primary Immunodeficiency Research Lab, Ghent University, Ghent, Belgium.

Tessa Kerre (T)

Department of Haematology, Ghent University Hospital, Ghent, Belgium.

Steven Van Laecke (S)

Department of Nephrology, Ghent University Hospital, Ghent, Belgium.

Wim Van Biesen (W)

Department of Nephrology, Ghent University Hospital, Ghent, Belgium.

Peggy Jacques (P)

Department of Rheumatology, Ghent University Hospital, Ghent, Belgium.

Bruno Verhasselt (B)

Department of Laboratory Medicine, Ghent University Hospital, Ghent, Belgium.

Elizaveta Padalko (E)

Department of Laboratory Medicine, Ghent University Hospital, Ghent, Belgium.

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