Cytomegalovirus seropositivity is associated with reduced risk of multiple sclerosis-a presymptomatic case-control study.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
09 2021
Historique:
revised: 12 05 2021
received: 02 03 2021
accepted: 07 06 2021
pubmed: 10 6 2021
medline: 21 10 2021
entrez: 9 6 2021
Statut: ppublish

Résumé

Epstein-Barr virus (EBV) and human herpesvirus 6A (HHV-6A) are associated with increased risk of multiple sclerosis (MS). Conversely, infection with cytomegalovirus (CMV) has been suggested to reduce the risk of MS but supporting data from presymptomatic studies are lacking. Here, it was sought to increase the understanding of CMV in MS aetiology. A nested case-control study was performed with presymptomatically collected blood samples identified through crosslinkage of MS registries and Swedish biobanks. Serological antibody response against CMV, EBV and HHV-6A was determined using a bead-based multiplex assay. Odds ratio (OR) with 95% confidence interval (CI) for CMV seropositivity as a risk factor for MS was calculated by conditional logistic regression and adjusted for EBV and HHV-6A seropositivity. Potential interactions on the additive scale were analysed by calculating the attributable proportion due to interaction (AP). Serum samples from 670 pairs of matched cases and controls were included. CMV seropositivity was associated with a reduced risk for MS (OR = 0.70, 95% CI 0.56-0.88, p = 0.003). Statistical interactions on the additive scale were observed between seronegativity for CMV and seropositivity against HHV-6A (AP 0.34, 95% CI 0.06-0.61) and EBV antigen EBNA-1 (amino acid 385-420) at age 20-39 years (AP 0.37, 95% CI 0.09-0.65). Cytomegalovirus seropositivity is associated with a decreased risk for MS. The protective role for CMV infection in MS aetiology is further supported by the interactions between CMV seronegativity and EBV and HHV-6A seropositivity.

Sections du résumé

BACKGROUND AND PURPOSE
Epstein-Barr virus (EBV) and human herpesvirus 6A (HHV-6A) are associated with increased risk of multiple sclerosis (MS). Conversely, infection with cytomegalovirus (CMV) has been suggested to reduce the risk of MS but supporting data from presymptomatic studies are lacking. Here, it was sought to increase the understanding of CMV in MS aetiology.
METHODS
A nested case-control study was performed with presymptomatically collected blood samples identified through crosslinkage of MS registries and Swedish biobanks. Serological antibody response against CMV, EBV and HHV-6A was determined using a bead-based multiplex assay. Odds ratio (OR) with 95% confidence interval (CI) for CMV seropositivity as a risk factor for MS was calculated by conditional logistic regression and adjusted for EBV and HHV-6A seropositivity. Potential interactions on the additive scale were analysed by calculating the attributable proportion due to interaction (AP).
RESULTS
Serum samples from 670 pairs of matched cases and controls were included. CMV seropositivity was associated with a reduced risk for MS (OR = 0.70, 95% CI 0.56-0.88, p = 0.003). Statistical interactions on the additive scale were observed between seronegativity for CMV and seropositivity against HHV-6A (AP 0.34, 95% CI 0.06-0.61) and EBV antigen EBNA-1 (amino acid 385-420) at age 20-39 years (AP 0.37, 95% CI 0.09-0.65).
CONCLUSIONS
Cytomegalovirus seropositivity is associated with a decreased risk for MS. The protective role for CMV infection in MS aetiology is further supported by the interactions between CMV seronegativity and EBV and HHV-6A seropositivity.

Identifiants

pubmed: 34107122
doi: 10.1111/ene.14961
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

3072-3079

Informations de copyright

© 2021 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.

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Auteurs

Viktor Grut (V)

Department of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.

Martin Biström (M)

Department of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.

Jonatan Salzer (J)

Department of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.

Pernilla Stridh (P)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Daniel Jons (D)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Rasmus Gustafsson (R)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Anna Fogdell-Hahn (A)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Jesse Huang (J)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Nicole Brenner (N)

Infections and Cancer Epidemiology Division, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Julia Butt (J)

Infections and Cancer Epidemiology Division, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Noemi Bender (N)

Infections and Cancer Epidemiology Division, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Anna Lindam (A)

Department of Public Health and Clinical Medicine, Unit of Research, Education and Development Östersund Hospital, Umeå University, Umeå, Sweden.

Lucia Alonso-Magdalena (L)

Department of Neurology, Skåne University Hospital in Malmö/Lund and Institution of Clinical Sciences, Neurology, Lund University, Lund, Sweden.

Martin Gunnarsson (M)

Department of Neurology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.

Magnus Vrethem (M)

Department of Neurology and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.

Tomas Bergström (T)

Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Oluf Andersen (O)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Ingrid Kockum (I)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Tim Waterboer (T)

Infections and Cancer Epidemiology Division, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Tomas Olsson (T)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Peter Sundström (P)

Department of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.

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