Smoking and Epstein-Barr virus infection in multiple sclerosis development.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
03 07 2020
Historique:
received: 18 11 2019
accepted: 29 05 2020
entrez: 5 7 2020
pubmed: 6 7 2020
medline: 15 12 2020
Statut: epublish

Résumé

It is unclear whether smoking interacts with different aspects of Epstein-Barr virus (EBV) infection with regard to multiple sclerosis (MS) risk. We aimed to investigate whether smoking acts synergistically with elevated EBNA-1 antibody levels or infectious mononucleosis (IM) history regarding MS risk. Two Swedish population-based case-control studies were used (6,340 cases and 6,219 matched controls). Subjects with different smoking, EBNA-1 and IM status were compared regarding MS risk, by calculating odds ratios (OR) with 95% confidence intervals (CI) employing logistic regression. Potential interaction on the additive scale was evaluated by calculating the attributable proportion due to interaction (AP). Current and past smokers had higher EBNA-1 antibody levels than never smokers (p < 0.0001). There was an additive interaction between current smoking and high EBNA-1 antibody levels (AP 0.3, 95% CI 0.2-0.4), but not between past smoking and high EBNA-1 antibody levels (AP 0.01, 95% CI - 0.1 to 0.1), with regard to MS risk. An interaction also occurred between current smoking and IM history (AP 0.2, 95% CI 0.004-0.4), but not between past smoking and IM history (AP - 0.06, 95% CI - 0.4 to 0.3). Current smoking increases EBNA-1 antibody levels and acts synergistically with both aspects of EBV infection to increase MS risk, indicating that there is at least one pathway to disease in which both risk factors are involved.

Identifiants

pubmed: 32620875
doi: 10.1038/s41598-020-67883-w
pii: 10.1038/s41598-020-67883-w
pmc: PMC7335184
doi:

Substances chimiques

Antibodies, Viral 0
Epstein-Barr Virus Nuclear Antigens 0
Immunoglobulin G 0
EBV-encoded nuclear antigen 1 O5GA75RST7

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

10960

Références

Hedström, A. K., Hillert, J., Olsson, T. & Alfredsson, L. Smoking and multiple sclerosis susceptibility. Eur. J. Epidemiol. 28, 867–874 (2013).
pubmed: 24146047 pmcid: 3898140
Levin, L. I. et al. Primary infection with the Epstein–Barr virus and risk of multiple sclerosis. Ann. Neurol. 67, 824–830 (2010).
pubmed: 20517945 pmcid: 3089959
Handel, A.E., et al. An updated meta-analysis of risk of multiple sclerosis following infectious mononucleosis. PLoS One. 5, e12496 (2010).
pubmed: 20824132 pmcid: 2931696
Simon, K. C. et al. Combined effects of smoking, anti-EBNA antibodies, and HLA-DRB1*1501 on multiple sclerosis risk. Neurology. 74, 1365–1371 (2010).
pubmed: 20375311 pmcid: 2875934
Sundqvist, E. et al. Lack of replication of interaction between EBNA1 IgG and smoking in risk for multiple sclerosis. Neurology. 79, 1363–1368 (2012).
pubmed: 22933744
Simon, K. C., Schmidt, H., Lound, S. & Ascherio, A. Risk factors for multiple sclerosis, neuromyelitis optica and transverse myelitis. Mult. Scler. 21, 703–709 (2015).
pubmed: 25305254
van der Mei, I. et al. Population attributable fractions and joint effects of key risk factors for multiple sclerosis. Mult. Scler. 22, 461–469 (2016).
pubmed: 26199349
Salzer, J., Stenlund, H. & Sundström, P. The interaction between smoking and Epstein–Barr virus as multiple sclerosis risk factors may depend on age. Mult. Scler. 20, 747–750 (2014).
pubmed: 24107308
Bjornevik, K. et al. Negative interaction between smoking and EBV in the risk of multiple sclerosis: The EnvIMS study. Mult. Scler. 23, 1018–1024 (2017).
pubmed: 27663872
Thomson, A. J. et al. Diagnostic criteria for primary progressive multiple sclerosis: A position paper. Ann. Neurol. 47, 831–835 (2000).
Patsopoulos, N.A., et al. Multiple sclerosis genomic map implicates peripheral immune cells and migroglia in susceptibility. Science. 365, eaav7188 (2019).
Dilthey, A. et al. Multi-population classical HLA type imputation. PLoS Comput. Biol. 9, e1002877 (2013).
pubmed: 23459081 pmcid: 3572961
Waterboer, T. et al. Multiplex human papillomavirus serology based on in situ-purified glutathione s-transferase fusion proteins. Clin. Chem. 51, 1845–1853 (2005).
pubmed: 16099939
Tengvall, K. et al. Molecular mimicry between anoctamin 2 and Epstein–barr virus nuclear antigen 1 associates with multiple sclerosis risk. Proc. Natl. Acad. Sci. USA. 116, 16955–16960 (2019).
pubmed: 31375628
Sundqvist, E. et al. Epstein–Barr virus and multiple sclerosis: Interactions with HLA. Genes Immun. 13, 14–20 (2012).
pubmed: 21776012
Rothman, K. J. et al. (eds) Modern Epidemiology 3rd edn. (Lippincott Wolliams & Wilkins, Philadelphia, 2008).
Ahlbom, A. & Alfredsson, L. Interaction: A word with two meanings creates confusion. Eur. J. Epidemiol. 20, 583–584 (2005).
VanderWeele, T. J. Sufficient cause interactions and statistical interactions. Epidemiology. 20, 6–13 (2009).
pubmed: 19234396
Moutsianas, L. et al. Class II HLA interactions modulate genetic risk for multiple sclerosis. Nat. Genet. 47, 1107–1113 (2015).
pubmed: 26343388 pmcid: 4874245
Hedström, A. K. Smoking and its interaction with genetics in MS etiology. Mult. Scler. 25, 180–186 (2019).
pubmed: 30251921
Hedström, A. K. et al. High levels of Epstein–Barr virus nuclear antigen-1-specific antibodies and infectious mononucleosis act both independently and synergistically to increase multiple sclerosis risk. Front. Neurol. 10, 1368 (2019).
pubmed: 32038456
Hedström, A.K., et al. The influence of human leukocyte antigen-DRB1*15:01 and its interaction with smoking in MS development is dependent on DQA1*01:01 status. Mult. Scler. https://doi.org/10.1177/1352458519877685 (2019).
doi: 10.1177/1352458519877685 pubmed: 31573825
Hedström, A. K. et al. The interaction between smoking and HLA genes in multiple sclerosis: Replication and refinement. Eur. J. Epidemiol. 32, 909–919 (2017).
pubmed: 28597127 pmcid: 5680370
Hedström, A. K. et al. Organic solvents and MS susceptibility; interaction with MS risk HLA genes. Neurology. 91, e455–e462 (2018).
pubmed: 29970406 pmcid: 6093765
Enders, C. K., Mistler, S. A. & Keller, B. T. Multilevel multiple imputation: A review and evaluation of joint modeling and chained equations imputation. Psychol. Methods. 21, 222–240 (2016).
pubmed: 26690775
He, Y. Q. et al. The relationship between environmental factors and the profile of Epstein–Barr virus antibodies in the lytic and latent infection periods in healthy populations from endemic and non-endemic nasopharyngeal carcinoma areas in China. EBioMedicine. 30, 184–191 (2018).
pubmed: 29606628 pmcid: 5952216
Nielsen, T. R., Pedersen, M., Rostgaard, K., Frisch, M. & Hjalgrim, H. Correlations between Epstein–Barr virus antibody levels and risk factors for multiple sclerosis in healthy individuals. Mult. Scler. 13, 420–423 (2007).
pubmed: 17439912
Chan, K. C. A., Chu, S. W. I. & Lo, Y. M. D. Ambient temperature and screening for nasopharyngeal cancer. N. Engl. J. Med. 378, 962–963 (2018).
pubmed: 29514031
He, Y. Q., Liao, X. Y. & Xue, W. Q. Association between environmental factors and oral Epstein–Barr virus DNA loads: A multicenter cross-sectional study in China. J. Infect. Dis. 219, 400–409 (2019).
pubmed: 30307559
Xu, F. H. et al. An epidemiological and molecular study of the relationship between smoking, risk of nasopharyngeal carcinoma, and Epstein–Barr virus activation. J. Natl. Cancer Inst. 104, 1396–1410 (2012).
pubmed: 22972969
Hu, T. et al. Smoking can increase nasopharyngeal carcinoma risk by repeatedly reactivating Epstein–Barr virus: An analysis of a prospective study in southern China. Cancer Med. 8, 2561–2571 (2019).
pubmed: 30843658 pmcid: 6536979
Qiu, F., Liang, C. L. & Liu, H. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down?. Oncotarget. 8, 268–284 (2017).
pubmed: 27902485
Smets, I., Fiddes, B. & Garcia-Perez, J. E. Multiple sclerosis risk variants alter expression of co-stimulatory genes in B cells. Brain 141, 786–796 (2018).
pubmed: 29361022 pmcid: 5837558
Li, G., Wulan, H. & Song, Z. Regulatory B cells function is suppressed by smoking and obesity in H. pylori-infected subjects and is correlated with elevated risk of gastric cancer. PLoS ONE 10, e0134591 (2015).
pubmed: 26226399 pmcid: 4520600
Grimaldi, C. M., Cleary, J., Dagtas, A. S., Moussai, D. & Diamond, B. Estrogen alters thresholds for B cell apoptosis and activation. J. Clin. Investig. 109, 1625–1633 (2002).
pubmed: 12070310
Prasad, S. et al. Impact of cigarette smoke extract and hyperglycemic conditions on blood–brain barrier endothelial cells. Fluids Barriers CNS. 12, 18 (2015).
pubmed: 26206552 pmcid: 4513397
Gao, X., Jia, M. & Zhang, Y. DNA methylation changes of whole blood cells in response to active smoking exposure in adults: A systematic review of DNA methylation studies. Clin. Epigenet. 7, 113 (2015).
Joehanes, R. et al. Epigenetic signatures of cigarette smoking. Circ. Cardiovasc. Genet. 9, 436–447 (2016).
pubmed: 27651444 pmcid: 5267325
Su, D. et al. Distinct epigenetic effects of tobacco smoking in whole blood and among leukocyte subtypes. PLoS ONE 11, e0166486 (2016).
pubmed: 27935972 pmcid: 5147832
Kreft, K. L. et al. Elevated EBNA-1 IgG in MS is associated with genetic MS risk variants. Neurol. Neuroimmunol. Neuroinflamm. 4, e406 (2017).
pubmed: 29379819 pmcid: 5778394
Zhou, Y. et al. Genetic loci for Epstein–Barr virus nuclear antigen-1 are associated with risk of multiple sclerosis. Mult. Scler. 22, 1655–1664 (2016).
pubmed: 26819262
McAulay, K. A. et al. HLA class I polymorphisms are associated with development of infectious mononucleosis upon primary EBV infection. J. Clin. Investig. 117, 3042–3048 (2007).
pubmed: 17909631
Agostini, S. et al. HLA alleles modulate EBV viral load in multiple sclerosis. J. Transl. Med. 16, 80 (2018).
pubmed: 29587799 pmcid: 5870171
Internet based information. https://www.scb.se . Accessed 16 Apr 2019.

Auteurs

Anna Karin Hedström (AK)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden. anna.hedstrom@ki.se.
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. anna.hedstrom@ki.se.

Jesse Huang (J)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska Institutet at Karolinska University Hospital, Stockholm, Sweden.

Nicole Brenner (N)

German Cancer Research Center (DKFZ), Heidelberg, Germany.

Julia Butt (J)

German Cancer Research Center (DKFZ), Heidelberg, Germany.

Jan Hillert (J)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska Institutet at Karolinska University Hospital, Stockholm, Sweden.

Tim Waterboer (T)

German Cancer Research Center (DKFZ), Heidelberg, Germany.

Ingrid Kockum (I)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska Institutet at Karolinska University Hospital, Stockholm, Sweden.

Tomas Olsson (T)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Center for Molecular Medicine, Karolinska Institutet at Karolinska University Hospital, Stockholm, Sweden.

Lars Alfredsson (L)

Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

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