Functional polymorphisms in the interleukin-6 and serotonin transporter genes, and depression and fatigue induced by interferon-α and ribavirin treatment
Open accessAbstract
Depression and fatigue are frequent side effects of interferon-alpha (IFN-alpha) treatment, and there is compelling evidence that the inflammatory response system (including interleukin-6, IL-6) and the serotonergic system is important in the pathophysiology of such symptoms. Functional polymorphisms in the promoter region of the IL-6 gene (rs1800795) and serotonin transporter gene (5-HTTLPR) have been identified as regulating these systems. The present study aimed to determine if these polymorphisms were associated with the development of depression and fatigue during IFN-alpha and ribavirin treatment. Ninety-eight Caucasian patients receiving pegylated IFN-alpha and ribavirin treatment for chronic hepatitis C virus at King's College Hospital, London, and Emory University Hospital, Atlanta, participated in this prospective cohort study. Symptoms of depression and fatigue were measured before treatment and at weeks 4, 8, 12 and 24 during treatment. The 'low IL-6' synthesizing genotype (CC) was associated with significantly fewer symptoms of depression (effect size = 0.7 at week 24; F = 9.4, d.f. = 436, P = 0.002). The 'high transcription' serotonin transporter (5-HTT) genotype (LL) was also associated with significantly fewer symptoms of depression, but with a much smaller effect (effect size = 0.2 at week 24; F = 4.5, d.f. = 436, P = 0.03). Neither polymorphisms were associated with symptoms of fatigue (IL-6: F = 1.2, d.f. = 430, P = 0.2; 5-HTT: F = 0.5, d.f. = 430, P = 0.5). The smaller effects of the 5-HTT polymorphism on depression may be explained by an interaction between the genes (F = 5.0, d.f. = 434, P = 0.02): the 'protective' effect of the 5-HTTLPR polymorphism was evident only in the presence of the 'low IL-6' genotype (F = 5.4, d.f. = 64, P = 0.02), not in the presence of the 'high IL-6' genotype (F = 2.2, d.f. = 369, P = 0.1). The association between the IL-6 polymorphism and reduced risk of depressive symptoms confirms the role of the inflammatory response system in the pathophysiology of IFN-alpha-induced depression; in contrast, the effect of the 5-HTT gene was small and perhaps dependent on the status of the inflammatory response.
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Functional SNPs in the promoter regions of the genes encoding IDO (rs9657182) and IL-6 (rs1800795) moderate the effects of IFNα treatment on depression.
“functional SNPs in the promoter regions of the genes encoding both IDO (rs9657182) and IL-6 (rs1800795) have also been found to moderate the effects of IFNα treatment on depression”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Bull et al., 2009
The Introduction identifies IL-6 rs1800795 as a functional promoter SNP, and the Discussion reports that it is associated with fewer depressive symptoms during IFN-α treatment. The paper does not report an association for IDO rs9657182; its Discussion mentions IDO activity, not an IDO promoter SNP. The cited source therefore supports only the IL-6 part of the claim. (LLM, conf=0.90)
Experimental — accuracy not yet measuredPolymorphisms in the 5-HT transporter and IL-6 genes contribute to the fatigue and depressive symptoms observed after IFN-α administration.
“Polymorphisms in the 5-hydroxytryptamine (5-HT) transporter and IL-6 genes contribute to the fatigue and depressive symptoms that are observed after IFN-α administration[22].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [22]
The functional G-174C polymorphism (rs1800795) in the promoter region of the IL-6 gene predicts depressive symptoms in patients taking interferon-alpha for chronic viral hepatitis.
“the functional G-174C polymorphism (rs1800795) in the promoter region of the IL-6 gene predicts depressive symptoms in patients taking interferon-alpha for chronic viral hepatitis (Bull et al., 2009).”
From Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation (2017) · cites this paper as Bull et al., 2009
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- Authors
- Bull, S. J., Huezo-Diaz, P., Binder, E. B., Cubells, J. F., Ranjith, G., Maddock, C., Miyazaki, C., Alexander, N., Hotopf, M., Cleare, A. J., Norris, S., Cassidy, E., Aitchison, K. J., Miller, A. H., & Pariante, C. M.
- Affiliations
- King's College London (GB)
- Emory University (US)
- St. James's Hospital (IE)
- Cork University Hospital (IE)
- Corresponding author
- Pariante, C M
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2008-05-06
- Volume
- 14
- Issue
- 12
- Pages
- 1095-1104
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC3513412
- OpenAlex
- W2166667138
- Cited by
- 228
- References
- 67
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 8 · 2021: 4 · 2020: 5 · 2019: 10 · 2018: 13 · 2017: 13 · 2016: 24 · 2015: 14 · 2014: 18 · 2013: 22 · 2012: 29
- FWCI
- 6.46
- Type
- journal article
- Language
- en
- Update notices
- erratum (2009-11-18)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Lenus, The Irish Health Repository (Dr Steevens Hospital Library) (submittedVersion)
- Funders
- National Institute of Mental Health (R01MH060723, K05MH069124)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Hepatology › Hepatitis C virus research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- interleukin-6, serotonin transporter, 5-HTTLPR, rs1800795, functional polymorphisms, depression, fatigue, interferon-alpha, ribavirin, chronic hepatitis C, pegylated interferon, genetic susceptibility, gene-gene interaction, inflammation, serotonergic system, genotype-phenotype correlation
- MeSH terms
- Adult, Antiviral Agents, Depression, Fatigue, Female, Gene Frequency, Genotype, Humans, Interferon Type I, Male, Middle Aged, Polymorphism, Genetic, Psychiatric Status Rating Scales, Recombinant Proteins, Ribavirin, Cohort Studies, Interleukin-6, Hepatitis C, Chronic, Serotonin Plasma Membrane Transport Proteins
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