Association of a polymorphism in the indoleamine- 2,3-dioxygenase gene and interferon-α-induced depression in patients with chronic hepatitis C
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Interferon (IFN)-α treatment for infectious diseases and cancer is associated with significant depressive symptoms that can limit therapeutic efficacy. Multiple mechanisms have been implicated in IFN-α-induced depression including immune, neuroendocrine and neurotransmitter pathways. To further explore mechanisms of IFN-α-induced depression and establish associated genetic risk factors, single nucleotide polymorphisms in genes encoding proteins previously implicated in IFN-α-induced depression were explored in two self-reported ethnic groups, Caucasians (n=800) and African Americans (n=232), participating in a clinical trial on the impact of three pegylated IFN-α treatment regimens on sustained viral response in patients with chronic hepatitis C. Before treatment, all subjects were free of psychotropic medications and had a score ≤20 on the Center for Epidemiologic Studies Depression Scale (CES-D), which was used to assess depressive symptom severity throughout the study. In Caucasians, a polymorphism (rs9657182) in the promoter region of the gene encoding indoleamine-2,3-dioxygenase (IDO1) was found to be associated with moderate or severe IFN-α-induced depressive symptoms (CES-D>20) at 12 weeks of IFN-α treatment (P=0.0012, P<0.05 corrected). Similar results were obtained for treatment weeks 24, 36 and 48. In subjects homozygous for the risk allele (CC, n=150), the odds ratio for developing moderate or severe depressive symptoms at treatment week 12 was 2.91 (confidence interval: 1.48-5.73) compared with TT homozygotes (n=270). rs9657182 did not predict depression in African Americans, who exhibited a markedly lower frequency of the risk allele at this locus. The findings in Caucasians further support the notion that IDO has an important role in cytokine-induced behavioral changes.
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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 A. K. Smith et al., 2012
The Discussion reports that the IDO1 promoter SNP rs9657182 predicted depressive symptoms during IFN-α therapy in Caucasian patients with chronic hepatitis C. It also says the study did not replicate a previous finding for IL-6 rs1800795, and that whether rs9657182 alters IDO1 function remains unclear. Thus the claim overstates both the evidence for the IL-6 SNP in this study and the characterization of the IDO1 SNP as functional. (LLM, conf=0.88)
Experimental — accuracy not yet measuredOne study observed no association between the development of IFN-alpha-induced depression and polymorphic regions examined in the genes encoding TNF, IL6, IL1A, IL1B, MCP-1/CCL2, or IFN-AR1.
“However, it is worthy to note that one study observed no association between the development of IFN-alpha-induced depression and polymorphic regions examined in the genes encoding TNF (rs1799964, rs1800629, rs3093662, rs769178), IL6 (rs1800795, rs1800796, rs1800797), IL1A (rs3783516, rs3783546), IL1B (rs1143643, rs1143644, rs16944, rs4848306), chemokine MCP-1/CCL2 (rs1024611, rs2530797,rs4586), or”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Smith et al., 2012
A polymorphism (rs9657182) in the promoter region of the gene encoding IDO1 was found to be associated with IFN-alpha-induced depression in Caucasian subjects homozygous for the C risk allele, but not African Americans who exhibited a markedly lower frequency of the risk allele at this locus.
“Interestingly, a polymorphism (rs9657182) in the promoter region of the gene encoding IDO1 was found to be associated with IFN-alpha-induced depression in Caucasian subjects homozygous for the C risk allele, but not African Americans who exhibited a markedly lower frequency of the risk allele at this locus (Smith et al., 2012)(see Table 1 for details).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Smith et al., 2012
In IFN-alpha-treated patients, CSF MHPG was not related to behavioral symptoms, and DBH SNPs were not associated with development of depression.
“MHPG has been examined in the CSF of IFN-alpha-treated patients but was not related to behavioral symptoms (Raison et al., 2009). SNPs of the gene for DA beta-hydroxylase, the enzyme that converts DA to NE, was examined in IFN-alpha-treated HCV+ subjects but was not associated with the development of depression (Smith et al., 2012).”
From Inflammatory cytokines in depression: neurobiological mechanisms and therapeutic implications (2013) · cites this paper as Smith et al., 2012
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- Authors
- Smith, A. K., Simon, J. S., Gustafson, E. L., Noviello, S., Cubells, J. F., Epstein, M. P., Devlin, D. J., Qiu, P., Albrecht, J. K., Brass, C. A., Sulkowski, M. S., McHutchinson, J. G., & Miller, A. H.
- Affiliations
- Emory University (US)
- Eisai (United States) (US)
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- Johns Hopkins University (US)
- Duke Medical Center (US)
- Corresponding author
- Miller, A H
- Venue
- Molecular Psychiatry
- Published
- 2011-06-21
- Volume
- 17
- Issue
- 8
- Pages
- 781-789
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC3179823
- OpenAlex
- W2030438646
- Cited by
- 84
- References
- 69
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 9 · 2020: 2 · 2019: 5 · 2018: 6 · 2017: 4 · 2016: 8 · 2015: 10 · 2014: 11 · 2013: 5 · 2012: 10
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL073921)
- National Institute of Mental Health (K01MH085806, R01MH060723, K05MH069124)
- National Institute on Drug Abuse (K02DA015766, K01DA015766)
- National Cancer Institute (P30CA138292)
- National Center for Research Resources (UL1RR025008)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Hepatology › Hepatitis C virus research
- Keywords
- indoleamine 2,3-dioxygenase, IDO1, promoter polymorphism, chronic hepatitis C, pegylated interferon-alpha, genetic susceptibility, African Americans, Caucasians
- MeSH terms
- Interferon alpha-2, Adult, Alleles, Antiviral Agents, Black or African American, Depression, Female, Genotype, Humans, Male, Middle Aged, Polyethylene Glycols, Polymorphism, Genetic, Promoter Regions, Genetic, Psychiatric Status Rating Scales, Recombinant Proteins, Randomized Controlled Trials as Topic, Interferon-alpha, Hepatitis C, Chronic, Genetic Predisposition to Disease, White People, Indoleamine-Pyrrole 2,3,-Dioxygenase
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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