Amanda M Simanek1, Caroline Cheng2, Robert Yolken3, Monica Uddin4, Sandro Galea5, Allison E Aiello6. 1. Joseph J. Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, WI, USA. Electronic address: simaneka@uwm.edu. 2. Department of Epidemiology, University of Michigan-School of Public Health, Ann Arbor, MI, USA; Center for Social Epidemiology & Population Health, University of Michigan-School of Public Health, Ann Arbor, MI, USA. 3. Department of Pediatrics, Stanley Division of Developmental Neurovirology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 4. Department of Psychology, University of Illinois Urbana-Champaign, Champaign, IL, USA; Institute of Genomic Biology, University of Illinois Urbana-Champaign, Urbana IL. 5. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA. 6. Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA. Electronic address: aaiello@email.unc.edu.
Abstract
BACKGROUND: Depression is predicted to become the leading cause of disability worldwide by 2030 and moreover, socioeconomic inequalities in depression persist. Herpesviruses, which are more prevalent among socioeconomically disadvantaged populations, subject to stress-induced reactivation and are associated with increased levels of pro-inflammatory cytokines implicated in the etiology of depression, may serve as novel risk factors for depression onset. METHODS: Data are from individuals in the Detroit Neighborhood Health Study tested for herpes simplex virus-1 (HSV-1) and cytomegalovirus (CMV) seropositivity/immunoglobulin G (IgG) antibody levels (N=263) as well as interleukin-6 (IL-6) (N=245) and C-reactive protein (CRP) (N=236) levels and assessed for incident depression via the Patient Health Questionnaire-9. Linear and logistic regression models were used to examine associations between pathogen seropositivity/IgG antibody levels, pro-inflammatory markers and incident depression over approximately one-year of follow-up. RESULTS: For every one unit increase in CMV IgG antibody level, the odds of incident depression increased by 26% and individuals with IgG antibody levels in the highest quartile had over three times greater odds of incident depression (odds ratio 3.87, 95% confidence interval 1.47, 10.19), compared to those in the lower three quartiles. Neither CMV or HSV-1 seropositivity nor HSV-1 IgG antibody level were associated with IL-6 or CRP levels at Wave 1, nor were IL-6 or CRP levels associated with incident depression at Wave 2. CONCLUSIONS: Further examination of the biological pathways linking CMV and depression are warranted.
BACKGROUND:Depression is predicted to become the leading cause of disability worldwide by 2030 and moreover, socioeconomic inequalities in depression persist. Herpesviruses, which are more prevalent among socioeconomically disadvantaged populations, subject to stress-induced reactivation and are associated with increased levels of pro-inflammatory cytokines implicated in the etiology of depression, may serve as novel risk factors for depression onset. METHODS: Data are from individuals in the Detroit Neighborhood Health Study tested for herpes simplex virus-1 (HSV-1) and cytomegalovirus (CMV) seropositivity/immunoglobulin G (IgG) antibody levels (N=263) as well as interleukin-6 (IL-6) (N=245) and C-reactive protein (CRP) (N=236) levels and assessed for incident depression via the Patient Health Questionnaire-9. Linear and logistic regression models were used to examine associations between pathogen seropositivity/IgG antibody levels, pro-inflammatory markers and incident depression over approximately one-year of follow-up. RESULTS: For every one unit increase in CMV IgG antibody level, the odds of incident depression increased by 26% and individuals with IgG antibody levels in the highest quartile had over three times greater odds of incident depression (odds ratio 3.87, 95% confidence interval 1.47, 10.19), compared to those in the lower three quartiles. Neither CMV or HSV-1 seropositivity nor HSV-1 IgG antibody level were associated with IL-6 or CRP levels at Wave 1, nor were IL-6 or CRP levels associated with incident depression at Wave 2. CONCLUSIONS: Further examination of the biological pathways linking CMV and depression are warranted.
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