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Abstract
Human cytomegalovirus (HCMV) is a neurotropic herpes virus known to cause neuropathology in patients with impaired immunity. Previously, we reported a reduction in the gray matter volume (GMV) of several brain regions in two independent samples of participants who were seropositive for HCMV (HCMV+) compared to matched participants who were seronegative for HCMV (HCMV−). In addition to an independent replication of the GMV findings, this study aimed to examine whether HCMV+ was associated with differences in resting-state functional connectivity (rsfMRI-FC). After balancing on 11 clinical/demographic variables using inverse probability of treatment weighting (IPTW), GMV and rsfMRI-FC were obtained from 99 participants with major depressive disorder (MDD) who were classified into 42 HCMV+ and 57 HCMV− individuals. Relative to the HCMV− group, the HCMV+ group showed a significant reduction of GMV in nine cortical regions. Volume reduction in the right lateral orbitofrontal cortex (standardized beta coefficient (SBC) = −0.32, [95%CI, −0.62 to −0.02]) and the left pars orbitalis (SBC = −0.34, [95%CI, −0.63 to −0.05]) in the HCMV+ group was also observed in the previous study. Regardless of the parcellation method or analytical approach, relative to the HCMV− group, the HCMV+ group showed hypoconnectivity between the hubs of the sensorimotor network (bilateral postcentral gyrus) and the hubs of the salience network (bilateral insula) with effect sizes ranging from SBC = −0.57 to −0.99. These findings support the hypothesis that a positive HCMV serostatus is associated with altered connectivity of regions that are important for stress and affective processing and further supports a possible etiological role of HCMV in depression.
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1 Laureate Institute for Brain Research, Tulsa, USA (GRID:grid.417423.7) (ISNI:0000 0004 0512 8863)
2 Laureate Institute for Brain Research, Tulsa, USA (GRID:grid.417423.7) (ISNI:0000 0004 0512 8863); Oklahoma State Univerisity, Department of Pharmacology and Physiology, Tulsa, USA (GRID:grid.65519.3e) (ISNI:0000 0001 0721 7331)
3 the University of California, San Francisco, School of Medicine, Department of Medicine, San Francisco, USA (GRID:grid.266102.1) (ISNI:0000 0001 2297 6811)
4 Laureate Institute for Brain Research, Tulsa, USA (GRID:grid.417423.7) (ISNI:0000 0004 0512 8863); Stephenson School of Biomedical Engineering, University of Oklahoma, Norman, USA (GRID:grid.266900.b) (ISNI:0000 0004 0447 0018)
5 University of Oklahoma School of Community Medicine, Department of Surgery, Tulsa, USA (GRID:grid.266900.b) (ISNI:0000 0004 0447 0018); University of Oklahoma School of Community Medicine, Department of Psychiatry, Tulsa, USA (GRID:grid.266900.b) (ISNI:0000 0004 0447 0018); Oklahoma State University Center for Health Sciences, Department of Biochemistry and Microbiology, Tulsa, USA (GRID:grid.261367.7) (ISNI:0000 0004 0542 825X)
6 Cousins Center for Psychoneuroimmunology at UCLA, Los Angeles, USA (GRID:grid.19006.3e) (ISNI:0000 0000 9632 6718); Semel Institute for Neuroscience at UCLA, Los Angeles, USA (GRID:grid.19006.3e) (ISNI:0000 0000 9632 6718); David Geffen School of Medicine, Los Angeles, USA (GRID:grid.19006.3e) (ISNI:0000 0000 9632 6718)
7 Stanley Division of Developmental Neurovirology, Johns Hopkins School of Medicine, Baltimore, USA (GRID:grid.21107.35) (ISNI:0000 0001 2171 9311)
8 Laureate Institute for Brain Research, Tulsa, USA (GRID:grid.417423.7) (ISNI:0000 0004 0512 8863); Oxley College of Health Sciences, The University of Tulsa, Tulsa, USA (GRID:grid.267360.6) (ISNI:0000 0001 2160 264X)