Tumor Necrosis Factor-α Receptor 1 Mediates Borna Disease Virus 1-Induced Changes in Peroxisomal and Mitochondrial Dynamics in Neurons

Author:

Osei Dominic12ORCID,Baumgart-Vogt Eveline1ORCID,Ahlemeyer Barbara1ORCID,Herden Christiane23ORCID

Affiliation:

1. Institute for Anatomy and Cell Biology, Justus Liebig University Giessen, 35392 Giessen, Germany

2. Institute of Veterinary Pathology, Justus Liebig University Giessen, 35392 Giessen, Germany

3. Center for Mind, Brain and Behavior, Justus Liebig University Giessen, 35392 Giessen, Germany

Abstract

Borna disease virus 1 (BoDV1) causes a persistent infection in the mammalian brain. Peroxisomes and mitochondria play essential roles in the cellular antiviral immune response, but the effect of BoDV1 infection on peroxisomal and mitochondrial dynamics and their respective antioxidant capacities is still not clear. Using different mouse lines—i.e., tumor necrosis factor-α transgenic (TNFTg; to pro-inflammatory status), TNF receptor-1 knockout (TNFR1ko), and TNFR2ko mice in comparison to wild-type (Wt) mice—we analyzed the abundances of both organelles and their main antioxidant enzymes, catalase and superoxide dismutase 2 (SOD2), in neurons of the hippocampal, cerebral, and cerebellar cortices. In TNFTg mice, a strong increase in mitochondrial (6.9-fold) and SOD2 (12.1-fold) abundances was detected; meanwhile, peroxisomal abundance increased slightly (1.5-fold), but that of catalase decreased (2.9-fold). After BoDV1 infection, a strong decrease in mitochondrial (2.1–6.5-fold), SOD2 (2.7–9.1-fold), and catalase (2.7–10.3-fold) abundances, but a slight increase in peroxisomes (1.3–1.6-fold), were detected in Wt and TNFR2ko mice, whereas no changes occurred in TNFR1ko mice. Our data suggest that the TNF system plays a crucial role in the biogenesis of both subcellular organelles. Moreover, TNFR1 signaling mediated the changes in peroxisomal and mitochondrial dynamics after BoDV1 infection, highlighting new mechanisms by which BoDV1 may achieve immune evasion and viral persistence.

Funder

Graduate School Scholarship Program of the German Academic Exchange Service

Publisher

MDPI AG

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