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. 2023 Nov 9;61(5):2881–2903. doi: 10.1007/s12035-023-03761-6

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Neurotropic viral infection induces neurodegeneration through a variety of cellular mechanisms. Viral infection affects several host cell response mechanisms to attenuate neuronal functions, including (i) increasing reactive oxygen species (ROS) by interfering with the electron transport system and disrupting the production of antioxidants, (ii) promoting neuroinflammation by increasing proinflammatory cytokine secretion from infiltrated inflammatory cells and infected neuronal cells such as microglia and astrocytes, which then (iii) activates the apoptosis signaling pathway by inducing both intrinsic and extrinsic signaling pathways leading to neuronal death in the CNS. Abbreviation: Cyt c, cytochrome c; CoQ, coenzyme Q; BCL-2, B-cell lymphoma 2; BAX, BCL-2 associated X; FAD, flavin adenine dinucleotide; FADH, flavin adenine dinucleotide hydride; NADH, reduced nicotinamide adenine dinucleotide; NAD+, nicotinamide adenine dinucleotide; TNF-α, tumor necrosis factor alpha; TRADD, TNF receptor-associated death domain; CAT, catalase; SOD, superoxide dismutase; GPx, glutathione peroxidase; GR, glutathione reductase; TRX, thioredoxin; TLRs, toll-like receptors; TCA, tricarboxylic acid