In this review, we discuss how viruses can also directly contribute to disease-associated protein misfolding and subsequent processes of protein aggregate spreading.ĪD affects 40 million people worldwide and is associated with extracellular deposition of Aβ amyloid as plaques and the intracellular deposition of hyperphosphorylated Tau protein as neurofibrillary tangles. Some viruses can enter the CNS and affect neurodegeneration via lytic egress from infected neurons by impairing neuronal processes or by inducing neuronal apoptosis. Viral infections can activate astrocytes and microglia or induce CNS infiltration by peripheral immune cells, thereby causing neuroinflammation (reviewed in ). An impressive number of studies highlights that viruses, through their capacity to hijack the host cell machinery and induce inflammation, trigger and/or contribute to degenerative processes. Pathogens, and especially viruses, are suspected to act as etiological factors in several NDs. NDs are multifactorial diseases, triggered by enhanced age as well as genetic and environmental risk factors. The etiology of idiopathic NDs remains unknown. Approximately 90% of NDs occur sporadically, and only few cases are linked to mutations in aggregation-prone proteins or proteins involved in their processing or trafficking. Protein aggregation occurs sequentially in anatomically connected areas, suggesting a progressive spreading throughout the CNS of affected individuals. Amyloid fibrils then act as seeds that bind and convert proteins of the same kind into their abnormal isoforms (seeding).

Protein aggregation follows a nucleated polymerization process, in which misfolded proteins spontaneously coassemble into oligomers (nucleation) that reorganize into beta-sheet-rich fibrils. A hallmark of NDs is the intra- or extracellular deposition of cellular proteins into ordered high-molecular weight fibrils, termed amyloid. Neurodegenerative diseases (NDs) are fatal chronic diseases of the central nervous system (CNS), including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and transmissible spongiform encephalopathies (TSEs).

19195304.1”.Įvidence for an association of viral infections with neurodegenerative diseases PCT/EP2020/074809, claiming priority to “European Application No. 17/640,119 based on PCT International application No. Vorberg holds pending patent applications for “HERV inhibitors for use in treating tauopathies”: “US Patent Application No. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: I have read the journal’s policy and have the following conflicts: I.

PL received the support of the Association pour la recherche sur la SLA and the Association Française contre les Myopathies (AFM), MyoNeurAlp Alliance. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: This work was supported by the CNRS and the INSERM (PL) and DZNE (IMV). Haigh, National Institutes of Health, UNITED STATESĬopyright: © 2022 Leblanc, Vorberg. Citation: Leblanc P, Vorberg IM (2022) Viruses in neurodegenerative diseases: More than just suspects in crimes.

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