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Reactivated endogenous retroviruses promote protein aggregate spreading
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Abstract
Prion-like spreading of protein misfolding is a characteristic of neurodegenerative diseases, but the exact mechanisms of intercellular protein aggregate dissemination remain unresolved. Evidence accumulates that endogenous retroviruses, remnants of viral germline infections that are normally epigenetically silenced, become upregulated in neurodegenerative diseases such as amyotrophic lateral sclerosis and tauopathies. Here we uncover that activation of endogenous retroviruses affects prion-like spreading of proteopathic seeds. We show that upregulation of endogenous retroviruses drastically increases the dissemination of protein aggregates between cells in culture, a process that can be inhibited by targeting the viral envelope protein or viral protein processing. Human endogenous retrovirus envelopes of four different clades also elevate intercellular spreading of proteopathic seeds, including pathological Tau. Our data support a role of endogenous retroviruses in protein misfolding diseases and suggest that antiviral drugs could represent promising candidates for inhibiting protein aggregate spreading.
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The endogenous murine leukemia virus was found to potently increase spreading of Sup35 and tau between cells.
“The endogenous murine leukemia virus was found to potently increase spreading of Sup35 and tau between cells.”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as Liu et al. 2023
While the overexpression of Gag/Pol and ENV elevated tau propagation, spreading was found to be most efficient when active viral particles were produced by donor cells.
“While the overexpression of Gag/Pol and ENV elevated tau propagation, spreading was found to be most efficient when active viral particles were produced by donor cells.”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as Liu et al. 2023
Overexpression of HERV-W-, -K-, -R-, and -H-encoded ENV glycoproteins was also found to facilitate the spread of tau between cells in coculture.
“Overexpression of HERV-W-, -K-, -R-, and -H-encoded ENV glycoproteins was also found to facilitate the spread of tau between cells in coculture.”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as Liu et al. 2023
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Metadata
- Authors
- Liu, S., Heumüller, S.-E., Hossinger, A., Müller, S. A., Buravlova, O., Lichtenthaler, S. F., Denner, P., & Vorberg, I. M.
- Affiliations
- German Federal Institute for Risk Assessment (BfR) (DE)
- German Center for Neurodegenerative Diseases (DE)
- University of Bonn (DE)
- Corresponding author
- Vorberg, Ina M.
- Venue
- Nature Communications
- Published
- 2023-08-18
- Volume
- 14
- Issue
- 1
- Pages
- 5034-5034
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC10439213
- OpenAlex
- W4385971153
- Cited by
- 48
- References
- 111
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 13 · 2023: 3
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion, cc-by)
- DZNE Pub (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Deutsche Forschungsgemeinschaft (EXC 2145 SyNergy– ID 390857198)
- Bundesministerium für Bildung und Forschung (CLINSPECT-M (FKZ161L0214C))
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- endogenous retroviruses, prion-like spreading, protein misfolding, neurodegenerative diseases, amyotrophic lateral sclerosis, tauopathy, pathological tau, viral envelope proteins, antiviral agents
- MeSH terms
- Amyotrophic Lateral Sclerosis, Antiviral Agents, Humans, Prions, Endogenous Retroviruses, Protein Aggregates
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