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Reactivated endogenous retroviruses promote protein aggregate spreading
Shu Liu1,2, Stefanie-Elisabeth Heumüller1, André Hossinger1
1German Center for Neurodegenerative Diseases Bonn (DZNE), Venusberg Campus 1/ 99, 53127, Bonn, Germany.
Nature Communications
|August 18, 2023
Summary
Activation of endogenous retroviruses accelerates protein misfolding spread in neurodegenerative diseases. Targeting viral proteins with antiviral drugs may inhibit this intercellular dissemination of proteopathic seeds.
Area of Science:
- Neurobiology
- Molecular Biology
- Virology
Background:
- Prion-like spreading of misfolded proteins characterizes neurodegenerative diseases.
- Mechanisms of intercellular protein aggregate dissemination are not fully understood.
- Endogenous retroviruses (ERVs) are upregulated in neurodegenerative conditions like ALS and tauopathies.
Purpose of the Study:
- To investigate the role of endogenous retrovirus activation in the prion-like spreading of protein misfolding.
- To determine if ERVs influence the intercellular dissemination of proteopathic seeds.
Main Methods:
- Assessing the effect of ERV upregulation on protein aggregate spreading in cell culture.
- Testing the efficacy of targeting viral envelope proteins and viral protein processing in inhibiting spread.
- Evaluating the impact of human endogenous retrovirus envelopes from different clades on proteopathic seed spreading.
Main Results:
- Upregulation of endogenous retroviruses significantly increased the dissemination of protein aggregates between cells.
- Inhibition of viral envelope protein or viral protein processing reduced this intercellular spreading.
- Human endogenous retrovirus envelopes enhanced the spreading of proteopathic seeds, including pathological Tau.
Conclusions:
- Endogenous retroviruses play a role in the progression of protein misfolding diseases.
- Antiviral drugs targeting ERVs could be a potential therapeutic strategy to inhibit protein aggregate spreading in neurodegenerative diseases.
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