ArticleProceedings of the National Academy of Sciences of the United States of America2023
Chaperone-assisted selective autophagy targets filovirus VP40 as a client and restricts egress of virus particles.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Conserved Filovirus Proteins as Targets of Broad-Spectrum Antivirals.bioRxiv : the preprint server for biology · 2025Article
- Marburg virus exploits the Rab11-mediated endocytic pathway in viral-particle production.Microbiology spectrum · 2024Article
- Hippo signaling pathway regulates Ebola virus transcription and egress.Nature communications · 2024Article
- Molecular insights into the Ebola virus life cycle.Nature microbiology · 2024Review
- Chaperoning the driver of filovirus egress to a dead end.Autophagy · 2023Article
- Autophagy induced by human adenovirus B7 structural protein VI inhibits viral replication.Virologica Sinica · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The filovirus VP40 protein directs virion egress, which is regulated either positively or negatively by select VP40-host interactions. We demonstrate that host BAG3 and HSP70 recognize VP40 as a client and inhibit the egress of VP40 virus-like particles (VLPs) by promoting degradation of VP40 via Chaperone-assisted selective autophagy (CASA). Pharmacological inhibition of either the early stage formation of the VP40/BAG3/HSP70 tripartite complex, or late stage formation of autolysosomes, rescued VP40 VLP egress back to WT levels. The mechanistic target of rapamycin complex 1 (mTORC1) is a master regulator of autophagy, and we found that surface expression of EBOV GP on either VLPs or an infectious VSV recombinant virus, activated mTORC1. Notably, pharmacological suppression of mTORC1 signaling by rapamycin activated CASA in a BAG3-dependent manner to restrict the egress of both VLPs and infectious EBOV in Huh7 cells. In sum, our findings highlight the involvement of the mTORC1/CASA axis in regulating filovirus egress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.