ArticleVirologica Sinica2023
Ebola virus VP35 perturbs type I interferon signaling to facilitate viral replication.
Article in Virologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Mapping the global evidence base of bundibugyo ebolavirus disease: a systematic scoping review of research gaps and preparedness priorities.BMC infectious diseases · 2026Article
- Review
- Review
- 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025Review
- Thermal tolerance and inactivation of Ebola virus.Virologica Sinica · 2025Article
- Herpes simplex virus 1 encodes a STING antagonist that can be therapeutically targeted.Cell reports. Medicine · 2025Article
- A comparative analysis of Marburg virus-infected bat and human models from public high-throughput sequencing data.International journal of medical sciences · 2025Article
- Emerging and reemerging infectious diseases: global trends and new strategies for their prevention and control.Signal transduction and targeted therapy · 2024Review
- Development of a Měnglà virus minigenome and comparison of its polymerase complexes with those of other filoviruses.Virologica Sinica · 2024Article
- Virome analysis provides new insights into the pathogenesis mechanism and treatment of SLE disease.Frontiers in cellular and infection microbiology · 2024Article
- Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As one of the deadliest viruses, Ebola virus (EBOV) causes lethal hemorrhagic fevers in humans and nonhuman primates. The suppression of innate immunity leads to robust systemic virus replication of EBOV, leading to enhanced transmission. However, the mechanism of EBOV-host interaction is not fully understood. Here, we identified multiple dysregulated genes in early stage of EBOV infection through transcriptomic analysis, which are highly clustered to Jak-STAT signaling. EBOV VP35 and VP30 were found to inhibit type I interferon (IFN) signaling. Moreover, exogenous expression of VP35 blocks the phosphorylation of endogenous STAT1, and suppresses nuclear translocation of STAT1. Using serial truncated mutations of VP35, N-terminal 1-220 amino acid residues of VP35 were identified to be essential for blocking on type I IFN signaling. Remarkably, VP35 of EBOV suppresses type I IFN signaling more efficiently than those of Bundibugyo virus (BDBV) and Marburg virus (MARV), resulting in stable replication to facilitate the pathogenesis. Altogether, this study enriches understanding on EBOV evasion of innate immune response, and provides insights into the interplay between filoviruses and host.
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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.