ArticleNature microbiology2026
Host-virus determinants of Ebola virus persistence in a human cerebral organoid model.
Article in Nature microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Article
- Ebola virus persistence and the hidden cost of immune privilege.Nature microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors.
Funding
Abstract
Ebola virus (EBOV) causes Ebola virus disease (EVD), a multisystemic human disease associated with an extraordinarily high case-fatality rate. EVD survivors may experience recrudescent inflammation with viral persistence in immune-privileged tissues, including the central nervous system (CNS). Persistence, defined by ongoing replication of the EBOV genome beyond the acute disease phase, may lead to virion production. Productive persistence has been linked to re-initiation of EVD outbreaks. We developed a human cerebral organoid model to investigate the host and viral determinants of EBOV CNS persistence. In this model, EBOV persistence for 120 days was sustained by continuous infection of astrocytes and neurons and the recruitment and infection of microglia. This was accompanied by the emergence of EBOV defective viral genomes and genomic subvariants, cell-to-cell transmission, activation of cell-specific innate immunity, and late brain organoid inflammation, indicating that persistent infection of EBOV within immune-privileged niches drives local inflammation.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.