TY - JOUR
KW - Ebola virus
KW - Viral pathogenesis
KW - Virus–host interactions
AU - Lina Widerspick
AU - Santiago Vidal Freire
AU - Johanna F. Steffen
AU - Shruti Shirsathe
AU - Petra Allartz
AU - Molly A. Vickers
AU - Christoph Henkel
AU - Pedro Neira Pelén
AU - Julia Nave
AU - Monika Rottstegge
AU - Michelle Heung
AU - Stephanie Wurr
AU - Dennis Tappe
AU - Lisa Oestereich
AU - Jonas Müller
AU - Angelique Hoelzemer
AU - Leonore Mensching
AU - Thomas Hoenen
AU - Nicole C. Kleinstreuer
AU - Ian Crozier
AU - John G. Bernbaum
AU - Gabriella Worwa
AU - Jens H. Kuhn
AU - Gustavo Palacios
AU - César Muñoz-Fontela
AB - 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.
BT - Nature Microbiology
DA - 2026-06-12
DO - 10.1038/s41564-026-02388-2
LA - en
N2 - 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.
PY - 2026
SP - 1
EP - 16
T2 - Nature Microbiology
TI - Host–virus determinants of Ebola virus persistence in a human cerebral organoid model
UR - https://www.nature.com/articles/s41564-026-02388-2
Y2 - 2026-07-02
SN - 2058-5276
ER -