02366nas a2200469   4500000000100000000000100001008004100002260001500043653001600058653002300074653003000097100002000127700002600147700002300173700002100196700001800217700002100235700002100256700002300277700001500300700002200315700001900337700001900356700001700375700002000392700001800412700002400430700002200454700001800476700002700494700001600521700002100537700002000558700001700578700002100595700002600616245009200642856005500734300000900789520108400798022001401882       2026                            d  c2026-06-1210aEbola virus10aViral pathogenesis10aVirus–host interactions1 aLina Widerspick1 aSantiago Vidal Freire1 aJohanna F. Steffen1 aShruti Shirsathe1 aPetra Allartz1 aMolly A. Vickers1 aChristoph Henkel1 aPedro Neira Pelén1 aJulia Nave1 aMonika Rottstegge1 aMichelle Heung1 aStephanie Wurr1 aDennis Tappe1 aLisa Oestereich1 aJonas Müller1 aAngelique Hoelzemer1 aLeonore Mensching1 aThomas Hoenen1 aNicole C. Kleinstreuer1 aIan Crozier1 aJohn G. Bernbaum1 aGabriella Worwa1 aJens H. Kuhn1 aGustavo Palacios1 aCésar Muñoz-Fontela00aHost–virus determinants of Ebola virus persistence in a human cerebral organoid model  uhttps://www.nature.com/articles/s41564-026-02388-2  a1-163 aEbola 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.  a2058-5276