Brain-like organoids reveal how Ebola persists and spreads for 120 days
· Medical Xpressby Anna Hein, Bernhard-Nocht-Institut für Tropenmedizin
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Following infection, the Ebola virus can survive unnoticed in the human body for months or even years, hiding in areas with little immune surveillance like the central nervous system. The danger is that those affected may have an Ebola virus disease relapse or even trigger a new outbreak. Using a cerebral organoid model, researchers at the Bernhard Nocht Institute for Tropical Medicine (BNITM) and the Icahn School of Medicine at Mount Sinai (ISMMS), together with other collaborators, gained valuable insights into the mechanisms of such Ebola virus persistence. Their findings were recently published in Nature Microbiology.
Ebola virus is a filovirus that causes Ebola virus disease, a severe and often fatal infection. Even if those affected survive the acute phase of the disease, the virus can remain in the body. Infectious Ebola virus has been detected in semen for months or even a year after infection. The virus can also persist in other immune-privileged organs such as the central nervous system, particularly the brain.
Immune-privileged means the immune system reacts in a weakened and controlled manner in these areas in order to protect sensitive tissue. As a result, it cannot always eliminate the virus completely. This persistent viral presence increases the risk of late inflammatory disease and relapses in individual patients and, albeit rarely, of retransmission to others.
Cerebral organoids suitable for investigating Ebola persistence
Little is known about the mechanisms that allow the Ebola virus to survive long term in its host. Does it persist in tissues or in individual cells? Does it produce new infectious particles? Does it alter its genome to evade detection by our immune system? As research on the human central nervous system is highly complicated, suitable model systems are required instead.
This is precisely where the researchers focused their efforts. They successfully used an established cerebral organoid model to perform long-term infection studies. To make these organoids, they stimulated so-called human-induced pluripotent stem cells so they developed into spherical, brain-like structures consisting of various cells of the central nervous system.
"These cerebral organoids enable us to investigate in detail the mechanisms that the Ebola virus and other filoviruses use to persist in the human central nervous system. Through experiments in this model system, we can gain insights that help us improve our understanding of the long-term effects of persistence, like the severe and sometimes fatal inflammation seen in Ebola virus disease survivors with meningoencephalitis," explains Dr. Lina Widerspick, first author of the publication and former researcher at the BNITM.
She carried out part of the experiments during a research visit to the Integrated Research Facility (IRF)-Frederick of the National Institutes of Health (NIH) in the U.S. She is now based at the Bundeswehr Institute of Microbiology in Munich.
Organoids give the unique opportunity to study this phenomenon in a human background rather than in an animal model. This may help in reassessing and optimizing treatments like antivirals and further opens avenues to reduce the use of animal models in infectious disease research in the future.
Ebola virus can survive long term in cerebral organoids
The researchers showed that Ebola virus and other filoviruses, such as Sudan, Reston and Marburg virus, can replicate in cerebral organoids for up to 120 days. They also found that the Ebola virus infected various cell types in the cerebral organoids—neurons as well as astrocytes. Microglia, the brain's immune cells, were also attracted to the site and infected by the virus.
The Ebola virus was able to spread in the cerebral organoids in two ways: directly from an infected cell to a neighboring cell (cell-to-cell transmission) and by budding from the host cell, which is the classical way the virus spreads. Thus, this represents a "productive persistence," meaning Ebola virus is not present in an inactive state within cells, but remains infectious.
The cerebral organoids produced pro-inflammatory cytokines, but the immune response was unable to successfully eliminate the virus during the persistent infection. "We observed elevated immune and inflammatory responses in the late stages of cerebral organoid culture. We therefore conclude that a persistent Ebola virus infection in immune-privileged tissues can lead to local inflammation.
"This observation is consistent with the fact that some Ebola virus disease survivors develop inflammation of the eye, meninges or brain months after infection with Ebola virus," says Prof. César Muñoz-Fontela, head of the Virus Immunology research group at BNITM and co–last author of the study.
How Ebola adapts to survive
Defective viral genomes are considered a well-known mechanism used by many viruses to suppress their replication. This enables the viruses to survive in the body in an attenuated but long-lasting form. It is also known that Ebola virus genomes mutate when they replicate for a long time because their genetic machinery cannot proofread the genomes as human machinery would. The research team has now identified defective viral genomes and particles, and mutations in the Ebola virus genomes, in late-stage persistently infected cerebral organoids.
"Many of these mutations had been proposed to reduce or prevent viral replication in naturally occurring infections. Because Ebola virus behaves similarly in this model system to how it does in human infections, this underscores the suitability of our cerebral organoids for investigating filovirus persistence," explains Prof. Gustavo Palacios, expert on Ebola virus genomics, professor of microbiology at ISMMS in New York, and co–last author of the publication.
The researchers also identified mutations that have not been described in Ebola virus disease survivors. Further investigations are now needed to determine whether these mutations are causally linked to filovirus persistence.
"Our work in human cerebral organoids highlights the potential of this model system to investigate persistent infections in immune-privileged tissues," concludes Muñoz-Fontela. "Further studies are now important to investigate the long-term interactions between virus and host, expanding our studies toward less-studied filoviruses like Reston, Taï Forest, Bombali and Bundibugyo virus, and to deepen our understanding of filoviral persistence mechanisms."
Publication details
Lina Widerspick et al, Host–virus determinants of Ebola virus persistence in a human cerebral organoid model, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02388-2
Journal information: Nature Microbiology
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