Journal
CELL HOST & MICROBE
Volume 24, Issue 3, Pages 405-+Publisher
CELL PRESS
DOI: 10.1016/j.chom.2018.08.003
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Funding
- Joint Science and Technology Office for Chemical and Biological Defense (JSTO-CBD) of the Defense Threat Reduction Agency (DTRA)
- Medical Countermeasure Systems (MCS) of the Joint Program Executive Office for Chemical and Biological Defense (JPEO-CBD)
- Battelle Memorial Institute's prime contract
- US National Institute of Allergy and Infectious Diseases (NIAID) [HHSN272200700016I]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZICAI009006] Funding Source: NIH RePORTER
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Sexual transmission of filoviruses was first reported in 1968 after an outbreak of Marburg virus (MARV) disease and recently caused flare-ups of Ebola virus disease in the 2013-2016 outbreak. How filoviruses establish testicular persistence and are shed in semen remain unknown. We discovered that persistent MARV infection of seminiferous tubules, an immune-privileged site that harbors sperm production, is a relatively common event in crab-eating macaques that survived infection after antiviral treatment. Persistence triggers severe testicular damage, including spermatogenic cell depletion and inflammatory cell invasion. MARV mainly persists in Sertoli cells, leading to breakdown of the blood-testis barrier formed by inter-Sertoli cell tight junctions. This disruption is accompanied by local infiltration of immunosuppressive CD4(+)Foxp3(+) regulatory T cells. Our study elucidates cellular events associated with testicular persistence that may promote sexual transmission of filoviruses and suggests that targeting immunosuppression may be warranted to clear filovirus persistence in damaged immune-privileged sites.
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