The sexual transmission of filoviruses was first reported in 1968 following an outbreak of Marburg virus (MARV) disease and has been highlighted again more recently by the flare-ups of Ebolavirus disease following the 2013 outbreak. However it is still not clear how filoviruses establish persistence in the testes and then are able to be shed in semen. The authors found that persistent MARV infection of seminiferous tubules, an immune-privileged site and centre of sperm production, is a relatively common event in crab-eating macaques that have survived infection following antiviral treatment. They found that this persistence triggers severe testicular damage, including spermatogenic cell depletion and inflammatory cell invasion. The virus was found to mainly persist in Sertoli cells, which leads to the breakdown of the blood-testis barrier formed by inter-Sertoli cell tight junctions. This disruption is also accompanied by local infiltration by immunosuppressive CD4+Foxp3+ regulatory T cells. Therefore these cellular events associated with testicular persistence may promote the sexual transmission of filoviruses.
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