Abstract
Reticuloendotheliosis virus (REV) causes immune-suppression disease in poultry, leading to a significant economic burden worldwide. Recent evidence demonstrated that the REV can enter the semen and then induce artificial insemination, but how the virus gets into semen was little known. Accumulating studies indicated that exosomes serve as vehicles for virus transmission, but the role of exosomes in viral shedding through the semen remains unclear. In this study, exosomes purified from the REV-positive semen were shown with reverse transcription-PCR and mass spectrometry to contain viral genomic RNA and viral proteins, which could also establish productive infections both in vivo and in vitro and escape from the REV-specific neutralizing antibodies. More importantly, compared with the infection caused by free virions, the exosome is more efficient for the virus to ensure effective infection and replication, which can also help the REV compromise the efficacy of the host immune response. In summary, this study demonstrated that semen-derived exosomes can medicate the transmission and immune escape of REV, implicating a novel mechanism for REV entering the semen and leading to vertical transmission.
Highlights
The first member of the reticuloendotheliosis virus (REV), including several closely related amphotropic avian retroviruses [1], was isolated from a turkey in 1957 [2]
Liquid chromatography-tandem mass spectrometry (LC-MS/MS) combined with Gene Ontology (GO) analysis was performed to characterize the proteins of semen-derived exosomes
Consistent with previous studies suggesting that viral nucleic acids are present in exosomes from infected cells [35, 36], the REV wholegenome RNAs were detected in REV-positive semen-derived exosomes (Figure 1E)
Summary
The first member of the reticuloendotheliosis virus (REV), including several closely related amphotropic avian retroviruses (family Retroviridae) [1], was isolated from a turkey in 1957 [2]. REV was reported in a diverse range of hosts including chicken [3], duck [4], geese [5], turkey [6], and wild birds [7]. Historical, phylogenetic, and paleovirological evidence totally supports a scenario wherein REVs originated as mammalian retroviruses (e.g., type C retroviruses) that were iatrogenically introduced into avian hosts [10].
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