Abstract
We have investigated the role of vif in maedi-visna virus (MVV), a lentivirus of sheep, by studying in vitro replication of vif-deleted MVV in several cell types, and the effects of vif deletion on in vivo infection. By measuring RT activity, we found that in comparison to wild-type MVV, growth of vif-deleted MVV was similar in fetal ovine synovial (FOS) cells, highly attenuated in sheep choroid plexus (SCP) cells, and not detectable in macrophages, natural target cells of MVV. Productive infection by vif-deleted MVV could not be demonstrated in sheep. An increased mutation frequency was observed in DNA produced by endogenous reverse transcription of viral RNA in vif-deleted virions, indicating the existence of a factor comparable in action to human APOBEC3G. These results suggest that the vif gene of MVV is essential for infectivity and that the Vif protein protects the viral genome from enpackaged mutagenic activities.
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