Disruption of the putative splice acceptor site for SIV(mac239)Vif reveals tight control of SIV splicing and impaired replication in Vif non-permissive cells

Vif is dispensable for simian immunodeficiency virus (SIV) replication in some cells, termed permissive (i.e., CEM-SS), but not in others, termed non-permissive (i.e., H9, CEMx174, and peripheral blood lymphocytes). Non-permissive cells express the RNA editing enzyme, APOBEC3G. To determine whether...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2005-08, Vol.338 (2), p.281-291
Main Authors: Victoria, Joseph G, Robinson, Jr, W Edward
Format: Article
Language:English
Subjects:
Alternative Splicing
Animals
Base Sequence
Binding Sites
Cell Line
Consensus Sequence
DNA Replication
Gene Products, vif - genetics
Humans
Kinetics
Molecular Sequence Data
RNA, Messenger - genetics
RNA, Viral - genetics
Simian Immunodeficiency Virus - genetics
Transcription, Genetic
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Summary:Vif is dispensable for simian immunodeficiency virus (SIV) replication in some cells, termed permissive (i.e., CEM-SS), but not in others, termed non-permissive (i.e., H9, CEMx174, and peripheral blood lymphocytes). Non-permissive cells express the RNA editing enzyme, APOBEC3G. To determine whether vif mRNA could be alternatively spliced, a mutation altering the putative vif splice acceptor site (SA1) was introduced into SIV(mac239) (SIV(Deltavif-SA)). Despite three consensus splice acceptor sites nearby SA1, SIV(Deltavif-SA) did not efficiently generate alternatively spliced vif mRNA. SIV(Deltavif-SA) was growth attenuated in CEMx174 and H9 cells but not in CEM-SS cells. Following SIV(Deltavif-SA), but not SIV(mac239), infection in either H9 or CEMx174 cells viral cDNA contained numerous G to A mutations; no such differences were observed in CEM-SS cells. This pattern is consistent with mutations generated by APOBEC3G in the absence of Vif. Therefore, efficient splicing of SIV vif mRNA is tightly controlled and requires the SA1 site.
ISSN:0042-6822