کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9288148 | 1227457 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Disruption of the putative splice acceptor site for SIVmac239Vif reveals tight control of SIV splicing and impaired replication in Vif non-permissive cells
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ویروس شناسی
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چکیده انگلیسی
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 SIVmac239 (SIVÎvif-SA). Despite three consensus splice acceptor sites nearby SA1, SIVÎvif-SA did not efficiently generate alternatively spliced vif mRNA. SIVÎvif-SA was growth attenuated in CEMx174 and H9 cells but not in CEM-SS cells. Following SIVÎvif-SA, but not SIVmac239, 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Virology - Volume 338, Issue 2, 1 August 2005, Pages 281-291
Journal: Virology - Volume 338, Issue 2, 1 August 2005, Pages 281-291
نویسندگان
Joseph G. Victoria, W. Edward Jr.,