T Lymphocytes transduced with a lentiviral vector expressing F12-Vif are protected from HIV-1 infection in an APOBEC3G-independent manner
- PMID: 16039909
- DOI: 10.1016/j.ymthe.2005.05.014
T Lymphocytes transduced with a lentiviral vector expressing F12-Vif are protected from HIV-1 infection in an APOBEC3G-independent manner
Abstract
The viral infectivity factor (Vif) is an essential component of the HIV-1 infectious cycle. Vif counteracts the action of the cytidine deaminase APOBEC3G (AP3G), which confers nonimmune antiviral defense against HIV-1 to T lymphocytes. Disabling or interfering with the function of Vif could represent an alternative therapeutic approach to AIDS. We have expressed a natural mutant of Vif, F12-Vif, in a VSV-G-pseudotyped lentiviral vector under the Tat-inducible control of the HIV-1 LTR. Conditional expression of F12-Vif prevents replication and spreading of both CXCR4 and CCR5 strains of HIV-1 in human primary T lymphocyte and T cell lines. T cells transduced with F12-Vif release few HIV-1 virions and with reduced infectivity. Several lines of evidence indicate that HIV-1 interference requires the presence of both wild-type and F12-Vif proteins, suggesting a dominant-negative feature of the F12-Vif mutant. Surprisingly, however, the F12-Vif-mediated inhibition does not depend on the reestablishment of the AP3G function.
Similar articles
-
Functional domains of APOBEC3G required for antiviral activity.J Cell Biochem. 2004 Jun 1;92(3):560-72. doi: 10.1002/jcb.20082. J Cell Biochem. 2004. PMID: 15156567
-
Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein.Nature. 2002 Aug 8;418(6898):646-50. doi: 10.1038/nature00939. Epub 2002 Jul 14. Nature. 2002. PMID: 12167863
-
A new approach to an AIDS vaccine: creating antibodies to HIV vif will enable apobec3G to turn HIV-infection into a benign problem.Med Hypotheses. 2005;64(2):261-3. doi: 10.1016/j.mehy.2004.07.015. Med Hypotheses. 2005. PMID: 15607551
-
New insights into the role of Vif in HIV-1 replication.AIDS Rev. 2004 Jan-Mar;6(1):34-9. AIDS Rev. 2004. PMID: 15168739 Review.
-
APOBEC deaminases as cellular antiviral factors: a novel natural host defense mechanism.Med Sci Monit. 2006 May;12(5):RA92-8. Med Sci Monit. 2006. PMID: 16641889 Review.
Cited by
-
Cell activation and HIV-1 replication in unstimulated CD4+ T lymphocytes ingesting exosomes from cells expressing defective HIV-1.Retrovirology. 2014 Jun 12;11:46. doi: 10.1186/1742-4690-11-46. Retrovirology. 2014. PMID: 24924541 Free PMC article.
-
Heterogeneity of signal transducer and activator of transcription binding sites in the long-terminal repeats of distinct HIV-1 subtypes.Open Virol J. 2007;1:26-32. doi: 10.2174/1874357900701010026. Epub 2007 Oct 20. Open Virol J. 2007. PMID: 19440456 Free PMC article.
-
Prospects for Foamy Viral Vector Anti-HIV Gene Therapy.Biomedicines. 2016 Mar 29;4(2):8. doi: 10.3390/biomedicines4020008. Biomedicines. 2016. PMID: 28536375 Free PMC article. Review.
-
Identification of dominant negative human immunodeficiency virus type 1 Vif mutants that interfere with the functional inactivation of APOBEC3G by virus-encoded Vif.J Virol. 2010 May;84(10):5201-11. doi: 10.1128/JVI.02318-09. Epub 2010 Mar 10. J Virol. 2010. PMID: 20219919 Free PMC article.
-
Mutational analysis of the HIV-1 auxiliary protein Vif identifies independent domains important for the physical and functional interaction with HIV-1 reverse transcriptase.Nucleic Acids Res. 2009 Jun;37(11):3660-9. doi: 10.1093/nar/gkp226. Epub 2009 Apr 15. Nucleic Acids Res. 2009. PMID: 19369217 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Miscellaneous