Anti-APOBEC3G activity of HIV-1 Vif protein is attenuated in elite controllers

HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectiv...

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Published inJournal of virology Vol. 89; no. 9; pp. 4992 - 5001
Main Authors Kikuchi, Tadashi, Iwabu, Yukie, Tada, Takuya, Kawana-Tachikawa, Ai, Koga, Michiko, Hosoya, Noriaki, Nomura, Shigeru, Brumme, Zabrina L, Jessen, Heiko, Pereyra, Florencia, Trocha, Alicja, Walker, Bruce D, Iwamoto, Aikichi, Tokunaga, Kenzo, Miura, Toshiyuki
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.05.2015
Subjects
APOBEC-3G Deaminase
Cell Line
Cytidine Deaminase - antagonists & inhibitors
Cytidine Deaminase - immunology
Gene Expression Profiling
Genes, Reporter
Genetic Vectors
HIV Infections - immunology
HIV-1 - immunology
Human immunodeficiency virus
Human immunodeficiency virus 1
Humans
Luciferases - analysis
Luciferases - genetics
Molecular Sequence Data
Polymorphism, Genetic
RNA, Viral - genetics
Sequence Analysis, DNA
Vesicular stomatitis virus
Vesiculovirus - genetics
vif Gene Products, Human Immunodeficiency Virus - genetics
vif Gene Products, Human Immunodeficiency Virus - metabolism
Virus-Cell Interactions
Online AccessGet full text

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Abstract HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectivity through anti-retroviral factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) degradation; however, little is known regarding Vif function in EC. Here, the anti-APOBEC3G activities of clonal, plasma HIV RNA-derived Vif sequences from 46 EC, 46 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfecting 293T cells with expression plasmids encoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif/env-deficient luciferase-reporter HIV-1 proviral DNA clone. Viral stocks were used to infect 293T cells, and Vif anti-APOBEC3G activity was quantified in terms of luciferase signal. On average, the anti-APOBEC3G activities of EC-derived Vif sequences (median log10 relative light units [RLU], 4.54 [interquartile range {IQR}, 4.30 to 4.66]) were significantly lower than those of sequences derived from NC (4.75 [4.60 to 4.92], P < 0.0001) and AI (4.74 [4.62 to 4.94], P < 0.0001). Reduced Vif activities were not associated with particular HLA class I alleles expressed by the host. Vif functional motifs were highly conserved in all patient groups. No single viral polymorphism could explain the reduced anti-APOBEC3G activity of EC-derived Vif, suggesting that various combinations of minor polymorphisms may underlie these effects. These results further support the idea of relative attenuation of viral protein function in EC-derived HIV sequences. HIV-1 elite controllers (EC) are rare individuals who are able to control plasma viremia to undetectable levels without antiretroviral therapy. Understanding the pathogenesis and mechanisms underpinning this rare phenotype may provide important insights for HIV vaccine design. The EC phenotype is associated with beneficial host immunogenetic factors (such as HLA-B*57) as well as with functions of attenuated viral proteins (e.g., Gag, Pol, and Nef). In this study, we demonstrated that HIV-1 Vif sequences isolated from EC display relative impairments in their ability to counteract the APOBEC3G host restriction factor compared to Vif sequences from normal progressors and acutely infected individuals. This result extends the growing body of evidence demonstrating attenuated HIV-1 protein function in EC and, in particular, supports the idea of the relevance of viral factors in contributing to this rare HIV-1 phenotype.
AbstractList HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectivity through anti-retroviral factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) degradation; however, little is known regarding Vif function in EC. Here, the anti-APOBEC3G activities of clonal, plasma HIV RNA-derived Vif sequences from 46 EC, 46 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfecting 293T cells with expression plasmids encoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif/env-deficient luciferase-reporter HIV-1 proviral DNA clone. Viral stocks were used to infect 293T cells, and Vif anti-APOBEC3G activity was quantified in terms of luciferase signal. On average, the anti-APOBEC3G activities of EC-derived Vif sequences (median log10 relative light units [RLU], 4.54 [interquartile range {IQR}, 4.30 to 4.66]) were significantly lower than those of sequences derived from NC (4.75 [4.60 to 4.92], P < 0.0001) and AI (4.74 [4.62 to 4.94], P < 0.0001). Reduced Vif activities were not associated with particular HLA class I alleles expressed by the host. Vif functional motifs were highly conserved in all patient groups. No single viral polymorphism could explain the reduced anti-APOBEC3G activity of EC-derived Vif, suggesting that various combinations of minor polymorphisms may underlie these effects. These results further support the idea of relative attenuation of viral protein function in EC-derived HIV sequences. IMPORTANCE HIV-1 elite controllers (EC) are rare individuals who are able to control plasma viremia to undetectable levels without antiretroviral therapy. Understanding the pathogenesis and mechanisms underpinning this rare phenotype may provide important insights for HIV vaccine design. The EC phenotype is associated with beneficial host immunogenetic factors (such as HLA-B*57) as well as with functions of attenuated viral proteins (e.g., Gag, Pol, and Nef). In this study, we demonstrated that HIV-1 Vif sequences isolated from EC display relative impairments in their ability to counteract the APOBEC3G host restriction factor compared to Vif sequences from normal progressors and acutely infected individuals. This result extends the growing body of evidence demonstrating attenuated HIV-1 protein function in EC and, in particular, supports the idea of the relevance of viral factors in contributing to this rare HIV-1 phenotype.
HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectivity through anti-retroviral factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) degradation; however, little is known regarding Vif function in EC. Here, the anti-APOBEC3G activities of clonal, plasma HIV RNA-derived Vif sequences from 46 EC, 46 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfecting 293T cells with expression plasmids encoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif / env -deficient luciferase -reporter HIV-1 proviral DNA clone. Viral stocks were used to infect 293T cells, and Vif anti-APOBEC3G activity was quantified in terms of luciferase signal. On average, the anti-APOBEC3G activities of EC-derived Vif sequences (median log 10 relative light units [RLU], 4.54 [interquartile range {IQR}, 4.30 to 4.66]) were significantly lower than those of sequences derived from NC (4.75 [4.60 to 4.92], P < 0.0001) and AI (4.74 [4.62 to 4.94], P < 0.0001). Reduced Vif activities were not associated with particular HLA class I alleles expressed by the host. Vif functional motifs were highly conserved in all patient groups. No single viral polymorphism could explain the reduced anti-APOBEC3G activity of EC-derived Vif, suggesting that various combinations of minor polymorphisms may underlie these effects. These results further support the idea of relative attenuation of viral protein function in EC-derived HIV sequences. IMPORTANCE HIV-1 elite controllers (EC) are rare individuals who are able to control plasma viremia to undetectable levels without antiretroviral therapy. Understanding the pathogenesis and mechanisms underpinning this rare phenotype may provide important insights for HIV vaccine design. The EC phenotype is associated with beneficial host immunogenetic factors (such as HLA-B*57) as well as with functions of attenuated viral proteins (e.g., Gag, Pol, and Nef). In this study, we demonstrated that HIV-1 Vif sequences isolated from EC display relative impairments in their ability to counteract the APOBEC3G host restriction factor compared to Vif sequences from normal progressors and acutely infected individuals. This result extends the growing body of evidence demonstrating attenuated HIV-1 protein function in EC and, in particular, supports the idea of the relevance of viral factors in contributing to this rare HIV-1 phenotype.
UNLABELLEDHIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectivity through anti-retroviral factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) degradation; however, little is known regarding Vif function in EC. Here, the anti-APOBEC3G activities of clonal, plasma HIV RNA-derived Vif sequences from 46 EC, 46 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfecting 293T cells with expression plasmids encoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif/env-deficient luciferase-reporter HIV-1 proviral DNA clone. Viral stocks were used to infect 293T cells, and Vif anti-APOBEC3G activity was quantified in terms of luciferase signal. On average, the anti-APOBEC3G activities of EC-derived Vif sequences (median log10 relative light units [RLU], 4.54 [interquartile range {IQR}, 4.30 to 4.66]) were significantly lower than those of sequences derived from NC (4.75 [4.60 to 4.92], P < 0.0001) and AI (4.74 [4.62 to 4.94], P < 0.0001). Reduced Vif activities were not associated with particular HLA class I alleles expressed by the host. Vif functional motifs were highly conserved in all patient groups. No single viral polymorphism could explain the reduced anti-APOBEC3G activity of EC-derived Vif, suggesting that various combinations of minor polymorphisms may underlie these effects. These results further support the idea of relative attenuation of viral protein function in EC-derived HIV sequences.IMPORTANCEHIV-1 elite controllers (EC) are rare individuals who are able to control plasma viremia to undetectable levels without antiretroviral therapy. Understanding the pathogenesis and mechanisms underpinning this rare phenotype may provide important insights for HIV vaccine design. The EC phenotype is associated with beneficial host immunogenetic factors (such as HLA-B*57) as well as with functions of attenuated viral proteins (e.g., Gag, Pol, and Nef). In this study, we demonstrated that HIV-1 Vif sequences isolated from EC display relative impairments in their ability to counteract the APOBEC3G host restriction factor compared to Vif sequences from normal progressors and acutely infected individuals. This result extends the growing body of evidence demonstrating attenuated HIV-1 protein function in EC and, in particular, supports the idea of the relevance of viral factors in contributing to this rare HIV-1 phenotype.
ABSTRACT HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectivity through anti-retroviral factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) degradation; however, little is known regarding Vif function in EC. Here, the anti-APOBEC3G activities of clonal, plasma HIV RNA-derived Vif sequences from 46 EC, 46 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfecting 293T cells with expression plasmids encoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif / env -deficient luciferase -reporter HIV-1 proviral DNA clone. Viral stocks were used to infect 293T cells, and Vif anti-APOBEC3G activity was quantified in terms of luciferase signal. On average, the anti-APOBEC3G activities of EC-derived Vif sequences (median log 10 relative light units [RLU], 4.54 [interquartile range {IQR}, 4.30 to 4.66]) were significantly lower than those of sequences derived from NC (4.75 [4.60 to 4.92], P < 0.0001) and AI (4.74 [4.62 to 4.94], P < 0.0001). Reduced Vif activities were not associated with particular HLA class I alleles expressed by the host. Vif functional motifs were highly conserved in all patient groups. No single viral polymorphism could explain the reduced anti-APOBEC3G activity of EC-derived Vif, suggesting that various combinations of minor polymorphisms may underlie these effects. These results further support the idea of relative attenuation of viral protein function in EC-derived HIV sequences. IMPORTANCE HIV-1 elite controllers (EC) are rare individuals who are able to control plasma viremia to undetectable levels without antiretroviral therapy. Understanding the pathogenesis and mechanisms underpinning this rare phenotype may provide important insights for HIV vaccine design. The EC phenotype is associated with beneficial host immunogenetic factors (such as HLA-B*57) as well as with functions of attenuated viral proteins (e.g., Gag, Pol, and Nef). In this study, we demonstrated that HIV-1 Vif sequences isolated from EC display relative impairments in their ability to counteract the APOBEC3G host restriction factor compared to Vif sequences from normal progressors and acutely infected individuals. This result extends the growing body of evidence demonstrating attenuated HIV-1 protein function in EC and, in particular, supports the idea of the relevance of viral factors in contributing to this rare HIV-1 phenotype.
HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional attenuation of some HIV-1 proteins has been reported in EC. The HIV-1 accessory protein Vif (virion infectivity factor) enhances viral infectivity through anti-retroviral factor apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G (APOBEC3G) degradation; however, little is known regarding Vif function in EC. Here, the anti-APOBEC3G activities of clonal, plasma HIV RNA-derived Vif sequences from 46 EC, 46 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared. Vesicular stomatitis virus glycoprotein (VSV-G)-pseudotyped viruses were generated by cotransfecting 293T cells with expression plasmids encoding patient-derived Vif, human APOBEC3G, VSV-G, and a vif/env-deficient luciferase-reporter HIV-1 proviral DNA clone. Viral stocks were used to infect 293T cells, and Vif anti-APOBEC3G activity was quantified in terms of luciferase signal. On average, the anti-APOBEC3G activities of EC-derived Vif sequences (median log10 relative light units [RLU], 4.54 [interquartile range {IQR}, 4.30 to 4.66]) were significantly lower than those of sequences derived from NC (4.75 [4.60 to 4.92], P < 0.0001) and AI (4.74 [4.62 to 4.94], P < 0.0001). Reduced Vif activities were not associated with particular HLA class I alleles expressed by the host. Vif functional motifs were highly conserved in all patient groups. No single viral polymorphism could explain the reduced anti-APOBEC3G activity of EC-derived Vif, suggesting that various combinations of minor polymorphisms may underlie these effects. These results further support the idea of relative attenuation of viral protein function in EC-derived HIV sequences. HIV-1 elite controllers (EC) are rare individuals who are able to control plasma viremia to undetectable levels without antiretroviral therapy. Understanding the pathogenesis and mechanisms underpinning this rare phenotype may provide important insights for HIV vaccine design. The EC phenotype is associated with beneficial host immunogenetic factors (such as HLA-B*57) as well as with functions of attenuated viral proteins (e.g., Gag, Pol, and Nef). In this study, we demonstrated that HIV-1 Vif sequences isolated from EC display relative impairments in their ability to counteract the APOBEC3G host restriction factor compared to Vif sequences from normal progressors and acutely infected individuals. This result extends the growing body of evidence demonstrating attenuated HIV-1 protein function in EC and, in particular, supports the idea of the relevance of viral factors in contributing to this rare HIV-1 phenotype.
Author Iwabu, Yukie
Koga, Michiko
Nomura, Shigeru
Brumme, Zabrina L
Miura, Toshiyuki
Tokunaga, Kenzo
Kikuchi, Tadashi
Iwamoto, Aikichi
Tada, Takuya
Kawana-Tachikawa, Ai
Hosoya, Noriaki
Walker, Bruce D
Pereyra, Florencia
Jessen, Heiko
Trocha, Alicja
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  organization: National Institute of Infectious Diseases, Tokyo, Japan
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  organization: National Institute of Infectious Diseases, Tokyo, Japan
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  organization: The Institute of Medical Science, the University of Tokyo, Tokyo, Japan
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Cites_doi 10.1128/JVI.01471-08
10.1084/jem.20052319
10.1371/journal.ppat.1000377
10.1074/jbc.M313093200
10.1074/jbc.M602413200
10.1097/QAD.0b013e3282fbd1da
10.1016/j.immuni.2007.08.010
10.1038/nri1489
10.1097/COH.0b013e3283454cf5
10.1126/science.273.5283.1856
10.1128/JVI.02694-06
10.1007/s007050050692
10.1128/JVI.02587-12
10.1128/JVI.80.4.2069-2072.2006
10.1182/blood-2005-12-4818
10.1073/pnas.0502440102
10.1093/nar/gkm181
10.1074/jbc.M004895200
10.1086/426826
10.1016/S0092-8674(03)00515-4
10.1126/science.270.5238.988
10.1128/JVI.00676-12
10.1038/ng934
10.1371/journal.ppat.0010006
10.1186/1742-4690-10-1
10.1128/JVI.79.14.9006-9018.2005
10.1101/gad.1249904
10.1086/506616
10.1128/JVI.01543-07
10.2174/157016205774370456
10.1128/JVI.00800-08
10.1128/JVI.80.7.3617-3623.2006
10.1038/nm1520
10.1074/jbc.C500082200
10.1038/nm945
10.1084/jem.20081984
10.1128/JVI.79.17.11513-11516.2005
10.1101/gad.1250204
10.1073/pnas.1530509100
10.1128/JVI.00286-10
10.1073/pnas.050567397
10.1128/jvi.66.11.6489-6495.1992
10.1074/jbc.M109.058305
10.1186/1742-4690-4-81
10.1128/JVI.73.12.10489-10502.1999
10.1128/JVI.78.11.6073-6076.2004
10.1038/nature03113
10.1016/j.tibs.2007.01.004
10.1128/JVI.01401-07
10.1128/JVI.01249-10
10.1126/science.1195271
10.1128/JVI.76.20.10533-10539.2002
10.1086/433188
10.1126/science.1089591
10.1128/JVI.00535-08
10.1093/emboj/16.15.4531
10.1128/JVI.00465-07
10.1038/nm946
10.1128/JVI.79.3.1975-1980.2005
10.1016/j.jmb.2007.07.029
10.1056/NEJM199501263320405
10.1128/jvi.59.2.284-291.1986
10.1128/JVI.01970-08
10.1097/QAI.0b013e3181fe9450
10.1074/jbc.M110.173286
10.1128/JVI.02176-07
10.1074/jbc.M210164200
10.1128/JVI.02579-07
10.1038/nrmicro1594
10.1128/JVI.01041-08
10.1099/vir.0.027102-0
10.1128/JVI.00960-10
10.3855/jidc.471
10.1128/JVI.01369-07
10.1086/526786
10.1016/S1097-2765(03)00353-8
10.1128/JVI.80.6.3112-3115.2006
10.1186/1742-4690-1-27
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DocumentTitleAlternate Anti-APOBEC3G Activity of HIV Vif in Elite Controllers
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Present address: Yukie Iwabu, Department of Veterinary Medicine, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan; Toshiyuki Miura, ViiV Healthcare K.K., Tokyo, Japan.
Citation Kikuchi T, Iwabu Y, Tada T, Kawana-Tachikawa A, Koga M, Hosoya N, Nomura S, Brumme ZL, Jessen H, Pereyra F, Trocha A, Walker BD, Iwamoto A, Tokunaga K, Miura T. 2015. Anti-APOBEC3G activity of HIV-1 Vif protein is attenuated in elite controllers. J Virol 89:4992–5001. doi:10.1128/JVI.03464-14.
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References 21106806 - J Gen Virol. 2011 Feb;92(Pt 2):247-68
16250885 - Curr HIV Res. 2005 Oct;3(4):339-44
10559367 - J Virol. 1999 Dec;73(12):10489-502
15574593 - Genes Dev. 2004 Dec 1;18(23):2867-72
15994794 - J Virol. 2005 Jul;79(14):9006-18
7808489 - N Engl J Med. 1995 Jan 26;332(4):228-32
18353945 - J Virol. 2008 Jun;82(11):5398-407
21051598 - Science. 2010 Dec 10;330(6010):1551-7
17869271 - J Mol Biol. 2007 Oct 26;373(3):541-50
16439564 - J Virol. 2006 Feb;80(4):2069-72
19360131 - PLoS Pathog. 2009 Apr;5(4):e1000377
16682496 - J Exp Med. 2006 May 15;203(5):1357-69
17522211 - J Virol. 2007 Aug;81(15):8236-46
21430530 - Curr Opin HIV AIDS. 2011 May;6(3):214-20
18353964 - J Virol. 2008 Jun;82(11):5510-8
17439959 - Nucleic Acids Res. 2007;35(9):2955-64
19307327 - J Exp Med. 2009 Apr 13;206(4):909-21
19109381 - J Virol. 2009 Mar;83(6):2460-8
21124229 - J Acquir Immune Defic Syndr. 2011 Feb 1;56(2):100-8
16201018 - PLoS Pathog. 2005 Sep;1(1):e6
15781449 - J Biol Chem. 2005 May 13;280(19):18573-8
15574592 - Genes Dev. 2004 Dec 1;18(23):2861-6
14527406 - Mol Cell. 2003 Sep;12(3):591-601
16076960 - Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11444-9
18562530 - J Virol. 2008 Sep;82(17):8422-30
23152537 - J Virol. 2013 Feb;87(3):1508-17
15650227 - J Virol. 2005 Feb;79(3):1975-80
18036235 - Retrovirology. 2007;4:81
20592083 - J Virol. 2010 Sep;84(17):8561-70
17173051 - Nat Med. 2007 Jan;13(1):46-53
16103203 - J Virol. 2005 Sep;79(17):11513-6
15609224 - J Infect Dis. 2005 Jan 15;191(2):159-63
17928341 - J Virol. 2007 Dec;81(24):13904-15
16142675 - Clin Infect Dis. 2005 Oct 1;41(7):1053-6
16501124 - J Virol. 2006 Mar;80(6):3112-5
16636053 - J Biol Chem. 2006 Jun 23;281(25):17259-65
18614631 - J Virol. 2008 Sep;82(18):9216-27
17203103 - Nat Rev Microbiol. 2007 Feb;5(2):141-51
19762971 - J Infect Dev Ctries. 2009;3(7):531-8
15592417 - Nature. 2004 Dec 9;432(7018):769-75
14672928 - J Biol Chem. 2004 Feb 27;279(9):7792-8
12134147 - Nat Genet. 2002 Aug;31(4):429-34
15516966 - Nat Rev Immunol. 2004 Nov;4(11):868-77
18453855 - AIDS. 2008 May 11;22(8):957-62
12239333 - J Virol. 2002 Oct;76(20):10533-9
23097438 - J Virol. 2013 Jan;87(1):444-53
14564014 - Science. 2003 Nov 7;302(5647):1056-60
14528300 - Nat Med. 2003 Nov;9(11):1404-7
15141007 - J Virol. 2004 Jun;78(11):6073-6
23289738 - Retrovirology. 2013;10:1
12859895 - Cell. 2003 Jul 11;114(1):21-31
16467198 - Blood. 2006 Jun 15;107(12):4781-9
7481804 - Science. 1995 Nov 10;270(5238):988-91
16941337 - J Infect Dis. 2006 Sep 15;194(6):725-33
18495769 - J Virol. 2008 Aug;82(15):7395-410
19837671 - J Biol Chem. 2009 Dec 11;284(50):35060-72
17892849 - Immunity. 2007 Sep;27(3):406-16
20504921 - J Virol. 2010 Aug;84(15):7581-91
16537629 - J Virol. 2006 Apr;80(7):3617-23
14528301 - Nat Med. 2003 Nov;9(11):1398-403
12480936 - J Biol Chem. 2003 Feb 21;278(8):6596-602
9303297 - EMBO J. 1997 Aug 1;16(15):4531-9
12883005 - Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5
10881687 - Arch Virol. 2000;145(5):1021-7
1357189 - J Virol. 1992 Nov;66(11):6489-95
20702622 - J Virol. 2010 Nov;84(21):11067-75
11071884 - J Biol Chem. 2001 Feb 16;276(7):4889-93
8791590 - Science. 1996 Sep 27;273(5283):1856-62
18971283 - J Virol. 2009 Jan;83(1):140-9
15373943 - Retrovirology. 2004;1:27
18275276 - J Infect Dis. 2008 Feb 15;197(4):563-71
17303427 - Trends Biochem Sci. 2007 Mar;32(3):118-28
3016298 - J Virol. 1986 Aug;59(2):284-91
20833716 - J Biol Chem. 2010 Nov 12;285(46):35350-8
17804494 - J Virol. 2007 Nov;81(22):12382-93
17728232 - J Virol. 2007 Nov;81(22):12608-18
17507468 - J Virol. 2007 Aug;81(15):8346-51
10694578 - Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2709-14
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References_xml – ident: e_1_3_2_21_2
  doi: 10.1128/JVI.01471-08
– ident: e_1_3_2_3_2
  doi: 10.1084/jem.20052319
– ident: e_1_3_2_19_2
  doi: 10.1371/journal.ppat.1000377
– ident: e_1_3_2_28_2
  doi: 10.1074/jbc.M313093200
– ident: e_1_3_2_55_2
  doi: 10.1074/jbc.M602413200
– ident: e_1_3_2_40_2
  doi: 10.1097/QAD.0b013e3282fbd1da
– ident: e_1_3_2_2_2
  doi: 10.1016/j.immuni.2007.08.010
– ident: e_1_3_2_29_2
  doi: 10.1038/nri1489
– ident: e_1_3_2_4_2
  doi: 10.1097/COH.0b013e3283454cf5
– ident: e_1_3_2_6_2
  doi: 10.1126/science.273.5283.1856
– ident: e_1_3_2_70_2
  doi: 10.1128/JVI.02694-06
– ident: e_1_3_2_36_2
  doi: 10.1007/s007050050692
– ident: e_1_3_2_75_2
  doi: 10.1128/JVI.02587-12
– ident: e_1_3_2_78_2
  doi: 10.1128/JVI.80.4.2069-2072.2006
– ident: e_1_3_2_14_2
  doi: 10.1182/blood-2005-12-4818
– ident: e_1_3_2_52_2
  doi: 10.1073/pnas.0502440102
– ident: e_1_3_2_46_2
  doi: 10.1093/nar/gkm181
– ident: e_1_3_2_56_2
  doi: 10.1074/jbc.M004895200
– ident: e_1_3_2_79_2
  doi: 10.1086/426826
– ident: e_1_3_2_72_2
  doi: 10.1016/S0092-8674(03)00515-4
– ident: e_1_3_2_18_2
  doi: 10.1126/science.270.5238.988
– ident: e_1_3_2_74_2
  doi: 10.1128/JVI.00676-12
– ident: e_1_3_2_16_2
  doi: 10.1038/ng934
– ident: e_1_3_2_37_2
  doi: 10.1371/journal.ppat.0010006
– ident: e_1_3_2_20_2
  doi: 10.1186/1742-4690-10-1
– ident: e_1_3_2_60_2
  doi: 10.1128/JVI.79.14.9006-9018.2005
– ident: e_1_3_2_50_2
  doi: 10.1101/gad.1249904
– ident: e_1_3_2_41_2
  doi: 10.1086/506616
– ident: e_1_3_2_66_2
  doi: 10.1128/JVI.01543-07
– ident: e_1_3_2_31_2
  doi: 10.2174/157016205774370456
– ident: e_1_3_2_65_2
  doi: 10.1128/JVI.00800-08
– ident: e_1_3_2_67_2
  doi: 10.1128/JVI.80.7.3617-3623.2006
– ident: e_1_3_2_12_2
  doi: 10.1038/nm1520
– ident: e_1_3_2_33_2
  doi: 10.1074/jbc.C500082200
– ident: e_1_3_2_25_2
  doi: 10.1038/nm945
– ident: e_1_3_2_63_2
  doi: 10.1084/jem.20081984
– ident: e_1_3_2_77_2
  doi: 10.1128/JVI.79.17.11513-11516.2005
– ident: e_1_3_2_51_2
  doi: 10.1101/gad.1250204
– ident: e_1_3_2_49_2
  doi: 10.1073/pnas.1530509100
– ident: e_1_3_2_23_2
  doi: 10.1128/JVI.00286-10
– ident: e_1_3_2_10_2
  doi: 10.1073/pnas.050567397
– ident: e_1_3_2_24_2
  doi: 10.1128/jvi.66.11.6489-6495.1992
– ident: e_1_3_2_48_2
  doi: 10.1074/jbc.M109.058305
– ident: e_1_3_2_58_2
  doi: 10.1186/1742-4690-4-81
– ident: e_1_3_2_61_2
  doi: 10.1128/JVI.73.12.10489-10502.1999
– ident: e_1_3_2_44_2
  doi: 10.1128/JVI.78.11.6073-6076.2004
– ident: e_1_3_2_8_2
  doi: 10.1038/nature03113
– ident: e_1_3_2_73_2
  doi: 10.1016/j.tibs.2007.01.004
– ident: e_1_3_2_15_2
  doi: 10.1128/JVI.01401-07
– ident: e_1_3_2_76_2
  doi: 10.1128/JVI.01249-10
– ident: e_1_3_2_7_2
  doi: 10.1126/science.1195271
– ident: e_1_3_2_34_2
  doi: 10.1128/JVI.76.20.10533-10539.2002
– ident: e_1_3_2_9_2
  doi: 10.1086/433188
– ident: e_1_3_2_32_2
  doi: 10.1126/science.1089591
– ident: e_1_3_2_39_2
  doi: 10.1128/JVI.00535-08
– ident: e_1_3_2_45_2
  doi: 10.1093/emboj/16.15.4531
– ident: e_1_3_2_68_2
  doi: 10.1128/JVI.00465-07
– ident: e_1_3_2_26_2
  doi: 10.1038/nm946
– ident: e_1_3_2_30_2
  doi: 10.1128/JVI.79.3.1975-1980.2005
– ident: e_1_3_2_53_2
  doi: 10.1016/j.jmb.2007.07.029
– ident: e_1_3_2_17_2
  doi: 10.1056/NEJM199501263320405
– ident: e_1_3_2_43_2
  doi: 10.1128/jvi.59.2.284-291.1986
– ident: e_1_3_2_69_2
  doi: 10.1128/JVI.01970-08
– ident: e_1_3_2_22_2
  doi: 10.1097/QAI.0b013e3181fe9450
– ident: e_1_3_2_47_2
  doi: 10.1074/jbc.M110.173286
– ident: e_1_3_2_13_2
  doi: 10.1128/JVI.02176-07
– ident: e_1_3_2_57_2
  doi: 10.1074/jbc.M210164200
– ident: e_1_3_2_42_2
  doi: 10.1128/JVI.02579-07
– ident: e_1_3_2_62_2
  doi: 10.1038/nrmicro1594
– ident: e_1_3_2_38_2
  doi: 10.1128/JVI.01041-08
– ident: e_1_3_2_5_2
  doi: 10.1099/vir.0.027102-0
– ident: e_1_3_2_54_2
  doi: 10.1128/JVI.00960-10
– ident: e_1_3_2_35_2
  doi: 10.3855/jidc.471
– ident: e_1_3_2_64_2
  doi: 10.1128/JVI.01369-07
– ident: e_1_3_2_11_2
  doi: 10.1086/526786
– ident: e_1_3_2_27_2
  doi: 10.1016/S1097-2765(03)00353-8
– ident: e_1_3_2_59_2
  doi: 10.1128/JVI.80.6.3112-3115.2006
– ident: e_1_3_2_71_2
  doi: 10.1186/1742-4690-1-27
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Snippet HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC). Functional...
ABSTRACT HIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC)....
UNLABELLEDHIV-1-infected individuals who control viremia to below the limit of detection without antiviral therapy have been termed elite controllers (EC)....
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StartPage 4992
SubjectTerms APOBEC-3G Deaminase
Cell Line
Cytidine Deaminase - antagonists & inhibitors
Cytidine Deaminase - immunology
Gene Expression Profiling
Genes, Reporter
Genetic Vectors
HIV Infections - immunology
HIV-1 - immunology
Human immunodeficiency virus
Human immunodeficiency virus 1
Humans
Luciferases - analysis
Luciferases - genetics
Molecular Sequence Data
Polymorphism, Genetic
RNA, Viral - genetics
Sequence Analysis, DNA
Vesicular stomatitis virus
Vesiculovirus - genetics
vif Gene Products, Human Immunodeficiency Virus - genetics
vif Gene Products, Human Immunodeficiency Virus - metabolism
Virus-Cell Interactions
Title Anti-APOBEC3G activity of HIV-1 Vif protein is attenuated in elite controllers
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