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Establishment of HIV-1 resistance in CD4 super(+) T cells by genome editing using zinc-finger nucleases

Homozygosity for the naturally occurring [delta]32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and sp... Full description

Journal Title: Nature biotechnology 2008-07-01, Vol.26 (7), p.808-816
Main Author: Perez, Elena E
Other Authors: Wang, Jianbin , Miller, Jeffrey C , Jouvenot, Yann , Kim, Kenneth A , Liu, Olga , Wang, Nathaniel , Lee, Gary , Bartsevich, Victor V , Lee, Ya-Li , Guschin, Dmitry Y , Rupniewski, Igor , Waite, Adam J , Carpenito, Carmine , Carroll, Richard G , Orange, Jordan S , Urnov, Fyodor D , Rebar, Edward J , Ando, Dale , Gregory, Philip D , Riley, James L , Holmes, Michael C , June, Carl H
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1087-0156
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recordid: cdi_proquest_miscellaneous_19608767
title: Establishment of HIV-1 resistance in CD4 super(+) T cells by genome editing using zinc-finger nucleases
format: Article
creator:
  • Perez, Elena E
  • Wang, Jianbin
  • Miller, Jeffrey C
  • Jouvenot, Yann
  • Kim, Kenneth A
  • Liu, Olga
  • Wang, Nathaniel
  • Lee, Gary
  • Bartsevich, Victor V
  • Lee, Ya-Li
  • Guschin, Dmitry Y
  • Rupniewski, Igor
  • Waite, Adam J
  • Carpenito, Carmine
  • Carroll, Richard G
  • Orange, Jordan S
  • Urnov, Fyodor D
  • Rebar, Edward J
  • Ando, Dale
  • Gregory, Philip D
  • Riley, James L
  • Holmes, Michael C
  • June, Carl H
subjects:
  • Human immunodeficiency virus 1
ispartof: Nature biotechnology, 2008-07-01, Vol.26 (7), p.808-816
description: Homozygosity for the naturally occurring [delta]32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted [math]50% of CCR5 alleles in a pool of primary human CD4 super(+) T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo in a NOG model of HIV infection. HIV-1-infected mice engrafted with ZFN-modified CD4 super(+) T cells had lower viral loads and higher CD4 super(+) T-cell counts than mice engrafted with wild-type CD4 super(+) T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4 super(+) T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN-modified autologous CD4 super(+) T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection.
language: eng
source:
identifier: ISSN: 1087-0156
fulltext: no_fulltext
issn:
  • 1087-0156
  • 1546-1696
url: Link


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titleEstablishment of HIV-1 resistance in CD4 super(+) T cells by genome editing using zinc-finger nucleases
creatorPerez, Elena E ; Wang, Jianbin ; Miller, Jeffrey C ; Jouvenot, Yann ; Kim, Kenneth A ; Liu, Olga ; Wang, Nathaniel ; Lee, Gary ; Bartsevich, Victor V ; Lee, Ya-Li ; Guschin, Dmitry Y ; Rupniewski, Igor ; Waite, Adam J ; Carpenito, Carmine ; Carroll, Richard G ; Orange, Jordan S ; Urnov, Fyodor D ; Rebar, Edward J ; Ando, Dale ; Gregory, Philip D ; Riley, James L ; Holmes, Michael C ; June, Carl H
creatorcontribPerez, Elena E ; Wang, Jianbin ; Miller, Jeffrey C ; Jouvenot, Yann ; Kim, Kenneth A ; Liu, Olga ; Wang, Nathaniel ; Lee, Gary ; Bartsevich, Victor V ; Lee, Ya-Li ; Guschin, Dmitry Y ; Rupniewski, Igor ; Waite, Adam J ; Carpenito, Carmine ; Carroll, Richard G ; Orange, Jordan S ; Urnov, Fyodor D ; Rebar, Edward J ; Ando, Dale ; Gregory, Philip D ; Riley, James L ; Holmes, Michael C ; June, Carl H
descriptionHomozygosity for the naturally occurring [delta]32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted [math]50% of CCR5 alleles in a pool of primary human CD4 super(+) T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo in a NOG model of HIV infection. HIV-1-infected mice engrafted with ZFN-modified CD4 super(+) T cells had lower viral loads and higher CD4 super(+) T-cell counts than mice engrafted with wild-type CD4 super(+) T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4 super(+) T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN-modified autologous CD4 super(+) T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection.
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descriptionHomozygosity for the naturally occurring [delta]32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted [math]50% of CCR5 alleles in a pool of primary human CD4 super(+) T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo in a NOG model of HIV infection. HIV-1-infected mice engrafted with ZFN-modified CD4 super(+) T cells had lower viral loads and higher CD4 super(+) T-cell counts than mice engrafted with wild-type CD4 super(+) T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4 super(+) T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN-modified autologous CD4 super(+) T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection.
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titleEstablishment of HIV-1 resistance in CD4 super(+) T cells by genome editing using zinc-finger nucleases
authorPerez, Elena E ; Wang, Jianbin ; Miller, Jeffrey C ; Jouvenot, Yann ; Kim, Kenneth A ; Liu, Olga ; Wang, Nathaniel ; Lee, Gary ; Bartsevich, Victor V ; Lee, Ya-Li ; Guschin, Dmitry Y ; Rupniewski, Igor ; Waite, Adam J ; Carpenito, Carmine ; Carroll, Richard G ; Orange, Jordan S ; Urnov, Fyodor D ; Rebar, Edward J ; Ando, Dale ; Gregory, Philip D ; Riley, James L ; Holmes, Michael C ; June, Carl H
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9Lee, Ya-Li
10Guschin, Dmitry Y
11Rupniewski, Igor
12Waite, Adam J
13Carpenito, Carmine
14Carroll, Richard G
15Orange, Jordan S
16Urnov, Fyodor D
17Rebar, Edward J
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9Lee, Ya-Li
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abstractHomozygosity for the naturally occurring [delta]32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted [math]50% of CCR5 alleles in a pool of primary human CD4 super(+) T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo in a NOG model of HIV infection. HIV-1-infected mice engrafted with ZFN-modified CD4 super(+) T cells had lower viral loads and higher CD4 super(+) T-cell counts than mice engrafted with wild-type CD4 super(+) T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4 super(+) T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN-modified autologous CD4 super(+) T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection.
doi10.1038/nbt1410