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|a 10.1016/j.clim.2023.109741
|2 doi
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|a pubmed24n1203.xml
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|a (NLM)37611838
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|a (PII)S1521-6616(23)00504-1
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Khan, Amber
|e verfasserin
|4 aut
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|a Antiretrovirals to CCR5 CRISPR/Cas9 gene editing - A paradigm shift chasing an HIV cure
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|c 2023
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
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|2 rdacarrier
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|a Date Completed 11.10.2023
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|a Date Revised 10.11.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023 Elsevier Inc. All rights reserved.
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|a The evolution of drug-resistant viral strains and anatomical and cellular reservoirs of HIV pose significant clinical challenges to antiretroviral therapy. CCR5 is a coreceptor critical for HIV host cell fusion, and a homozygous 32-bp gene deletion (∆32) leads to its loss of function. Interestingly, an allogeneic HSCT from an HIV-negative ∆32 donor to an HIV-1-infected recipient demonstrated a curative approach by rendering the recipient's blood cells resistant to viral entry. Ex vivo gene editing tools, such as CRISPR/Cas9, hold tremendous promise in generating allogeneic HSC grafts that can potentially replace allogeneic ∆32 HSCTs. Here, we review antiretroviral therapeutic challenges, clinical successes, and failures of allogeneic and allogeneic ∆32 HSCTs, and newer exciting developments within CCR5 editing using CRISPR/Cas9 in the search to cure HIV
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|a Journal Article
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|a Research Support, N.I.H., Extramural
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|a Research Support, Non-U.S. Gov't
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|a Review
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|a Antiretroviral therapy
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|a CCR5
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|a CRISPR/Cas9
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|a HIV
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|a ∆32
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|a Anti-Retroviral Agents
|2 NLM
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|a CCR5 protein, human
|2 NLM
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|a Receptors, CCR5
|2 NLM
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1 |
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|a Paneerselvam, Nandagopal
|e verfasserin
|4 aut
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|a Lawson, Brian R
|e verfasserin
|4 aut
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773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 255(2023) vom: 15. Okt., Seite 109741
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:255
|g year:2023
|g day:15
|g month:10
|g pages:109741
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|u http://dx.doi.org/10.1016/j.clim.2023.109741
|3 Volltext
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 255
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