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Article: Suppression of Epstein-Barr virus DNA load in latently infected nasopharyngeal carcinoma cells by CRISPR/Cas9

TitleSuppression of Epstein-Barr virus DNA load in latently infected nasopharyngeal carcinoma cells by CRISPR/Cas9
Authors
KeywordsCRISPR/Cas9
EBNA1
Epstein-Barr virus
Nasopharyngeal carcinoma
Issue Date2018
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/virusres
Citation
Virus Research, 2018, v. 244, p. 296-303 How to Cite?
AbstractEpstein-Barr virus (EBV) infects more than 90% of the world's adult population. Once established, latent infection of nasopharyngeal epithelial cells with EBV is difficult to eradicate and might lead to the development of nasopharyngeal carcinoma (NPC) in a small subset of individuals. In this study we explored the anti-EBV potential of CRISPR/Cas9 targeting of EBV genome in infected NPC cells. We designed gRNAs to target different regions of the EBV genome and transfected them into C666-1 cells. The levels of EBV DNA in transfected cells were decreased by about 50%. The suppressive effect on EBV DNA load lasted for weeks but could not be further enhanced by re-transfection of gRNA. Suppression of EBV by CRISPR/Cas9 did not affect survival of C666-1 cells but sensitized them to chemotherapeutic killing by cisplatin and 5-fluorouracil. Our work provides the proof-of-principle for suppressing EBV DNA load with CRISPR/Cas9 and a potential new strategy to sensitize EBV-infected NPC cells to chemotherapy. © 2017 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/248324
ISSN
2017 Impact Factor: 2.484
2015 SCImago Journal Rankings: 1.259
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYuen, KS-
dc.contributor.authorWang, ZM-
dc.contributor.authorWong, NHM-
dc.contributor.authorZhang, ZQ-
dc.contributor.authorCheng, TF-
dc.contributor.authorLui, WY-
dc.contributor.authorChan, CP-
dc.contributor.authorJin, D-
dc.date.accessioned2017-10-18T08:41:25Z-
dc.date.available2017-10-18T08:41:25Z-
dc.date.issued2018-
dc.identifier.citationVirus Research, 2018, v. 244, p. 296-303-
dc.identifier.issn0168-1702-
dc.identifier.urihttp://hdl.handle.net/10722/248324-
dc.description.abstractEpstein-Barr virus (EBV) infects more than 90% of the world's adult population. Once established, latent infection of nasopharyngeal epithelial cells with EBV is difficult to eradicate and might lead to the development of nasopharyngeal carcinoma (NPC) in a small subset of individuals. In this study we explored the anti-EBV potential of CRISPR/Cas9 targeting of EBV genome in infected NPC cells. We designed gRNAs to target different regions of the EBV genome and transfected them into C666-1 cells. The levels of EBV DNA in transfected cells were decreased by about 50%. The suppressive effect on EBV DNA load lasted for weeks but could not be further enhanced by re-transfection of gRNA. Suppression of EBV by CRISPR/Cas9 did not affect survival of C666-1 cells but sensitized them to chemotherapeutic killing by cisplatin and 5-fluorouracil. Our work provides the proof-of-principle for suppressing EBV DNA load with CRISPR/Cas9 and a potential new strategy to sensitize EBV-infected NPC cells to chemotherapy. © 2017 Elsevier B.V.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/virusres-
dc.relation.ispartofVirus Research-
dc.rightsPosting accepted manuscript (postprint): © <year>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectCRISPR/Cas9-
dc.subjectEBNA1-
dc.subjectEpstein-Barr virus-
dc.subjectNasopharyngeal carcinoma-
dc.titleSuppression of Epstein-Barr virus DNA load in latently infected nasopharyngeal carcinoma cells by CRISPR/Cas9-
dc.typeArticle-
dc.identifier.emailYuen, KS: samyuen@hku.hk-
dc.identifier.emailChan, CP: chancp10@hku.hk-
dc.identifier.emailJin, D: dyjin@hku.hk-
dc.identifier.authorityChan, CP=rp02031-
dc.identifier.authorityJin, D=rp00452-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.virusres.2017.04.019-
dc.identifier.pmid28456574-
dc.identifier.scopuseid_2-s2.0-85018973792-
dc.identifier.hkuros280134-
dc.identifier.volume244-
dc.identifier.spage296-
dc.identifier.epage303-
dc.identifier.isiWOS:000425575400037-
dc.publisher.placeNetherlands-

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