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Article: Inhibition of hepatitis B virus replication in 2.2.15 cells by expressed shRNA

TitleInhibition of hepatitis B virus replication in 2.2.15 cells by expressed shRNA
Authors
KeywordsMolecular Sequence Numbers
Issue Date2005
PublisherBlackwell Publishing Ltd
Citation
Journal of Viral Hepatitis, 2005, v. 12 n. 3, p. 236-242 How to Cite?
AbstractHepatitis B virus (HBV) infection is a worldwide health problem. To determine whether RNA interference (RNAi) could inhibit ongoing HBV replication in 2.2.15 cells, we constructed shRNA-producing vector pU6P based on the mouse U6 RNA promoter and cloned 12 targeted sequences against HBV into the vector, resulting in a series of pU6-siHBV vectors. The recombinant vectors were transfected into 2.2.15 cells, HBsAg and HBeAg in cultured media were assayed using enzyme-linked immunosorbent assay at various days after transfection. The amount of HBV DNA in the culture medium was quantitated by real-time polymerase chain reaction, HBsAg and HBeAg expression were inhibited by 72.8 ± 5.4% (P = 0.00003) and 55.8 ± 6.2% (P = 0.000026), respectively, 4 days after transfection with pU6-siHBV5. The greatest inhibition of HBV DNA was decreased by approximately 1.9-fold (P = 0.013) on day 6 post transfection with pU6-siHBV11 compared with that of empty vector. No change was found for HBV protein expression and DNA replication on pU6-siGFP (negative control) transfected cells. Our data demonstrate that the transfection of HBV-targeted shRNA-producing vector in 2.2.15 cells could inhibit the HBV protein expression and HBV DNA replication specifically. RNAi may be considered as a potential antiviral approach for human HBV infection. © 2005 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/91082
ISSN
2015 Impact Factor: 4.179
2015 SCImago Journal Rankings: 1.815
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRen, X-Ren_HK
dc.contributor.authorZhou, L-Jen_HK
dc.contributor.authorLuo, G-Ben_HK
dc.contributor.authorLin, Ben_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2010-09-17T10:12:46Z-
dc.date.available2010-09-17T10:12:46Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal of Viral Hepatitis, 2005, v. 12 n. 3, p. 236-242en_HK
dc.identifier.issn1352-0504en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91082-
dc.description.abstractHepatitis B virus (HBV) infection is a worldwide health problem. To determine whether RNA interference (RNAi) could inhibit ongoing HBV replication in 2.2.15 cells, we constructed shRNA-producing vector pU6P based on the mouse U6 RNA promoter and cloned 12 targeted sequences against HBV into the vector, resulting in a series of pU6-siHBV vectors. The recombinant vectors were transfected into 2.2.15 cells, HBsAg and HBeAg in cultured media were assayed using enzyme-linked immunosorbent assay at various days after transfection. The amount of HBV DNA in the culture medium was quantitated by real-time polymerase chain reaction, HBsAg and HBeAg expression were inhibited by 72.8 ± 5.4% (P = 0.00003) and 55.8 ± 6.2% (P = 0.000026), respectively, 4 days after transfection with pU6-siHBV5. The greatest inhibition of HBV DNA was decreased by approximately 1.9-fold (P = 0.013) on day 6 post transfection with pU6-siHBV11 compared with that of empty vector. No change was found for HBV protein expression and DNA replication on pU6-siGFP (negative control) transfected cells. Our data demonstrate that the transfection of HBV-targeted shRNA-producing vector in 2.2.15 cells could inhibit the HBV protein expression and HBV DNA replication specifically. RNAi may be considered as a potential antiviral approach for human HBV infection. © 2005 Blackwell Publishing Ltd.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltden_HK
dc.relation.ispartofJournal of Viral Hepatitisen_HK
dc.subjectMolecular Sequence Numbersen_HK
dc.titleInhibition of hepatitis B virus replication in 2.2.15 cells by expressed shRNAen_HK
dc.typeArticleen_HK
dc.identifier.emailLin, B:blin@hku.hken_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2893.2005.00587.xen_HK
dc.identifier.pmid15850463-
dc.identifier.scopuseid_2-s2.0-18344394782en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-18344394782&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue3en_HK
dc.identifier.spage236en_HK
dc.identifier.epage242en_HK
dc.identifier.isiWOS:000228559700002-
dc.identifier.citeulike167189-

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