一般而言，HBV/HCV共感染下，HCV复制占主导地位，HBV的复制受到抑制。对于HCV和HBV在细胞内到底是如何相互作用的，到目前还未知，其中一个重要原因是没有一个好的细胞感染模型用于HBV/HCV共感染研究。
该团队基于HepG2细胞，通过过表达HBV受体NTCP及HCV感染相关分子，筛选出一株可以支持HBV/HCV共感染的细胞株（HepG2-NTCP/CD81/Mir）。此细胞不仅支持HBV/HCV单感染，而且还支持HBV/HCV在同一细胞内同时感染。两种病毒相互不影响感染效率，但是共感染后HBV的复制能力明显下降，与临床报道一致。此外，该细胞模型还可以模拟临床用药后HBV复制反弹的机制研究，为解释其机制及优化临床用药等提供理论基础。该团队的硕士研究生张凯和博士研究生赖鑫源为论文的共同第一作者，向宽辉副研究员、李彤副教授和庄辉教授为论文共同通讯作者。该研究工作同时得医院张佳医院的李传云医生的支持和帮助。
附文献信息：题目：AnovelcellculturemodelrevealstheviralinterferenceduringhepatitisBandCviruscoinfection.DOI：10./j.antiviral..Highlights：（1）ThisnovelcellmodelfullysupportsHBVandHCVcoinfection.（2）HBVreplicationwassuppressedbyHCVandreboundedduringtheinterferonαanddirect-actingantiviraldrugstreatment.（3）HBVcorepromoterandSpromoterIIactivitieswereinhibitedwhencoinfectedwithHCV.（4）ThiscellmodelprovidesopportunitytostudymoleculardetailsoftheinteractionofHBVandHCVincoinfectedcells.Abstract:CoinfectionofhepatitisBvirus(HBV)andhepatitisCvirus(HCV)mayresultinsevereliverdiseaseandfrequentprogressiontocirrhosisandhepatocellularcarcinoma.ClinicalevidencesuggeststhatHBVreplicationissuppressedbyreplicatingHCVandoftenreboundsaftertreatmentwithdrugsagainstHCV.Thus,ahighlyefficientcellculturesystempermissiveforHBV/HCVwouldfacilitateinvestigationontheinteractionandpathogenesisaftercoinfection.HerewereportedarobustHBV/HCVcoinfectioncellculturemodelbyoverexpressinghumansodium-taurocholatecotransportingpolypeptide(NTCP),CD81andMirintoHepG2cellsandinvestigatedinteractionsbetweenHBVandHCV.Inthissystem,HepG2-NTCP/CD81/MircellsnotonlysupportedrobustinfectionandreplicationofHBVandHCV,butalsoallowedHBV/HCVcoinfectioninthesinglecelllevel.OurresultshowedcellswithreplicatingHBVstillsupportedHCVinfection.However,HBVreplicationwassuppressedbyHCVthroughtheinhibitionofHBVcorepromoterandSpromoterIIactivity,andthisinhibitionwasattenuatedbytheinterferonalpha(IFNα)treatment,suggestingHCVinfluenceonHBVattranscriptionallevel.CoinfectionofHBV/HCVinthissystemdidnotblockIFNstimulatedgenesexpression.InhibitionofHCVbydirect-actingantiviraldrugsrestoredHBVreplicationandexpressionofviralgenes.Conclusions:HepG2-NTCP/CD81/MirfullysupportsHBV/HCVcoinfection,replicationandinteraction.Thisnovelcellmodeloffersaplatformtoadvanceourunderstandingofthemoleculardetailsoftheinteraction,pathogenesisandout