简介：Theaimofthisstudyistoinvestigatewhetherthreemononucleotidepolymorphismsatthelocus-1082,-819and-592inthepromoterregionoftheIL-10geneareassociatedwithchronicseverehepatitis.TheIL-10-592andIL-10-1082polymorphismsweregenotypedbypolymerasechainreaction-restrictionfragmentlengthpolymorphismanalysis(PCR-RFLP)whilepolymerasechainreaction-se-quencespecificprimer(PCR-SSP)assaywasusedtotesttheIL-10-819polymorphism.Thepolymor-phismsofIL-10-1082,-819and-592genesweredetectedin98patientswithchronicseverehepatitis(CSH),478patientswithchronichepatitisB(CHB),223asymptomatic(chronic)HBVcarriers(ASC)and267patientswithself-restrictedHBV.Therewassignificantdifferenceofthepolymor-phismsofIL-10-1082,IL-10-819andIL-10-592genesbetweenCSHgroupandothergroups.Thefre-quencyofAAgenotypeatIL-10genepromoter-1082locusinchronicseverehepatitispatientswashigherthanthatinasymptomaticHBVcarriers(X~2=13.314,P=0.001),andself-restrictedHBVpatients(X~2=13.545,P=0.000);thefrequencyofCCandACgenotypeatIL-10genepromoter-592locusinchronicseverehepatitispatientswashigherthanthatinchronichepatitispatients(X~2=15.970,P=0.000)(X~2=20.414,P=0.000),asymptomaticHBVcarriers(X~2=21.283,P=0.000)(X~2=28.309,P=0.000)andself-restrictedHBVpatients(X~2=17.047,P=0.000)(X~2=16.528,P=0.000);thefrequencyofTCgenotypeatIL-10genepromoter-819locusinchronicseverehepatitispatientswashigherthanthatinchronichepatitispatients(X~2=58.961,P=0.000),asymptomaticHBVcarriers(X~2=53.255,P=0.001)andself-restrictedHBVpatients(X~2=39.616,P=0.001).Sointerleukine-10genepolymorphismwasassociatedwiththechronicsevereheoatitis.

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简介：HepatitisBvirus（HBV）isasignificantglobalpathogenandefficientcureforHBVpatientsisstillachallenginggoal.Wepreviouslyreportedthatacidicmucopolysaccharidefromstichopusjaponicusselenka（SJAMP）couldinhibitHBsAgandHBeAgexpressioninvitro.However,thepotentialanti-HBVeffectsofSJAMPinvivohavenotyetbeenexplored.Inthisstudy,weshowthatSJAMPexhibitspotentanti-HBVactivityinHBVtransgenicmiceinadose-dependentmanner.Specifically,sixtyHBVtransgenicmaleBALB/cmicewererandomlyselectedtoreceivethetreatmentofPBS,lowdoseSJAMP(30mgkg-1),middledoseSJAMP(40mgkg-1),highdoseSJAMP(50mgkg-1)andIFN(45IUkg-1)for30d.SJAMPtreatmentsuppressedserumHBV-DNA,andliverHBsAgandHBcAglevelsinHBV-transgenicmice.ThepresentstudyhighlightsthepotentialapplicationofSJAMPinHBVtherapy.

简介：DuckhepatitisBvims(DHBV)DNAwasdetectedindifferenttumorousnodulesofduckswithhepaticmulticentriccancerorintrahepaticmetastasisbySouthernblottechnique.Among7duckswithhepatocellularcarcinomaofmultipletumornodules,thehybridizationpatternofIntegratedDHBVDNAIndifferenttumorousnoduleswasidenticalin3casesanddifferentin2cases.OnecaseshowedasimilarhybridizationpatternintwotumorousnodulesandotheronewasnegativetorDHBVDNA.IntegratedDHBVDNAwasalsoidentifiedinametastaticlungcancerofduckswithhepatocellularcarcinoma.Thehybridizationpatternofmetastasisoflungswasasthesomeasthatinprimaryhepatocellularcarcinoma.ThesamediscretehybridizationbandsInthedifferenttumorousnodulesindicatethatthesenodulesmightarisefromonetransformedcell.ThedifferenthybridizationpatternsInvarioustumorousnodulesshowthatthesetumorousnodulesmightarisefromvarioustransformedcells.Theresultssuggestthatthehyb

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简介：INTRODUCTIONMolecularbiologyhasmadeatremendousimpactonthediagnosisandtreatmentofliverdiseases.Inparticular,advancesinmolecularbiologymadepossiblethediscovery

简介：AbstractChronic hepatitis B virus (HBV) infection caused by mother-to-child transmission (MTCT, also known as vertical transmission) during the perinatal period is a major public health problem worldwide. Despite the availability of the combined active-passive immunization with a hepatitis B vaccine and hepatitis B immunoglobulin after birth, about 9% of newborns are still infected with HBV, especially those born to hepatitis B e antigen (HBeAg)-positive mothers. Currently, the management of HBV infection during pregnancy remains controversial. This article briefly reviews the recent advances in the epidemiology of HBV, immunization against it, and management strategies in the third trimester.

简介：HepatitisB(HB)virus(HBV)infection,whichcauseslivercirrhosisandhepatocellularcarcinoma,isendemicworldwide.HepatitisBvaccinesbecamecommerciallyavailableinthe1980s.TheWorldHealthOrganizationrecommendedtheintegrationoftheHBvaccineintothenationalimmunisationprogramsinallcountries.HBVpreventionstrategiesareclassifiedintothreegroups:(1)universalvaccinationalone;(2)universalvaccinationwithscreeningofpregnantwomenplusHBimmuneglobulin(HBIG)atbirth;and(3)selectivevaccinationwithscreeningofpregnantwomenplusHBIGatbirth.Mostlow-incomecountrieshaveadopteduniversalvaccineprogramswithoutscreeningofpregnantwomen.However,HBvaccinesarenotwidelyusedinlow-incomecountries.TheGlobalAllianceforVaccineandImmunizationwaslaunchedin2000,andby2012,theglobalcoverageofathree-doseHBvaccinehadincreasedto79%.Thenextchallengesaretofurtherincreasethecoveragerate,closethegapbetweenrecommendationsandroutinepractices,approachhighriskindividuals,screenandtreatchronicallyinfectedindividuals,andpreventbreakthroughinfections.ToeradicateHBVinfections,strenuouseffortsarerequiredtoovercomesocioeconomicbarrierstotheHBvaccine;thistaskisexpectedtotakeseveraldecadestocomplete.

简介：瞄准：由transfecting观察肝炎B复制和表示的抑制基于向量的小干扰RNA(siRNA)pGenesil-HBVX指向HBVX基因区域进HepG2.2.15房间。方法：pGenesil-HBVX被构造并且transfected进经由lipofection的HepG2.2.15房间。HBV抗原分泌物被决定在由解决时间的immunofluorometric试金(TRFIA)的transfection以后的24，48，和72h。HBV复制被荧光检验细胞质的病毒的蛋白质的量的PCR，和表示被免疫组织化学决定。结果：进上层清液的HBsAg和HBeAg的分泌物被发现被28.5%和32.2%禁止(P<0.01)，并且在38.67%(P<0.05)并且42.86%(P<0.01)在在pGenesil-HBVXtransfection以后的48h和72h分别地。为细胞质的HBsAg染色的Immunohistochemical在HepG2.2.15房间显示出类似的衰落在transfection以后的48h。在文化上层清液以内的HBV染色体的数字显著地也被减少48h和由荧光PCR确定了的72hpost-transfection(P<0.05)。结论：在HepG2.2.15房间，HBV复制和表示被指向编码区域的HBVX的基于向量的siRNApGenesil-HBVX禁止。

简介：Objective:ToassesstheeffectofantiviraltherapyforhepatitisBvirus(HBV)-relatedhepatocellularcarcinoma(HCC)afterradicalhepatectomy.Methods:Atotalof478HBV-relatedHCCpatientstreatedbyradicalhepatectomywereretrospectivelycollected.Patientsinthetreatmentgroup(n=141)receivedpostoperativelamivudinetreatment(100mg/d),whereaspatientsinthecontrolgroup(n=337)didnot.Recurrence-freesurvival(RFS)rates,overallsurvival(OS)rates,treatmentsforrecurrentHCCandcauseofdeathwerecomparedbetweenthetwogroups.Propensityscorematching(PSM)analysiswasalsoconductedtoreduceconfoundingbiasbetweenthetwogroups.Results:The1-,3-,and5-yearRFSratesdidn’tsignificantlydifferbetweenthetwogroups(P=0.778);however,the1-,3-,and5-yearOSratesinthetreatmentgroupweresignificantlyhigherthanthoseinthecontrolgroup(P=0.002).Similarresultswereobservedinthematcheddata.SubgroupanalysisshowedthatantiviraltreatmentconferredasignificantsurvivalbenefitforBarcelonaClinicalLiverCancerstageA/Bpatients.FollowingHCCrecurrence,morepeopleinthetreatmentgroupwereabletochoosecurativetreatmentsthanthoseinthecontrolgroup(P=0.031).Forcauseofdeath,fewerpeopleinthetreatmentgroupdiedofliverfailurethanthoseinthecontrolgroup(P=0.041).Conclusion:PostoperativeantiviraltherapyincreaseschancesofreceivingcurativetreatmentsforrecurrentHCCandpreventsdeathbecauseofliverfailure,therebysignificantlyprolongingOS,especiallyinearly-orintermedian-stagetumors.

简介：AbstractLow-level viremia (LLV) was defined as persistent or intermittent episodes of detectable hepatitis B virus (HBV) DNA (<2000 IU/mL, detection limit of 10 IU/mL) after 48 weeks of antiviral treatment. Effective antiviral therapies for chronic hepatitis B (CHB) patients, such as entecavir (ETV), tenofovir disoproxil fumarate (TDF), and tenofovir alafenamide (TAF), have been shown to inhibit the replication of HBV DNA and prevent liver-related complications. However, even with long-term antiviral therapy, there are still a number of patients with persistent or intermittent LLV. At present, the research on LLV to address whether adversely affect the clinical outcome is limited, and the follow-up treatment for these patients is open to question. At the same time, the mechanism of LLV is not clear. In this review, we summarize the incidence of LLV, the association between LLV and long-term outcomes, possible mechanisms, and management strategies in these patient populations.

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简介：AIM:ToelucidatethemolecularmechanismsunderlyinghepatitisBvirus(HBV)occultinfectionofgenotypeC.METHODS:Atotalof10typesofhepatitisBsurfaceantigen(HBsAg)variantsfromaKoreanoccultcohortwereused.AfteracompleteHBVgenomeplasmidmutatedsuchthatitdoesnotexpressHBsAgandplasmidencoding,eachHBsAgvariantwastransientlyco-transfectedintoHuH-7cells.ThesecretioncapacityandintracellularexpressionoftheHBVvirionsandHBsAgsintheirrespectivevariantswereanalyzedusingreal-timequantitativepolymerasechainreactionassaysandcommercialHBsAgenzyme-linkedimmunosorbentassays,respectively.RESULTS:AllvariantsexhibitedlowerlevelsofHBsAgsecretionintothemediumcomparedwiththewildtype.Inparticular,ineightofthetenvariants,verylowlevelsofHBsAgsecretionthatweresimilartothenegativecontrolweredetected.Incontrast,mostvariants(9/10)exhibitednormalvirionsecretioncapacitiescomparablewith,orevenhigherthan,thewildtype.ThisprovidednewinsightintotheintrinsicnatureofoccultHBVinfection,whichleadstoHBsAgsero-negativenessbuthashorizontalinfectivity.Furthermore,mostvariantsgeneratedhigherreactiveoxidativespeciesproductionthanthewildtype.ThisfindingprovidespotentiallinksbetweenoccultHBVinfectionandliverdiseaseprogression.CONCLUSION:ThepresentlyobtaineddataindicatethatdeficiencyinthesecretioncapacityofHBsAgvariantsmayhaveapivotalfunctionintheoccultinfectionsofHBVgenotypeC.

简介：Thereversetranscriptase(RT)proteinofhepatitisBvirus(HBV)hasbeensuccessfullyexpressedbyrecombinanttechnologyinEschericahiacoli(E.coli).Inthisstudyweaimedtodevelopasemi-quantitativeassayforthestudyofHBVRTproteinusingthissystem.CompleteHBVpolymerasegenefromawildtypevirus(rt306P)andthepolymerasegenefromamutant,withrt306Psubstitutedbyserine(rtP306S)wereseparatelyfusedtothemaltosebindingprotein(MBP)geneandexpressedinE.colirespectively.TheexpressionlevelsofHBVpolymerasegenesfromthewildtypevirusanditscounterpartmutantatrt306werecompared.Whentheseproteinsweresemi-quantifiedbyWesternblottingusingrabbitanti-TPserum,thertP306SmutantshoweddecreasedexpressionofMBP-HBVpolymerase.Bythismethod,wehaveshownthattheexpressionlevelofHBVRTcouldbeaffectedbysubstitutionsinitsaminoacidsequences,andthismethodcouldbeusedtostudythecharacteristicsofHBVRTprotein.

简介：AbstractBackground:Hepatitis C virus (HCV) genotype 3, particularly subtype 3b, is increasing in prevalence and distribution in China. This study evaluated the prevalence, regional distribution, clinical characteristics, host factors, treatment outcomes, and disease progression of patients with HCV genotype 3 in China.Methods:A 5-year follow-up was preceded by a cross-sectional study. Treatment choices were at the discretion of treating physicians. Estimated infection time to overall-disease-progression (defined by ≥1 of: newly diagnosed cirrhosis; cirrhosis at baseline, Child-Turcotte-Pugh score increased 2 points or more; progression from compensated cirrhosis to decompensated cirrhosis; hepatocellular carcinoma; liver transplantation; or death) was calculated using the Kaplan-Meier method. Cox regression analyses were conducted to evaluate the risk factors for disease progression.Results:The cross-sectional study enrolled 997 patients, including 91 with HCV genotype 3 infection. Among them, subtype 3b (57.1%) was more dominant than subtype 3a (38.5%). Five hundred and twelve patients were included into the follow-up phase. Among patients analyzed for estimated infection time to overall-disease-progression, 52/304 (17.1%) patients with HCV genotype 1 and 4/41 (9.8%) with HCV genotype 3 (4/26 with genotype 3b, 0/13 with genotype 3a, and 0/2 with undefined subtype of genotype 3) experienced overall-disease-progression. Patients with HCV genotype 3 were younger than those with genotype 1 (mean age: 39.5 ± 8.7 vs. 46.9 ± 13.6 years) and demonstrated more rapid disease progression (mean estimated infection time to overall-disease-progression 27.1 vs. 35.6 years).Conclusions:HCV genotype 3, specifically subtype 3b, is associated with more rapid progression of liver disease. Further analysis to compare HCV subtype 3a and 3b is needed in high prevalence regions.Trial registration:NCT01293279, https://clinicaltrials.gov/ct2/show/NCT01293279; NCT01594554, https://clinicaltrials.gov/ct2/show/NCT01594554.

简介：瞄准：为了为在肝炎B估计肝的纤维变性决定结缔组织生长因素(CCN2/CTGF)的用途，病毒(HBV)导致了长期的肝疾病(CLD-B)。方法：连接酶的immunosorbent试金被用来与导致HBV的活跃的肝肝硬化和30个健康个人与长期的肝炎B(CHB)和39个病人从107个病人在sera测量CCN2。从有CHB，有导致HBV的肝肝硬化的8个病人和有正常的肝组织学的8个HBV搬运人的31个病人的肝样品为转变生长因素-1(TGF-1)或CCN2mRNA层次由被检验在situ杂交，并且计算机图象分析被执行在肝纸巾测量CCN2mRNA积极的房间的综合最佳的密度(IOD)。组织学的发炎分级和纤维变性阶段被H并且E染色和凡·吉森斯方法评估。结果：分别地，浆液CCN2集中作为与健康个人相比在有CHB或活跃的肝肝硬化的病人更高是4.0褶层或4.9褶层(P<0.01)。在肝纸巾在在sera和CCN2mRNA表示的CCN2的层次之间有好一致性(r=0.87，P<0.01)。在sera的CCN2的层次与CLD-B在病人与组织学的纤维变性阶段的改进被增加(r=0.85，P<0.01)。浆液CCN2是为对肝纤维变性的评价的一个可靠标记，与在操作为从有F1阶段肝纤维变性的病人的分别地，区分的正常的肝控制的0.94或0.85的特征(巨鸟)曲线(AUC)或在温和、重要的纤维变性之间区别的接收装置下面的区域。结论：在有CLD-B的病人的浆液CCN2的察觉可以为对肝的纤维变性的严厉的评价有临床的意义。

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简介：AbstractBackground:The hepatitis B virus X (HBx) protein plays a critical role in the initiation and progression of hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). In the early stage of the disease, HBx facilitates tumor onset by inactivating the tumor suppressor p53. The p53-encoding gene, however, is frequently mutated or deleted as the cancer progresses to the late stage and, under such circumstance, the p53 homolog TAp63 can harness HCC growth by transactivating several important p53-target genes.Methods:To determine whether HBx regulates TAp63, we performed co-immunoprecipitation assay, real-time quantitative polymerase chain reaction, immunoblotting, and flow cytometry analysis in p53-null cancer cell lines, Hep3B and H1299.Results:HBx interacts with the transactivation domain of TAp63, as HBx was co-immunoprecipitated with TAp63 but not with ΔNp63. The interaction between HBx and TAp63 abolished transcriptional activity of TAp63, as evidenced by the reduction of the levels of its target genes p21 and PUMA, consequently leading to restricted apoptosis and augmented proliferation of HCC cells.Conclusion:HBV induces progression of HCC that harbors defective p53 by inhibiting the tumor suppressor TAp63.

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