Yang X.-H.,Key Laboratory of Molecular Biology for Infectious Diseases |
Yang X.-H.,Chongqing Medical University |
Xiao L.,Chongqing Medical University |
Xiao L.,Peoples Hospital of District of YuBei |
And 8 more authors.
European Journal of Internal Medicine | Year: 2014
Background/aims: Current results had demonstrated lamivudine (LAM) contributed to improve liver function and short-term prognosis in patients with hepatitis B virus-related acute-on-chronic liver failure (ACLF), but data concerning the outcome of long-term prognosis are limited. Our objective was to explore the prediction value of early viral response for prognosis and LAM resistance in ACLF patients with lamivudine treatment within 96 weeks. Methods: One hundred and forty consecutive subjects were recruited, 76 patients were treated with LAM and supportive treatment (LAM group) and 64 patients only received supportive treatment (non-NAs group). All the patients were followed up until death or 96 weeks. The primary end point was overall survival rate at 96 weeks, as well as the relationship between the virologic response at weeks 4 or 12 and prognosis and resistance at 96 weeks. Results: At 96 weeks, the cumulative survival was higher in the LAM group than that in the non-NA group (43/76 (56.58%) vs 9/64 (14.06%), respectively, p = 0.000). The survival rate of patients achieved complete viral response (CVR) at week 4 was higher than that of those with partial virologic response (PVR) during the 96-week follow-up (27/29 [93.10%] vs 16/45 [35.56%], p = 0.000). In CVR patients, there was a significant improvement in model for end-stage liver failure (MELD) scores compared to PVR. Logistic recurrence indicated that both 4-week CVR and MELD scores were an independent predictor of the 96-week survival. Twelve patients developed LAM resistance (22.22%); all of them came from the PVR at 4 weeks. Conclusion: LAM can significantly improve the long-term survival rate, and 4 weeks CVR can predict the long-term clinical outcome and LAM-resistant in patients with HBV-related ACLF. © 2014 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
Chen J.,Chongqing Medical and Pharmaceutical College |
Chen J.,Key Laboratory of Molecular Biology for Infectious Diseases |
Huang A.,Key Laboratory of Molecular Biology for Infectious Diseases |
Xu L.,Chongqing Medical and Pharmaceutical College |
And 7 more authors.
Journal of Central South University (Medical Sciences) | Year: 2011
Objective To detect the recombinant intermediates of hepatitis B virus (HBV) between genotype B and C in vitro. Methods Vector Plenti6/V5-D-topo-X was genetically modified by genotype B and C to transfect HepG2 cells. Then the HepG2 cells were amplified and sequence of the nucleic acid after the transinfection was tested and compared with RDP3Beta40 software package and bootscanning procedure in SimPIot program package. Results Three recombinant intermediates of HBV between genotype B and C were identified in vitro. Genotype C in the precore region plus the core gene spanning nucleotide positions from 1 740 - 1 838 to 2443 -2485 contributed to the recombination with genotype B. Isolate Rl recombinant intermediate had 2 break points at nt 2 170 -2 172 and nt2 188 -2 189. Nucleic acid changed from CAC to TGT and from GA to AC, respectively. Isolate R2 recombinant intermediate had a break point at nt 1 740 - 1 838, and 3 bases changed in different nucleic acid sites; from A to T at nt 1 740, from C to T at nt 1 753, and from G to A at nt 1 838, respectively. Isolate R3 recombinant intermediate had a break point at nt 2 443 -2 483, and 4 bases changed in different nucleic acid sites: from C to T at nt 2 443 , from A to G at nt 2 452, from T to C at nt 2 480, and from C to T at nt 2 483 , respectively. Conclusion The recombinant intermediates of HBV between genotype B and C have been detected in vitro and the changes have been identified in the precore region plus the core gene in genotype B and C.