Drugs may induce hepatitis B virus (HBV) reactivation (HBV-R). Here we have reviewed the definition and harm of HBV-R, the risk drugs and their underlying mechanism, the influence factors, as well as the early intervention measures. It is shown that multiple drugs, including chemotherapy drugs, immunotherapy drugs, directly acting antivirals, cell therapy, etc., can induce HBV-R by affecting host immunity or directly activating HBV transcription factors. HBV-R could cause severe liver damage, even interruption of treatment of original diseases, affecting the prognosis of patients. Through precisely identifying risk drugs, monitoring the influence factors, and prescribing preventive anti-HBV regimen if necessary, the incidence of HBV-R can be significantly reduced. It is also suggested that clinical physicians should not only pay attention to the early identification and intervention of HBV-R, but also further study the mechanism of HBV-R in depth, especially the underlying mechanism between host, HBV and risk factors. This will help to promote the discovery of more valuable markers for risk prediction and targets for early intervention, and to further reduce the risk of HBV-R and improve the prognosis of patients.
ObjectiveTo systematically review the efficacy of different nucleosides (acids) in preventing hepatitis B virus reactivation after chemotherapy in cancer patients. MethodsThe Cochrane Library, PubMed, EMbase, Web of Science, CNKI, WanFang Data, and VIP databases were electronically searched to collect randomized controlled trials (RCTs) of different nucleosides (acids) to prevent HBV reactivation after chemotherapy in cancer patients from inception to June 7th, 2021. Two reviewers independently screened literature, extracted data, and assessed the risk of bias of included studies. Network meta-analysis was then performed by using Stata 16.0 software. ResultsA total of 43 RCTs involving 3 269 patients were included. There were 7 interventions, namely entecavir (ETV), lamivudine (LAM), adefovir dipivoxil (ADV), telbivudine (LdT), tenofovir dipivoxil (TDF), lamivudine combined with entecavir (LAM+ETV), and lamivudine combined with adefovir dipivoxil (LAM+ADV). The results of network meta-analysis showed that the efficacy of reducing the reactivation rate of ETV, LAM, ADV, LdT, TDF, LAM+ETV, LAM+ADV were superior than the control group. The ETV, LAM and ADV were not as effective as LAM+ETV. The leading drug combinations were LAM+ETV (94.8%), LdT (81.5%) and LA+ADV (58.0%). ConclusionsCurrent evidence shows that LAM+ETV, LdT, and LA+ADV are more effective in preventing hepatitis B virus reactivation after chemotherapy in cancer patients. Due to limited quality and quantity of the included studies, more high-quality studies are required to verify the above conclusions.
ObjectiveTo analyze hepatitis B virus (HBV) genotype distribution and drug-resistant mutations in West China Hospital of Sichuan University, providing basis for hepatitis B individualized treatment.MethodsA total of 786 chronic hepatitis B patients admitted to West China Hospital of Sichuan University from January 2016 to December 2018 were enrolled in the study. Genotype and drug-resistant mutations were analyzed by Sanger sequencing, and statistical analysis was conducted by χ2 test.ResultsThree genotypes (B, C and D) were identified in 786 samples, 489 (62.2%) in genotype B, 291 (37.0%) in genotype C , and 6 (0.8%) in genotype D. The distribution differences of B and C genotypes in age and ethnic groups were statistically significant (P<0.05). Among them, 627 cases had drug-resistant mutations, with a drug-resistant mutation rate of 79.8%. A total of 262 cases (33.3%) were resistant to lamivudine and tibivudine, 102 cases (13.0%) were resistant to lamivudine, tibivudine and entecavir; 83 cases (10.6%) were resistant to adefovir dipivoxil. No tenofovir resistant strains were detected in 786 samples. There were statistically significant differences in drug resistance between B and C genotypes (χ2=14.356, P<0.01). The most common single mutation was M204I [179 cases (22.8%)], followed by 46 cases (5.9%) of A181V/T associated with adefovir dipivoxil resistance. The most common mixed mutation was L180M+M204V/I in 83 cases (10.6%), and another 102 cases (13.0%) showed M250V and/or V173L and/or T184A/G/S/I and/or S202G/I with L180M+M204V/I.ConclusionsHBV genotypes in West China Hospital of Sichuan University are mainly B and C, and the situation of drug resistance is severe and the mutation pattern is complex. Therefore, detecting HBV genotype and drug resistance mutation is necessary, which may develop better clinical treatments.
Objective To explore the relationship between the HBsAg positive patients suffering from hepatocellular carcinoma (HCC) and HBV DNA genotype. Methods By using PCR type-specific primers combined with sequencing of genotype, we analyzed the genotype of HBV DNA in the serum of 500 patients with positive HBsAg in our hospital. Among them, 150 cases suffered from HCC. Results Genotype B and C were both predominant genotypes in HBsAg positive patients. But in HCC group, the rate of genotype C was 65.33% （98/150）, which was significantly higher than that in non-HCC group (88/350, 25.14%), while genotype B, in contrast, was 28.67% （43/150） and 68.86% （241/350）， χ2=75.45， Plt;0.05. The distribution of HBV DNA genotype B or genotype C in different gender or different age groups were not statistically significantly different in cases of HCC (Pgt;0.05). Conclusion Genotype C of HBV DNA is more common in patients with HCC, and maybe there is relationship between genotype C and the occurrence of HCC.
Objective To investigate the prevention of HBV reinfection in the perioperative period of liver transplantation on HBV-related diseases． Methods Published papers were collected and reviewed． Results HBV-related diseases were the main indications of liver transplantation．The prevention for HBV reinfection affects the survivals remarkably. Nowadays, a lot of medication have been used in the prevention of HBV reinfection， and the therapeutic regimens were different from each other. Conclusion Liver transplantation is an effective treatment for HBV-related disease． Appropriate prevention of HBV reinfection in the perioperative period of liver transplantation is important for the survivals of patients．
Objective To evaluate the efficacy and safety of antiviral drugs for hepatitis B with YMDD motif variant. Methods We electronically searched MEDLINE (1989-April, 2004), EMBASE (1989-April, 2004), CBMdisc (expand) (1989-April, 2004), and handsearched unpublished Chinese conference proceedings. Randomized and quasi-randomized trials in patients with chronic hepatitis B with YMDD motif variant correlative to lamivudine were collected. Two reviewers extracted the data and assessed the quality of literature independently. The data were then analyzed by RevMan 4.2 software. Results Five studies involving 6 trials and 284 patients were included. According to the results of meta-analysis, antiviral therapy with adefovir plus lamivudine showed significantly better effects on the clearance of serum HBV-DNA and HBeAg and normalization of ALT than that of lamivudine alone (RR 16.61, 95%CI 2.29 to 120.71; RR 6.66, 95%CI 1.23 to 35.88 and RR 6.26, 95%CI 2.29 to 17.12 respectively); also, oxymatrine plus thymothin showed obviously better effects on the clearance of serum HBV-DNA and HBeAg (RR 2.96, 95%CI 1.26 to 6.93 and RR 2.51, 95%CI 1.05 to 5.98 respectively).But adefovir alone showed no better effects on clearance of serum HBV-DNA and HBeAg than that of lamivudine alone (RR 11.00, 95%CI 0.65 to 186.02 and RR 7.00, 95%CI 0.39 to 126.92 respectively); interferon plus lamivudine showed no better effects on the clearance of serum HBV-DNA, HBeAg and the normalization of ALT (RR 3.50, 95%CI 0.90 to 13.58; RR 4.90, 95%CI 0.70 to 35.10 and RR 2.80, 95%CI 0.91 to 8.12 respectively). Chinese herbs plus lamivudine showed no better effects on the clearance of serum HBV-DNA (RR 1.16, 95%CI 0.89 to 1.51). There were no significant side effects in the groups, except flu like symptom in the interferon group, slight kidney impairment in the adefovir group, and aggravation of rare cases in lamivudine group. Conclusions Antiviral therapy with adefovir plus lamivudine, or oxymatrine plus thymothin, shows better effects than with lamivudine alone in terms of antiviral therapy and clinical outcome improvement. However, the evidence is too weak to draw a definite conclusion in this systematic review. Larger sample size and rigorously designed randomized, double blind, placebo control trials are required for future study.
ObjectiveTo explore the single locus mutation that related to hepatitis B virus (HBV) co-infection by means of genome-wide association study (GWAS) in Chinese Han patients with pulmonary tuberculosis (TB).MethodsA total of 946 patients with pulmonary TB enrolled between March 2013 and March 2018 were genotyped by Illumina Human Omni Express gene chip. After quality control, 389 972 single nucleotide polymorphisms (SNPs) of 703 patients with single TB infection and 53 patients with TB-HBV co-infection were included in the follow-up association analysis.ResultsThe SNP with the strongest statistical correlation signal was rs118122819 (P=2.923×10−12, odds ratio=7.933) located on chromosome 8p23.1. Other potential susceptibility genes included CDH4 (rs73309833), MARCH1 (rs3797020), and DNER (rs13393112), etc. In addition, a strong linkage imbalance between rs118122819 and rs4840365 (D’=0.88, r2=0.76) was found, while rs4840365 was located in the MFHAS1 gene region.ConclusionsThis study provides evidence for the presence of susceptibility gene locus for HBV co-infection in pulmonary TB patients, and provides important clues for the mechanism research, disease prevention, and treatment of co-infection. But these associations must be replicated and validated in larger studies.
ObjectiveTo detect the expression of indoleamine2, 3-dioxygenase (IDO) and HBV preS mRNA in HepG2 cells and its inhibitory effect on the proliferation of human peripheral blood lymphocyte. MethodsThe AdIDOEGFPpreS was transfected to human hepatocarcinoma cell line HepG2 and the specific fragment of IDO mRNA and HBV preS mRNA in these HepG2 cells were detected by RT-PCR. Then the transfected HepG2 cells were cocultured with human peripheral blood lymphocyte and the inhibitory effect of IDO on the proliferation of human peripheral blood lymphocyte was observed. ResultsThe IDO and HBV preS mRNA were successfully transferred to HepG2 cells, so the specific fragment of IDO and HBV preS mRNA could be found in the transfected HepG2 cells but not in the control group HepG2 cells by RT-PCR. Furthermore, the relative expression intensity of IDO and HBV preS were 1.27 and 1.18, respectively. When co-cultured with human peripheral blood lymphocyte, the counts per minute in the transfected HepG2 cells 〔(7 471±1 375) beats/min〕 was significantly less than that in the control group 〔(13 821±1 997) beats/min〕, Plt;0.001. ConclusionThe target gene IDO and HBV preS can be transferred and expressed in HepG2 cells successfully, which can obviously suppress the proliferation of human peripheral blood lymphocyte.
Objective To study the relationship of hepatitis B virus （HBV） to spontaneous rupture of hepatocellular carcinoma （HCC-SR） and its mechanism. Method The related literatures about theory of HCC-SR were consulted and reviewed. Results The injury of small arteries was usually followed in patients with HCC-SR， which was related to vascular autoimmune injury caused by the HBV infection. The small arteries in which immune complex deposited were readily injured， as a result HCC-SR happened while vascular load increased. Conclusion The HBV infection resulted in vascular autoimmune injury maybe a important factor in the pathogenesis of HCC-SR.
Long non-coding RNA (lncRNA) is a type of nucleic acid sequence that exceeds 200 nucleotides in length and cannot encode any complete protein. In recent years, its important regulatory role in various pathophysiological processes has been gradually clarified, however, few studies have reported its role in carcinogenic virus infection. This article summarizes the currently known lncRNAs abnormally expressed in hepatitis B virus-induced hepatocellular carcinoma, and focuses on the mechanisms of lncRNAs regulating the occurrence and development of hepatitis B virus-related hepatocellular carcinoma such as controlling virus replication and host immunity, cell cycle and proliferation, invasion and metastasis, autophagy and apoptosis of liver cancer cells, hoping to provide a theoretical basis for the molecular targeted therapy of hepatocellular carcinoma.