Hepatitis B virus(HBV)reactivation is a clinically significant challenge in disease management.This review explores the immunological mechanisms underlying HBV reactivation,emphasizing disease progression and manageme...Hepatitis B virus(HBV)reactivation is a clinically significant challenge in disease management.This review explores the immunological mechanisms underlying HBV reactivation,emphasizing disease progression and management.It delves into host immune responses and reactivation’s delicate balance,spanning innate and adaptive immunity.Viral factors’disruption of this balance,as are interac-tions between viral antigens,immune cells,cytokine networks,and immune checkpoint pathways,are examined.Notably,the roles of T cells,natural killer cells,and antigen-presenting cells are discussed,highlighting their influence on disease progression.HBV reactivation’s impact on disease severity,hepatic flares,liver fibrosis progression,and hepatocellular carcinoma is detailed.Management strategies,including anti-viral and immunomodulatory approaches,are critically analyzed.The role of prophylactic anti-viral therapy during immunosuppressive treatments is explored alongside novel immunotherapeutic interventions to restore immune control and prevent reactivation.In conclusion,this compre-hensive review furnishes a holistic view of the immunological mechanisms that propel HBV reactivation.With a dedicated focus on understanding its implic-ations for disease progression and the prospects of efficient management stra-tegies,this article contributes significantly to the knowledge base.The more profound insights into the intricate interactions between viral elements and the immune system will inform evidence-based approaches,ultimately enhancing disease management and elevating patient outcomes.The dynamic landscape of management strategies is critically scrutinized,spanning anti-viral and immunomodulatory approaches.The role of prophylactic anti-viral therapy in preventing reactivation during immunosuppressive treatments and the potential of innovative immunotherapeutic interventions to restore immune control and proactively deter reactivation.展开更多
In this editorial,we offer a summary of the risk associated with hepatitis B reactivation(HBVr)in the setting of both solid and hematologic malignancies treated with Bruton tyrosine kinase(BTK)inhibitors,with insights...In this editorial,we offer a summary of the risk associated with hepatitis B reactivation(HBVr)in the setting of both solid and hematologic malignancies treated with Bruton tyrosine kinase(BTK)inhibitors,with insights derived from current studies.Furthermore,we emphasize the critical need for a framework regarding robust risk evaluation in patients undergoing such treatments.This framework is essential for identifying those at increased risk of HBVr,enabling healthcare providers to implement proactive measures to prevent reactivation and ensure the safe administration of BTK inhibitor therapy.展开更多
Rheumatoid arthritis(RA)is an autoimmune disease characterized by proliferative synovitis,which can cause cartilage and bone damage as well as functional limitations.Disease-modifying anti-rheumatic drugs have signifi...Rheumatoid arthritis(RA)is an autoimmune disease characterized by proliferative synovitis,which can cause cartilage and bone damage as well as functional limitations.Disease-modifying anti-rheumatic drugs have significantly improved the prognosis of RA patients.However,people with RA,when combined with hepatitis B virus(HBV)infection,may experience reactivation of HBV during treatment with anti-rheumatic drugs.The outcome of HBV reactivation(HBVr)varies from liver inflammation to liver failure,while insufficient HBV screening in RA patients has been reported in various countries.Therefore,it is necessary to identify patients at high risk before starting immunosuppressive therapy.The immune response plays an important role in anti-HBV infection.However,most anti-rheumatic drugs exert an inhibitory effect on the body’s immune system,resulting in HBVr.Therefore,it is necessary to conduct a comprehensive evaluation based on host factors,viral factors,and drug factors.In this paper,we summarize the mechanism of HBVr,the risk of HBVr caused by anti-rheumatic drugs,and the appropriate diagnosis and treatment process for RA patients so that clinicians can have a more comprehensive understanding of HBVr in RA patients.展开更多
Imatinib mesylate is a molecular targeted agent for treating chronic myeloid leukemia (CML) and gastrointestinal stromal tumor. Although imatinib mesylate is not regarded as an immunosuppressive agent, few studies h...Imatinib mesylate is a molecular targeted agent for treating chronic myeloid leukemia (CML) and gastrointestinal stromal tumor. Although imatinib mesylate is not regarded as an immunosuppressive agent, few studies have also shown that it may impair immune response. In this report, we present a case of transient hepatitis B virus (HBV) reactivation during imatinib mesylate treatment for CML.展开更多
Objective The current study aims to investigate the effect of Hemagglutinating virus of Japan envelope(HVJ-E) on induction of apoptosis and autophagy in human prostate cancer PC3 cells, and the underlying mechanisms...Objective The current study aims to investigate the effect of Hemagglutinating virus of Japan envelope(HVJ-E) on induction of apoptosis and autophagy in human prostate cancer PC3 cells, and the underlying mechanisms. Methods PC3 cells were treated with HVJ-E at various multiplicity of infection(MOI), and the generated reactive oxygen species(ROS), cell viability, apoptosis, and autophagy were detected, respectively. Next, the role of ROS played in the regulation of HVJ-E-induced apoptosis and autuphagy in PC3 cells were analysed. In the end, the relationship between HVJ-E-induced apoptosis and autuophagy was investigated by using rapamycin and chloroquine. Results Flow cytometry assay revealed that HVJ-E treatment induced dose-dependent apoptosis and that the JNK and p38 MAPK signaling pathways were involved in HVJ-E-induced apoptosis in PC3 cells. In addition, HVJ-E was able to induce autophagy in PC3 cells via the class III PI3 K/beclin-1 pathway. The data also implyed that HVJ-E-triggered autophagy and apoptosis were ROS dependent. When ROS was blocked with N-acetylcysteine(NAC), HVJ-E-induced LC3-II conversion and apoptosis were reversed. Interestingly, HVJ-E-induced apoptosis was significantly increased by an inducer of autophagy, rapamycin pretreatment, both in vitro and in vivo. Conclusion HVJ-E exerts anticancer effects via autophagic cell death in prostate cancer cells.展开更多
Background Immunotherapy shows promise as a treatment option for various cancers.However,there is growing concern over potential complications from hepatitis B virus(HBV)reactivation after checkpoint blockade immunoth...Background Immunotherapy shows promise as a treatment option for various cancers.However,there is growing concern over potential complications from hepatitis B virus(HBV)reactivation after checkpoint blockade immunotherapy.Although most of the previous clinical trials on immune checkpoint inhibitors(ICIs)excluded patients with HBV,a few case reports and retrospective studies of HBV reactivation have been published.The aim of this study is to assess the risk of hepatitis B virus reactivation(HBVr)in patients receiving ICIs for advanced cancer.Methods English and Chinese language literature published prior to April 30,2023,was searched in PubMed,EMBASE,Web of Science,Cochrane,SinoMed,CNKI and Wanfang Data for studies reporting HBVr rates in cancer patients treated with ICIs.A pooled risk estimate was calculated for HBVr rates with 95%confdence intervals(CI).Results Data from 34 studies including 7126 patients were retrieved and analyzed.The pooled HBVr rate in cancer patients treated with ICIs was 1.3%(I^(2)=90.44%,95%CI:0.2-2.9%,P<0.001).Subgroup analysis revealed that patients diagnosed with hepatocellular carcinoma(HCC),HBV carriers,and patients from Asian regions or in developing countries have a higher rate of HBVr.Conclusions Our meta-analysis demonstrated a low risk of HBVr in patients treated with ICIs for advanced cancer.ICI treatment may be safely used in patients with existing HBV infection or chronic hepatitis B,accompanied by regular monitoring and appropriate antiviral prophylaxis if necessary.展开更多
文摘Hepatitis B virus(HBV)reactivation is a clinically significant challenge in disease management.This review explores the immunological mechanisms underlying HBV reactivation,emphasizing disease progression and management.It delves into host immune responses and reactivation’s delicate balance,spanning innate and adaptive immunity.Viral factors’disruption of this balance,as are interac-tions between viral antigens,immune cells,cytokine networks,and immune checkpoint pathways,are examined.Notably,the roles of T cells,natural killer cells,and antigen-presenting cells are discussed,highlighting their influence on disease progression.HBV reactivation’s impact on disease severity,hepatic flares,liver fibrosis progression,and hepatocellular carcinoma is detailed.Management strategies,including anti-viral and immunomodulatory approaches,are critically analyzed.The role of prophylactic anti-viral therapy during immunosuppressive treatments is explored alongside novel immunotherapeutic interventions to restore immune control and prevent reactivation.In conclusion,this compre-hensive review furnishes a holistic view of the immunological mechanisms that propel HBV reactivation.With a dedicated focus on understanding its implic-ations for disease progression and the prospects of efficient management stra-tegies,this article contributes significantly to the knowledge base.The more profound insights into the intricate interactions between viral elements and the immune system will inform evidence-based approaches,ultimately enhancing disease management and elevating patient outcomes.The dynamic landscape of management strategies is critically scrutinized,spanning anti-viral and immunomodulatory approaches.The role of prophylactic anti-viral therapy in preventing reactivation during immunosuppressive treatments and the potential of innovative immunotherapeutic interventions to restore immune control and proactively deter reactivation.
文摘In this editorial,we offer a summary of the risk associated with hepatitis B reactivation(HBVr)in the setting of both solid and hematologic malignancies treated with Bruton tyrosine kinase(BTK)inhibitors,with insights derived from current studies.Furthermore,we emphasize the critical need for a framework regarding robust risk evaluation in patients undergoing such treatments.This framework is essential for identifying those at increased risk of HBVr,enabling healthcare providers to implement proactive measures to prevent reactivation and ensure the safe administration of BTK inhibitor therapy.
文摘Rheumatoid arthritis(RA)is an autoimmune disease characterized by proliferative synovitis,which can cause cartilage and bone damage as well as functional limitations.Disease-modifying anti-rheumatic drugs have significantly improved the prognosis of RA patients.However,people with RA,when combined with hepatitis B virus(HBV)infection,may experience reactivation of HBV during treatment with anti-rheumatic drugs.The outcome of HBV reactivation(HBVr)varies from liver inflammation to liver failure,while insufficient HBV screening in RA patients has been reported in various countries.Therefore,it is necessary to identify patients at high risk before starting immunosuppressive therapy.The immune response plays an important role in anti-HBV infection.However,most anti-rheumatic drugs exert an inhibitory effect on the body’s immune system,resulting in HBVr.Therefore,it is necessary to conduct a comprehensive evaluation based on host factors,viral factors,and drug factors.In this paper,we summarize the mechanism of HBVr,the risk of HBVr caused by anti-rheumatic drugs,and the appropriate diagnosis and treatment process for RA patients so that clinicians can have a more comprehensive understanding of HBVr in RA patients.
文摘Imatinib mesylate is a molecular targeted agent for treating chronic myeloid leukemia (CML) and gastrointestinal stromal tumor. Although imatinib mesylate is not regarded as an immunosuppressive agent, few studies have also shown that it may impair immune response. In this report, we present a case of transient hepatitis B virus (HBV) reactivation during imatinib mesylate treatment for CML.
基金supported by the National Key Research and Development Program of China[2017YFD0502303]National N atural Science Foundation of China[No.31302042]High-end Talent Support Program of Yangzhou University and the Young and Middle-aged Academic Leaders Plan of Yangzhou University and the Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)
文摘Objective The current study aims to investigate the effect of Hemagglutinating virus of Japan envelope(HVJ-E) on induction of apoptosis and autophagy in human prostate cancer PC3 cells, and the underlying mechanisms. Methods PC3 cells were treated with HVJ-E at various multiplicity of infection(MOI), and the generated reactive oxygen species(ROS), cell viability, apoptosis, and autophagy were detected, respectively. Next, the role of ROS played in the regulation of HVJ-E-induced apoptosis and autuphagy in PC3 cells were analysed. In the end, the relationship between HVJ-E-induced apoptosis and autuophagy was investigated by using rapamycin and chloroquine. Results Flow cytometry assay revealed that HVJ-E treatment induced dose-dependent apoptosis and that the JNK and p38 MAPK signaling pathways were involved in HVJ-E-induced apoptosis in PC3 cells. In addition, HVJ-E was able to induce autophagy in PC3 cells via the class III PI3 K/beclin-1 pathway. The data also implyed that HVJ-E-triggered autophagy and apoptosis were ROS dependent. When ROS was blocked with N-acetylcysteine(NAC), HVJ-E-induced LC3-II conversion and apoptosis were reversed. Interestingly, HVJ-E-induced apoptosis was significantly increased by an inducer of autophagy, rapamycin pretreatment, both in vitro and in vivo. Conclusion HVJ-E exerts anticancer effects via autophagic cell death in prostate cancer cells.
文摘Background Immunotherapy shows promise as a treatment option for various cancers.However,there is growing concern over potential complications from hepatitis B virus(HBV)reactivation after checkpoint blockade immunotherapy.Although most of the previous clinical trials on immune checkpoint inhibitors(ICIs)excluded patients with HBV,a few case reports and retrospective studies of HBV reactivation have been published.The aim of this study is to assess the risk of hepatitis B virus reactivation(HBVr)in patients receiving ICIs for advanced cancer.Methods English and Chinese language literature published prior to April 30,2023,was searched in PubMed,EMBASE,Web of Science,Cochrane,SinoMed,CNKI and Wanfang Data for studies reporting HBVr rates in cancer patients treated with ICIs.A pooled risk estimate was calculated for HBVr rates with 95%confdence intervals(CI).Results Data from 34 studies including 7126 patients were retrieved and analyzed.The pooled HBVr rate in cancer patients treated with ICIs was 1.3%(I^(2)=90.44%,95%CI:0.2-2.9%,P<0.001).Subgroup analysis revealed that patients diagnosed with hepatocellular carcinoma(HCC),HBV carriers,and patients from Asian regions or in developing countries have a higher rate of HBVr.Conclusions Our meta-analysis demonstrated a low risk of HBVr in patients treated with ICIs for advanced cancer.ICI treatment may be safely used in patients with existing HBV infection or chronic hepatitis B,accompanied by regular monitoring and appropriate antiviral prophylaxis if necessary.