Overview of the immunological mechanisms in hepatitis B virus reactivation:Implications for disease progression and management strategies

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.

Risk of hepatitis B virus reactivation in oncological patients treated with tyrosine kinase inhibitors:A case report and literature analysis

Hepatitis B virus(HBV)reactivation(HBVr)represents a severe and potentially life-threatening condition,and preventive measures are available through blood test screening or prophylactic therapy administration.The assessment of HBVr traditionally considers factors such as HBV profile,including hepatitis B surface antigen(HBsAg)and antibody to hepatitis B core antigen,along with type of medication(chemotherapy;immunomodulants).Nevertheless,consideration of possible patient’s underlying tumor and the specific malignancy type(solid or hematologic)plays a crucial role and needs to be assessed for decision-making process.

Investigating the reactivation of historical landslides during the 2022 Luding M_(S)6.8 earthquake

On September 5,2022,a strong earthquake with a magnitude of MS6.8 struck Luding County in Sichuan Province,China,triggering thousands of landslides along the Dadu River in the northwest-southeast(NW-SE)direction.We investigated the reactivation characteristics of historical landslides within the epicentral area of the Luding earthquake to identify the initiation mechanism of earthquake-induced landslides.Records of the two newly triggered and historical landslides were analyzed using manual and threshold methods;the spatial distribution of landslides was assessed in relation to topographical and geological factors using remote sensing images.This study sheds light on the spatial distribution patterns of landslides,especially those that occur above historical landslide areas.Our results revealed a similarity in the spatial distribution trends between historical landslides and new ones induced by earthquakes.These landslides tend to be concentrated within a range of 0.2 km from the river and 2 km from the fault.Notably,both rivers and faults predominantly influenced the reactivation of historical landslides.Remarkably,the reactivated landslides are characterized by their small to medium size and are predominantly situated in historical landslide zones.The number of reactivated landslides surpassed that of previously documented historical landslides within the study area.We provide insights into the critical factors responsible for historical landslides during the 2022 Luding earthquake,thereby enhancing our understanding of the potential implications for future co-seismic hazard assessments and mitigation strategies.

Navigating the complex terrain of hepatitis B virus reactivation in the era of Bruton tyrosine kinase inhibitors

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.

Prevention of hepatitis B reactivation in patients with hematologic malignancies treated with novel systemic therapies:Who and Why?

The risk of reactivation in patients with chronic or past/resolved hepatitis B virus(HBV)infection receiving chemotherapy or immunosuppressive drugs is a wellknown possibility.The indication of antiviral prophylaxis with nucleo(t)side analogue is given according to the risk of HBV reactivation of the prescribed therapy.Though the advent of new drugs is occurring in all the field of medicine,in the setting of hematologic malignancies the last few years have been characterized by several drug classes and innovative cellular treatment.As novel therapies,there are few data about the rate of HBV reactivation and the decision of starting or not an antiviral prophylaxis could be challenging.Moreover,patients are often treated with a combination of different drugs,so evaluating the actual role of these new therapies in increasing the risk of HBV reactivation is difficult.First results are now available,but further studies are still needed.Patients with chronic HBV infection[hepatitis B surface antigen(HBsAg)positive]are reasonably all treated.Past/resolved HBV patients(HBsAg negative)are the actual area of uncertainty where it could be difficult choosing between prophylaxis and pre-emptive strategy.

Hepatitis B virus reactivation in patients treated with monoclonal antibodies

Hepatitis B virus(HBV)reactivation poses a significant clinical challenge,espe-cially in patients undergoing immunosuppressive therapies,including mono-clonal antibody treatments.This manuscript briefly explores the complex rela-tionship between monoclonal antibody therapy and HBV reactivation,drawing upon current literature and clinical case studies.It delves into the mechanisms underlying this phenomenon,highlighting the importance of risk assessment,monitoring,and prophylactic measures for patients at risk.The manuscript aims to enhance the understanding of HBV reactivation in the context of monoclonal antibody therapy,ultimately facilitating informed clinical decision-making and improved patient care.This paper will also briefly review the definition of HBV activation,assess the risks of reactivation,especially in patients treated with monoclonal antibodies,and consider management for patients with regard to screening,prophylaxis,and treatment.A better understanding of patients at risk can help clinicians provide optimum management to ensure successful patient outcomes and prevent morbidity.

Involvement of X-chromosome reactivation in augmenting cancer testis antigens expression:A hy pothesis

Cancer testis antigens(CTAs)are attractive targets for tumor imm unotherapy because of their tumor specific expression,Since more than half of confirmed CTAs are located on the X-chromosome,we asked whether there is a link between CTA expression and X-chromosomes.Recent reports have shown that reactivation of the inactive X-chromosome,known as X-chromosome reactivation(XCR),a unique phenomenon that exists in many high-risk tumors in women,can transform the expression of many X-linked genes from monoallelic to biallelic.

Prevention and management of hepatitis B virus reactivation in patients with hematological malignancies treated with anticancer therapy

Hepatitis due to hepatitis B virus(HBV) reactivation can be severe and potentially fatal, but is preventable. HBV reactivation is most commonly reported in patients receiving cancer chemotherapy, especially rituximabcontaining therapy for hematological malignancies and those receiving stem cell transplantation. All patients with hematological malignancies receiving anticancer therapy should be screened for active or resolved HBV infection by blood tests for hepatitis B surface antigen(HBs Ag) and antibody to hepatitis B core antigen(antiHBc). Patients found to be positive for HBs Ag should be given prophylactic antiviral therapy to prevent HBV reactivation. For patients with resolved HBV infection, no standard strategy has yet been established to prevent HBV reactivation. There are usually two options. One is pre-emptive therapy guided by serial HBV DNA monitoring, whereby antiviral therapy is given as soon as HBV DNA becomes detectable. However, there is little evidence regarding the optimal interval and period of monitoring. An alternative approach is prophylactic antiviral therapy, especially for patients receiving highrisk therapy such as rituximab, newer generation of anti-CD20 monoclonal antibody, obinutuzumab or hematopoietic stem cell transplantation. This strategy may effectively prevent HBV reactivation and avoid the inconvenience of repeated HBV DNA monitoring. Entecavir or tenofovir are preferred over lamivudine as prophylactic therapy. Although there is no well-defined guideline on the optimal duration of prophylactic therapy, there is growing evidence to recommend continuing prophylactic antiviral therapy for at least 12 mo after cessation of chemotherapy, and even longer for those who receive rituximab or who had high serum HBV DNA levels before the start of immunosuppressive therapy. Many novel agents have recently become available for the treatment of hematological malignancies, and these agents may be associated with HBV reactivation. Although there is currently limited evidence to guide the optimal preventive measures, we recommend antiviral prophylaxis in HBs Ag-positive patients receiving novel treatments, especially the Bruton tyrosine kinase inhibitors and the phosphatidylinositol 3-kinase inhibitors, which are B-cell receptor signaling modulators and reduce proliferation of malignant B-cells. Further studies are needed to clarify the risk of HBV reactivation with these agents and the best prophylactic strategy in the era of targeted therapy for hematological malignancies.

Incidence and characteristics of HBV reactivation in hematological malignant patients in south Egypt

AIM:To investigate characteristics of hepatitis B virus(HBV)implicated in HBV reactivation in patients with hematological malignancies receiving immunosuppressive therapy.METHODS:Serum samples were collected from 53 patients with hematological malignancies negative for hepatitis B surface antigen(HBsAg)before the start of and throughout the chemotherapy course.HBV reactivation was diagnosed when the HBsAg status changed from negative to positive after the initiation of chemotherapy and/or when HBV DNA was detected by realtime detection polymerase chain reaction(RTD-PCR).For detecting the serological markers of HBV infection,HBsAg as well as antibodies to the core antigen(antiHBc)and to the surface antigen were measured in the sera by CEIA.Nucleic acids were extracted from sera,and HBV DNA sequences spanning the S gene were amplified by RTD-PCR.The extracted DNA was further subjected to PCR to amplify the complete genome as well as the specific genomic sequences bearing the enhancerⅡ/core promoter/pre-core/core regions(nt1628-2364).Amplicons were sequenced directly.RESULTS:Thirty-five(66%)of the 53 HBsAg-negative patients were found to be negative serologically for antiHBc,and the remaining 18(34%)patients were positive for anti-HBc.Five of the 53(9.4%)patients with hematologic malignancies experienced HBV reactivation.Genotype D1 was detected in all five patients.Four types of mutant strains were detected in the S gene product of HBV strains and were isolated from 3 patients with HBV reactivation:T/S120,L143,and I126.HBV DNA was detected in the pretreatment HBsAg-negative samples in one of the five patients with HBV reactivation.In this patient,sequences encompassing the HBV full genome obtained from sera before the start of chemotherapy and at the time of de novo HBV hepatitis were detected and it showed 100%homology.Furthermore,in the phylogenetic tree,the sequences were clustered together,thereby indicating that this patient developed reactivation from an occult HBV infection.CONCLUSION:Past infection with HBV is a risk factor for HBV reactivation in Egypt.Mandatory anti-HBc screening prior to chemotherapy in patients with hematological malignancies is recommended.

Post-partum reactivation of chronic hepatitis B virus infection among hepatitis B e-antigen-negative women

AIM: To investigate the frequency and timing of post-partum chronic hepatitis B virus(HBV) reactivation and identify its pre-partum predictors. METHODS: Forty-one hepatitis B e antigen(HBe Ag)-negative chronic HBV infected pregnant women were prospectively evaluated between the 28 th and the 32 nd week of gestation. Subjects were re-evaluated at 3-mo intervals during the first post-partum year and every 6 mo during the following years. HBV DNA was determined using real-time reverse transcription polymerase chain reaction(Cobas Taq Man HBV Test) with a lower detection limit of 8 IU/m L. Post-partum reactivation(PPR) was defined as abnormal alanine aminotransaminase(ALT) levels and HBV DNA above 2000 IU/m L. RESULTS: Fourteen out of 41 women(34.1%) had prepartum HBV DNA levels > 2000 IU/m L, 18(43.9%) had levels < 2000 IU/m L and 9(21.9%) had undetectable levels. Fourteen women were lost to follow-up(failure to return). PPR occurred in 8 of the 27(29.6%) women evaluated, all within the first 6 mo after delivery(5 at month 3; 3 at month 6). Five of the 6(83.3%) women with pre-partum HBV DNA > 10000 IU/m L exhibited PPR compared with 3 of the 21(14.3%) women with HBV DNA < 10000 IU/m L(two with HBV DNA > 2000 and the third with HBV DNA of 1850IU/m L), P = 0.004. An HBV DNA level ≥ 10000 IU/m L independently predicted post-partum HBV infection reactivation(OR = 57.02, P = 0.033). Mean pre-partum ALT levels presented a non-significant increase in PPR cases(47.3 IU/L vs 22.2 IU/L, respectively, P = 0.094).CONCLUSION: In the present study, PPR occurred in approximately 30% of HBe Ag-negative pregnant women; all events were observed during the first semester after delivery. Pre-partum HBV DNA level > 10000 IU/m L predicted PPR.

Hepatitis B reactivation in patients receiving direct-acting antiviral therapy or interferon-based therapy for hepatitis C:A systematic review and meta-analysis

AIM To assess the incidence of hepatitis B virus(HBV) reactivation in patients receiving direct-acting antiviral agent(DAA)-based therapy or interferon(IFN)-based therapy for hepatitis C and the effectiveness of preemptive antiHBV therapy for preventing HBV reactivation.METHODS The Pub Med, MEDLINE and EMBASE databases were searched, and 39 studies that reported HBV reactivation in HBV/hepatitis C virus coinfected patients receiving DAAbased therapy or IFN-based therapy were included. The primary outcome was the rate of HBV reactivation. The secondary outcomes included HBV reactivation-related hepatitis and the effectiveness of preemptive anti-HBV treatment with nucleos(t)ide analogues. The pooled effects were assessed using a random effects model. RESULTS The rate of HBV reactivation was 21.1% in hepatitis Bsurface antigen(HBs Ag)-positive patients receiving DAAbased therapy and 11.9% in those receiving IFN-based therapy. The incidence of hepatitis was lower in HBs Agpositive patients with undetectable HBV DNA compared to patients with detectable HBV DNA receiving DAA therapy(RR = 0.20, 95%CI: 0.06-0.64, P = 0.007). The pooled HBV reactivation rate in patients with previous HBV infection was 0.6% for those receiving DAA-based therapy and 0 for those receiving IFN-based therapy, and none of the patients experienced a hepatitis flare related to HBV reactivation. Preemptive anti-HBV treatment significantly reduced the potential risk of HBV reactivation in HBs Agpositive patients undergoing DAA-based therapy(RR = 0.31, 95%CI: 0.1-0.96, P = 0.042).CONCLUSION The rate of HBV reactivation and hepatitis flare occurrence is higher in HBs Ag-positive patients receiving DAA-based therapy than in those receiving IFN-based therapy, but these events occur less frequently in patients with previous HBV infection. Preemptive anti-HBV treatment is effective in preventing HBV reactivation.

Chemotherapy-related reactivation of hepatitis B infection: Updates in 2013

Hepatitis B reactivation is a potentially serious complication of anticancer chemotherapy,which occurs during and after therapy.This condition affects primarily hepatitis B surface antigen(HBsAg)-positive patients,but sometimes HBsAg-negative patients can be at risk,based only on evidence of past infection or occult infection with a low titer of detectable hepatitis B virus(HBV)DNA.The clinical outcomes vary with the different degrees of virologic and biochemical rebound,ranging from asymptomatic elevations in liver enzymes to hepatic failure and even death.Despite the remarkable advancement in the treatment of chronic hepatitis B over the past decade,proper strategies for the prevention and management of HBV reactivation remain elusive.Moreover,with the increasing use of rituximab in patients with lymphoma,HBV reactivation in occult or past infections has become increasingly problematic,especially in HBV-endemic regions.This review addresses the current knowledge on the clinical aspects and management of chemotherapy-related HBV reactivation,updates from recent reports,several unresolvedissues and future perspectives.

Reactivation of hepatitis B virus infection in patients with hemolymphoproliferative diseases, and its prevention

Reactivation of hepatitis B virus(HBV)replication is characterized by increased HBV-DNA serum values of about 1 log or by HBV DNA turning positive if previously undetectable in serum,possibly associated with liver damage and seldom life-threatening.Due to HBV reactivation,hepatitis B surface antigen(HBsAg)-negative/anti-HBc-positive subjects may revert to HBsAg-positive.In patients with hemo-lymphoproliferative disease,the frequency of HBV reactivation depends on the type of lymphoproliferative disorder,the individual's HBV serological status and the potency and duration of immunosuppression.In particular,it occurs in 10%-50%of the HBsAg-positive and in 2%-25%of the HBsAg-negative/anti-HBc-positive,the highest incidences being registered in patients receiving rituximab-based therapy.HBV reactivation can be prevented by accurate screening of patients at risk and by a pharmacological prophylaxis with anti-HBV nucleo(t)sides starting 2-3 wk before the beginning of immunosuppressive treatment and covering the entire period of administration of immunosuppressive drugs and a long subsequent period,the duration of which depends substantially on the degree of immunodepression achieved.Patients with significant HBV replication before immunosuppressive therapy should receive anti-HBV nucleo(t)sides as a long-term(may be life-long)treatment.This review article is mainly directed to doctors engaged every day in the treatment of patients with onco-lymphoproliferative diseases,so that they can broaden their knowledge on HBV infection and on its reactivation induced by the drugs with high immunosuppressive potential that they use in the care of their patients.

Hepatitis C virus reactivation in cancer patients in the era of targeted therapies

The purpose of this review is to summarize the evidence of hepatitis C reactivation in cancer patients in the era of targeted therapies.Targeted therapies are novel therapeutics frequently used in cancer patients.During treatment with targeted therapies,viral replication is one of the major problems that can occur.The PubMed database,ASCO,and ASCO Gastrointestinal Cancer Symposium abstracts were searched up until September 15,2013 using the following search keywords:"targeted therapies,rituximab,alemtuzumab,brentuximab,hepatitis,hepatitis C reactivation,tyrosine kinase inhibitors,imatinib,mammalian target of rapamycin(mTOR)inhibitors,everolimus,anti-HER therapies,trastuzumab,pertuzumab,lapatinib,antiepidermal growth factor receptor therapies,cetuximab,panitumumab,and ipilimumab".Papers considered relevant for the aim of this review were selected by the authors.The data about rituximab-induced hepatic flare in hepatitis C virus(HCV)positive patients is controver-sial.However,there is the possibility of life-threatening hepatic flare that can develop after HCV ribonucleic acid(HCV-RNA)viral load increases.Routine followup of liver function tests should be advised.Especially in high-risk patients,such as those with baseline chronic active hepatitis and cirrhosis,and where there are plans to administer rituximab concomitantly with corticosteroids,it is advised to have close follow-up of HCV viral load.The data is insufficient to make accurate statements about the association of alemtuzumab therapy and HCV reactivation.However,alemtuzumab may cause deep immunosuppression.Due to this,it is better to follow up with liver function tests and HCV RNA levels during alemtuzumab therapy.Brentuximab has effects on antibody dependent cellular toxicity and may decrease humoral immunity.Thus,we believe that during brentuximab treatment of HCV infected patients,clinicians may encounter hepatitis C reactivation.There have been no reported cases of hepatitis C reactivation with imatinib therapy.However,there are many reports of hepatitis B reactivation with imatinib treatment.Based on the evidence of hepatitis B reactivation with imatinib and the effects of imatinib on immune system functions,we suggest that imatinib therapy might be a risk factor for HCV reactivation.Anti-human epidermal growth factor receptor 2 therapies are not associated with hepatic flare in HCV infected patients.Post-transplant studies reported that mTOR was safely administered to patients with active hepatitis C without causing hepatic flare.Cetuximab and panitumumab have not been associated with HCV reactivation.Two cases of HCV infected melanoma were safely treated with ipilimumab without any HCV reactivation or hepatic flare.Targeted therapies are a new and emerging area of oncology treatment modalities.While treating HCV infected cancer patients,clinicians should be mindful of the immunosuppressive properties of targeted therapies.Further randomized trials are needed to establish algorithms for this issue.

Hepatitis B virus reactivation with a rituximab-containing regimen

Rituximab is currently used not only in the treatment of B-cell lymphoma but also for various other diseases, including autoimmune diseases, post-transplant graft vs host disease, and rejection following kidney transplants. Due to rituximab's widespread use, great progress has been made regarding research into complications that arise from its use, one of the most serious being the reactivation of hepatitis B virus(HBV), and efforts continue to establish guidelines for preventive treatment against this occurrence. This report discusses preventive measures against rituximab-induced HBV reactivation and future objectives.

Reactivation of hepatitis B after liver transplantation: Current knowledge, molecular mechanisms and implications in management

Chronic hepatitis B(CHB) is a major global health problem affecting an estimated 350 million people with more than 786000 individuals dying annually due to complications, such as cirrhosis, liver failure and hepatocellular carcinoma(HCC). Liver transplantation(LT) is considered gold standard for treatment of hepatitis B virus(HBV)-related liver failure and HCC. However, post-transplant viral reactivation can be detrimental to allograft function, leading to poor survival. Prophylaxis with high-dose hepatitis B immunoglobulin(HBIG) and anti-viral drugs have achieved remarkable progress in LT by suppressingviral replication and improving long-term survival. The combination of lamivudine(LAM) plus HBIG has been for many years the most widely used. However, life-long HBIG use is both cumbersome and costly, whereas long-term use of LAM results in resistant virus. Recently, in an effort to develop HBIG-free protocols, high potency nucleos(t)ide analogues, such as Entecavir or Tenofovir, have been tried either as monotherapy or in combination with low-dose HBIG with excellent results. Current focus is on novel antiviral targets, especially for covalently closed circular DNA(ccc DNA), in an effort to eradicate HBV infection instead of viral suppression. However, there are several other molecular mechanisms through which HBV may reactivate and need equal attention. The purpose of this review is to address post-LT HBV reactivation, its risk factors, underlying molecular mechanisms, and recent advancements and future of anti-viral therapy.

Three-dimensional distinct element modeling of fault reactivation and induced seismicity due to hydraulic fracturing injection and backflow

This paper presents a three-dimensional fully hydro-mechanical coupled distinct element study on fault reactivation and induced seismicity due to hydraulic fracturing injection and subsequent backflow process,based on the geological data in Horn River Basin,Northeast British Columbia,Canada.The modeling results indicate that the maximum magnitude of seismic events appears at the fracturing stage.The increment of fluid volume in the fault determines the cumulative moment and maximum fault slippage,both of which are essentially proportional to the fluid volume.After backflow starts,the fluid near the joint intersection keeps flowing into the critically stressed fault,rather than backflows to the wellbore.Although fault slippage is affected by the changes of both pore pressure and ambient rock stress,their contributions are different at fracturing and backflow stages.At fracturing stage,pore pressure change shows a dominant effect on induced fault slippage.While at backflow stage,because the fault plane is under a critical stress state,any minor disturbance would trigger a fault slippage.The energy analysis indicates that aseismic deformation takes up a majority of the total deformation energy during hydraulic fracturing.A common regularity is found in both fracturing-and backflow-induced seismicity that the cumulative moment and maximum fault slippage are nearly proportional to the injected fluid volume.This study shows some novel insights into interpreting fracturing-and backflowinduced seismicity,and provides useful information for controlling and mitigating seismic hazards due to hydraulic fracturing.

Hepatitis B reactivation related to everolimus

Reactivation of hepatitis B virus (HBV) during chemotherapy is a well known complication in patients with chronic hepatitis B and cancer.The clinical manifestations range from subclinical elevation of liver enzymes to severe,potentially fatal fulminant hepatitis.Reactivation can occur in a patient with previous inactive HBV infection;either an inactive carrier or a patient with resolved hepatitis.Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved in renal cell carcinoma,neuroendocrine tumours and breast cancer.mTOR inhibitors are a new generation of drugs for targeted treatment;therefore,little about their side effects is known.Here,we report a patient with renal cell carcinoma who experienced a flare of hepatitis B infection during treatment with everolimus.Clinicians should be aware of HBV reactivation in patients who are undergoing treatment with everolimus,and screening for hepatitis B infection and prophylactic antiviral treatment should be considered.

Reactivation of tuberculosis in hepatocellular carcinoma treated with transcatheter arterial chemoembolization: A report of 3 cases

Pulmonary tuberculosis is an opportunistic infection that can be reactivated in immunocompromised conditions, for example, in malignancy or after liver transplantation. Hepatocellular carcinoma (HCC) has a high mortality rate because it is frequently diagnosed at an advanced stage. Although surgical resection is the established curative measure for HCC, it is only feasible for earlystage HCC. Transcatheter arterial chemoembolization (TACE) is the most common treatment modality for patients with unresectable HCC. However, repeated TACE sessions and, occasionally, the tumor itself can further impair the reserve hepatic function and immunity. We report 3 recent cases of HCC with reactivation of pulmonary tuberculosis after TACE.

COVID-19 or treatment associated immunosuppression may trigger hepatitis B virus reactivation: A case report

BACKGROUND Since the initial recognition of coronavirus disease 2019(COVID-19)in Wuhan,this infectious disease has spread to most areas of the world.The pathogenesis of COVID-19 is yet unclear.Hepatitis B virus(HBV)reactivation occurring in COVID-19 patients has not yet been reported.CASE SUMMARY A 45-year-old hepatitis B man with long-term use of adefovir dipivoxil and entecavir for antiviral therapy had HBV reactivation after being treated with methylprednisolone for COVID-19 for 6 d.CONCLUSION COVID-19 or treatment associated immunosuppression may trigger HBV reactivation.