A previous study reported that while the HBV
reactivation rate in patients with resolved HBV
infection was 0% in those who received cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) treatment, it was 24% in patients administered R-CHOP treatment (17).
More than 9 million people in our country are living with HBV
and 10 million with HCV.8 The knowledge of infecting virus genotype is indispensable for effective treatment.
Although nearly two-thirds of patients developed HBV
reactivation, less than 5% developed alanine aminotransferase rises at least twice the upper limit of normal, and only one patient had symptomatic HBV
reactivation, which entecavir therapy resolved.
The aims of this study were to quantify the expression levels of lncRNA-HULC, lncRNA-HEIH, and HBXIP in patients with HBV
infection and hepatitis B-related diseases.
Following the completion of the SAD and MAD portion in healthy subjects, the study will evaluate safety, PK and antiviral data of EDP-514 in NUC-suppressed patients with chronic HBV
is a blood-borne pathogen that chronically infects approximately 350 million people worldwide, and more than 780,000 patients die annually due to HBV
related liver diseases.
The World Health Organisation (WHO) estimates that 240 million people are infected with HBV
and 170 million with hepatitis C (HCV).
The aim of this study was to evaluate the effects of the Milan criteria on the HBV
and HCC recurrence in patients who underwent LDLT due to HBV-induced cirrhosis and HCC.
Covalently closed circular HBV
DNA is a major determinant of persistence of the HBV
genome in infected cells, and necessitates long-term antiviral treatment in those infected individuals.
has a DNA genome, it replicates via an RNA intermediate, through the process of reverse transcription catalysed by a viral polymerase that lacks proofreading ability.
Plasmacytoid dendritic cells (pDC) are the most important cells to connect innate and adaptive immune responses, and also the main source of interferon (IFN)-a. IFN-a can suppress the activity of HBV
enhancers, control HBV-posttranscriptional replication,,, and inhibit HBV
nucleocapsid formation in virus replication. It can also limit virus infection by modulating both innate and adaptive immunity, directly activate natural killer (NK) cells to enhance their cytotoxicity to eliminate-infected cells, promote the maturation of DCs, stimulate naive cluster of differentiation antigen 8+ (CD8+) T cells, resulting in clonal expansion and proliferation, and increase expression of chemokines that recruit NK, T and B cells to the site of infection.