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Clinical Gastroenterology and... Jan 2020
Topics: Hepatitis B virus; Humans; Infections
PubMed: 31252194
DOI: 10.1016/j.cgh.2019.06.026 -
Serum Interleukins as Potential Prognostic Biomarkers in HBV-Related Acute-on-Chronic Liver Failure.Mediators of Inflammation 2022Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is relatively common in China and has complex pathogenesis, difficult clinical treatment, and poor... (Review)
Review
Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is relatively common in China and has complex pathogenesis, difficult clinical treatment, and poor prognosis. Immune status is an important factor affecting ACLF prognosis. Interleukins are a family of secreted lymphocyte factors that interact with a host of cell types including immune cells. These signaling molecules play important roles in transmitting information; regulating immune cells; mediating the activation, proliferation, and differentiation of T and B cells; and modulating inflammatory responses. Many studies have investigated the correlation between interleukin expression and the prognosis of HBV-ACLF. This review focuses on the potential use of interleukins as prognostic biomarkers in HBV-ACLF. References were mainly identified through PubMed and CNKI search, including relevant studies published until December 2021. We have summarized reports of several promising diagnostic interleukin biomarkers that predict susceptibility to HBV-ACLF. The use of biomarkers to understand early prognosis can help devise different therapeutic measures and improve patient survival. Ongoing research on prognostic biomarkers of HBV-ACLF is promising, and future preclinical and clinical studies are warranted.
Topics: Acute-On-Chronic Liver Failure; Biomarkers; Hepatitis B virus; Hepatitis B, Chronic; Humans; Interleukins; Prognosis
PubMed: 36117587
DOI: 10.1155/2022/7794890 -
International Journal of Infectious... Sep 2023
Topics: Humans; Hepatitis B virus; Mental Disorders
PubMed: 37507084
DOI: 10.1016/j.ijid.2023.07.028 -
Hepatology (Baltimore, Md.) Jun 2022
Topics: Hepatitis B; Hepatitis B Vaccines; Hepatitis B virus; Humans
PubMed: 35403231
DOI: 10.1002/hep.32346 -
Critical Reviews in Eukaryotic Gene... 2022We aimed to explore the relationship between free triiodothyronine (FT3) level and severity of hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF). A...
We aimed to explore the relationship between free triiodothyronine (FT3) level and severity of hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF). A total of 122 patients with HBV-ACLF who were hospitalized in Beijing You'an Hospital Affiliated to Capital Medical University from September 2018 to February 2020 were included in this study. The FT3 level and the number of organs involved in patients with different stages of liver failure were analyzed. The patients were divided into four groups, Q1, Q2, Q3, and Q4, according to FT3 level. Correlation analysis was used to compare the correlation between FT3 level and Model for End-Stage Liver Disease (MELD) score, chronic liver failure-sequential organ failure assessment (CLIF-SOFA) score, CLIF-consortium organ failure (CLIF-COF) score, and Asian Pacific Association for the Study of the Liver (APASL) acute-on-chronic liver failure (ACLF) Research Consortium (AARC) score. Multiple linear regression, logistic regression and receiver operating characteristic (ROC) curve were used to analyze the effect of FT3 on MELD score. The FT3 level was the lowest in patients with advanced HBV-ACLF, but the highest in patients with early-stage HBV-ACLF (P < 0.01). The more organs involved, the lower the level of FT3 (P < 0.01). The MELD score of Q4 group was the lowest, whereas that of Q1 group was the highest (P < 0.01). Pearson correlation coefficients of FT3 with MELD score, CLIF-SOFA score, CLIF-COF score and AARC score were -0.477, -0.359, -0.347, and -0.391, respectively (P < 0.001). Multiple linear regression analysis showed that the partial regression coefficients of FT3, natural log total bilirubin in milligrams per decaliter {ln[TBIL (mg/dL)]}, natural log creatinine in milligrams per decaliter {ln[CR (mg/dL)]}, and natural log international normalized ratio {ln[INR]} were -0.215, 0.346, 0.231, and 0.667, respectively (P < 0.001). The odds ratio (OR) values of FT3, ln[TBIL (mg/dL)], ln[CR (mg/dL)], and ln[INR] were 0.141 (0.082-0.244), 5.426 (2.697-9.059), 4.535 (2.432-8.455), and 8.642 (6.679-10.267) in the MELD ≥ 30 group compared with MELD < 30 group (P < 0.001). Furthermore, their area under the ROC curve (AUROC) values were 0.739 (0.686-0.792), 0.748 (0.696-0.800), 0.632 (0.562-0.702), and 0.933 (0.903-0.963), respectively (P < 0.001). FT3 level is correlated with the severity of HBV-ACLF, which may be one of the factors to judge the severity of this disease.
Topics: Acute-On-Chronic Liver Failure; End Stage Liver Disease; Hepatitis B virus; Humans; ROC Curve; Severity of Illness Index
PubMed: 35997117
DOI: 10.1615/CritRevEukaryotGeneExpr.2022041680 -
Frontiers in Cellular and Infection... 2022Numerous canonical cellular signaling pathways modulate hepatitis B virus (HBV) replication. HBV genome products are known to play a significant role in regulating these... (Review)
Review
Numerous canonical cellular signaling pathways modulate hepatitis B virus (HBV) replication. HBV genome products are known to play a significant role in regulating these cellular pathways for the liver's viral-related pathology and physiology and have been identified as the main factor in hepatocarcinogenesis. Signaling changes during viral replication ultimately affect cellular persistence, multiplication, migration, genome instability, and genome damage, leading to proliferation, evasion of apoptosis, block of differentiation, and immortality. Recent studies have documented that numerous signaling pathway agonists or inhibitors play an important role in reducing HBV replication and , and some have been used in phase I or phase II clinical trials. These optional agents as molecular therapeutics target cellular pathways that could limit the replication and transcription of HBV or inhibit the secretion of the small surface antigen of HBV in a signaling-independent manner. As principle-based available information, a combined strategy including antiviral therapy and immunomodulation will be needed to control HBV infection effectively. In this review, we summarize recent findings on interventions of molecular regulators in viral replication and the interactions of HBV proteins with the components of the various targeting cellular pathways, which may assist in designing novel agents to modulate signaling pathways to prevent HBV replication or carcinogenesis.
Topics: Hepatitis B; Hepatitis B virus; Humans; Signal Transduction; Virus Replication
PubMed: 35252042
DOI: 10.3389/fcimb.2022.847539 -
Alimentary Pharmacology & Therapeutics Aug 2022
Topics: Hepatitis B; Hepatitis B virus; Humans
PubMed: 35804475
DOI: 10.1111/apt.17081 -
Transplant Infectious Disease : An... Aug 2022
Topics: Hepacivirus; Hepatitis B; Hepatitis B virus; Humans; Tissue Donors; Viremia
PubMed: 35635505
DOI: 10.1111/tid.13871 -
Reviews in Medical Virology Jan 2022Innate immunity plays a major role in controlling viral infections. Recent exploration of sodium taurocholate co-transporting polypeptide receptor as specific hepatitis... (Review)
Review
Innate immunity plays a major role in controlling viral infections. Recent exploration of sodium taurocholate co-transporting polypeptide receptor as specific hepatitis B virus (HBV) receptor in human hepatocytes has provided appropriate cell culture tools to study the innate immunity of hepatocytes and its cross talk with HBV. In this review, we give a brief update on interaction between HBV and innate immunity using the currently available in vitro cellular models that support the complete life cycle of HBV. We will discuss how HBV can act as a 'stealth' virus to counteract the innate immune responses mediated by the pathogen recognition receptors of hepatocytes and escape the first line of surveillance of the host immune system. We give an overview of the cellular components of innate immunity that present in these in vitro models and discuss how activating these innate immunity components may contribute to the eradication of HBV infection.
Topics: Hepatitis B; Hepatitis B virus; Hepatocytes; Humans; Immunity, Innate
PubMed: 34021666
DOI: 10.1002/rmv.2256 -
Infectious Disease Clinics of North... Jun 2020Hepatitis B virus (HBV) reactivation can be a serious complication for patients with chronic or resolved HBV infection when treated with biologics. For HBsAg-positive... (Review)
Review
Hepatitis B virus (HBV) reactivation can be a serious complication for patients with chronic or resolved HBV infection when treated with biologics. For HBsAg-positive patients receiving biologics, the risk of HBV reactivation is moderate to high. HBsAg-negative/anti-HBc positive patients are at lower risk of HBV reactivation than HBsAg-positive patients. However, patients taking anti-CD20 agents, such as rituximab, have high risk of HBV reactivation (>10%), so antiviral prophylactic therapies are required. This review provides the different classes of biologics associated with HBV reactivation, stratifies the various reactivation risk levels by HBV status and biologic agent, and discusses management strategies.
Topics: Antibiotic Prophylaxis; Biological Factors; Hepatitis B; Hepatitis B virus; Humans; Nucleosides; Precision Medicine; Virus Activation
PubMed: 32334985
DOI: 10.1016/j.idc.2020.02.009