In this editorial, we comment on the article by Mu , published in the recent issue of the . We pay special attention to the immune tolerance mechanism caused by hepatitis B virus (HBV) infection, the pathogenesis of hepatocellular carcinoma (HCC), and the role of antiviral therapy in treating HCC related to HBV infection. HBV infection leads to systemic innate immune tolerance by directly inhibiting pattern recognition receptor recognition and antiviral signaling pathways, as well as by inhibiting the immune functions of macrophages, natural killer cells and dendritic cells. In addition, HBV leads to an immunosuppressive cascade by expressing inhibitory molecules to induce exhaustion of HBV-specific cluster of differentiation 8 + T cells, ultimately leading to long-term viral infection. The loss of immune cell function caused by HBV infection ultimately leads to HCC. Long-term antiviral therapy can improve the prognosis of patients with HCC and prevent tumor recurrence and metastasis.
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http://dx.doi.org/10.4251/wjgo.v17.i1.93983 | DOI Listing |
HPB (Oxford)
January 2025
Surgical Gastroenterology Unit, Division of General Surgery, University of Cape Town Faculty of Health Sciences and Groote Schuur Hospital, Cape Town, South Africa. Electronic address:
Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death globally, particularly in developing countries in Southeast Asia and sub-Saharan Africa (SSA), where chronic hepatitis B virus (HBV) dominates as a major aetiological factor.
Methods: We conducted a retrospective cohort study to quantify the metastatic profile of HCC in a South African patient population managed at a tertiary centre. Demographic, clinical and treatment data were extracted from an institutional registry.
J Med Virol
February 2025
Programa de Pós-Graduação em Medicina e Saúde, Universidade Federal da Bahia, Salvador, Brazil.
Human Immunodeficiency Virus (HIV), Human T Lymphotropic Virus (HTLV), Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) coinfection may lead to disease progression or worsen its clinical presentation. Viral coinfections screening during blood donation is critical. To identify risk factors for coinfection among blood donors, we assessed the blood donations at the Fundação de Hematologia e Hemoterapia da Bahia, from 2008 to 2017.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Hepatology, Center for Pathogen Biology and Infectious Diseases, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
The intricate link between cholesterol metabolism and host immune responses is well recognized, but the specific mechanisms by which cholesterol biosynthesis influences hepatitis B virus (HBV) replication remain unclear. In this study, we show that SREBP2, a key regulator of cholesterol metabolism, inhibits HBV replication by interacting directly with the HBx protein, thereby preventing its nuclear translocation. We also found that inhibiting the ER-to-Golgi transport of the SCAP-SREBP2 complex or blocking SREBP2 maturation significantly enhances HBV suppression.
View Article and Find Full Text PDFIndian J Nephrol
August 2024
Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Background: Viral infections can increase the likelihood of an individual developing membranous nephropathy (MN). Limited information is available regarding the treatment approaches for such cases. We conducted a review focusing on hepatitis B (HBV), hepatitis C (HCV), and human immunodeficiency virus (HIV)-associated MN.
View Article and Find Full Text PDFClin Cosmet Investig Dermatol
January 2025
Department of Dermatology, Guangzhou Dermatology Hospital, Guangzhou, Guangdong, People's Republic of China.
Scleromyxedema (SM) is a rare primary cutaneous mucinosis characterized by systemic papules and scleroderma-like manifestations, often associated with monoclonal gammopathy. We present the case of a 37-year-old male with SM who developed yellowish plaques on the neck and back over three years. Histopathological examination revealed mucin deposition, fibroblast proliferation, and fibrosis, supporting the diagnosis.
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