Article
Biochemistry & Molecular Biology
Yaojia Ma, Shingo Nakamoto, Junjie Ao, Na Qiang, Tadayoshi Kogure, Keita Ogawa, Miyuki Nakagawa, Kisako Fujiwara, Terunao Iwanaga, Ryuta Kojima, Hiroaki Kanzaki, Keisuke Koroki, Kazufumi Kobayashi, Naoya Kanogawa, Soichiro Kiyono, Masato Nakamura, Takayuki Kondo, Ryo Nakagawa, Sadahisa Ogasawara, Ryosuke Muroyama, Tetsuhiro Chiba, Jun Kato, Naoya Kato
Summary: In this study, antiviral compounds targeting HBx protein were identified by analyzing HBx binding activity. Tranilast, one of the identified compounds, was found to inhibit HBV replication and infection without affecting cell viability. These findings provide new insights into the development of drugs for the treatment of HBV infection.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Microbiology
Ellen Van Damme, Jolien Vanhove, Bryan Severyn, Lore Verschueren, Frederik Pauwels
Summary: Chronic hepatitis B, caused by HBV, is a major health issue globally, with the goal of treatment being functional cure. Understanding the virus's biology is crucial for identifying new therapeutic targets in order to achieve high rates of functional cure.
FRONTIERS IN MICROBIOLOGY
(2021)
Article
Pharmacology & Pharmacy
Lili He, Huanyu Shen, Hui Deng, Xiaoyan Zhang, Yang Xu, Chunwei Shi, Zhuqing Ouyang
Summary: The study investigated the interaction between the host structural maintenance of chromosomes 5/6 complex (Smc5/6) and the regulatory X protein (HBx) of hepatitis B virus (HBV). It was found that Smc5/6 interacts with HBx through multiple sites and the C-terminal of HBx is sufficient for the interaction. A key residue, Phe132, was identified as critical for the interaction and viral production. These findings provide valuable insights for both basic research and therapeutic drugs targeting HBx.
ANTIVIRAL RESEARCH
(2023)
Article
Virology
Geon-Woo Kim, Aleem Siddiqui
Summary: This study identifies an additional m6A site in the HBV genome at nt 1616, which negatively regulates HBx RNA and protein expression. In the absence of m6A methyltransferases (METTL3/14) and the reader protein (YTHDF2), HBx RNA and protein expression levels increase. Mutations in the m6A sites in the HBx coding region also lead to increased HBx RNA and protein expression. These findings reveal the unique positional effects of m6A modification on the regulation of HBx protein expression.
JOURNAL OF VIROLOGY
(2022)
Article
Genetics & Heredity
Zaheenul Islam Siddiqui, Syed Ali Azam, Wajihul Hasan Khan, Masarrat Afroz, Sabihur Rahman Farooqui, Fatima Amir, Md Iqbal Azmi, Ayesha Anwer, Saniya Khan, Mahboubeh Mehmankhah, Shama Parveen, Syed Naqui Kazim
Summary: Hepatitis B virus X protein C-terminal 127 amino acid truncation plays important roles in inducing cell proliferation, altering gene expression, modifying mitochondrial potential, inducing mitochondrial clustering and oxidative stress, and changing HBx expression pattern in the development of hepatitis B-related liver diseases.
FRONTIERS IN GENETICS
(2021)
Article
Microbiology
Qi Wei, Hongxiao Song, Yanli Gao, Fengchao Xu, Qingfei Xiao, Fei Wang, Bingxin Lei, Junqi Niu, Pujun Gao, Haichun Ma, Guangyun Tan
Summary: There is cross talk between HBV and the host through the CH25H-HBx axis. The expression of CH25H is increased in HBV-infected patients and is associated with low HBV replication. CH25H and its mutants interact with HBx protein and inhibit the nuclear translocation of HBx. 25HC promotes HBV infection but not replication.
Review
Gastroenterology & Hepatology
Masataka Tsuge
Summary: Chronic hepatitis B virus (HBV) infection is a global health issue that can lead to severe liver dysfunction and hepatocellular carcinoma. Current antiviral therapies are effective in suppressing viral replication, but difficulty in complete virus elimination, along with alterations in intracellular metabolism and signaling pathways, contribute to the development of hepatocarcinogenesis in chronic HBV infection.
LIVER INTERNATIONAL
(2021)
Review
Medicine, General & Internal
Mirjam B. Zeisel, Francesca Guerrieri, Massimo Levrero
Summary: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and is largely caused by chronic hepatitis B virus (HBV) infection. While antiviral therapies can suppress viral replication, there is currently no cure for chronic HBV infection. HBV contributes to liver carcinogenesis through direct and indirect effects on host epigenetic alterations, modulating gene expression.
JOURNAL OF CLINICAL MEDICINE
(2021)
Review
Biochemistry & Molecular Biology
Bouchra Kitab, Kyoko Tsukiyama-Kohara
Summary: Hepatitis C virus (HCV) causes chronic infection in the liver and can lead to advanced liver diseases such as fibrosis, cirrhosis, and hepatocellular carcinoma. HCV primarily infects quiescent hepatocytes and can regulate cell cycle genes and proliferation pathways, contributing to persistent infection. The expression levels of HCV RNA and viral proteins are influenced by the hepatocyte proliferation state and cell cycle phase.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Editorial Material
Virology
Adi Ariffianto, Lin Deng, Takayuki Abe, Chieko Matsui, Masahiko Ito, Akihide Ryo, Hussein Hassan Aly, Koichi Watashi, Tetsuro Suzuki, Masashi Mizokami, Yoshiharu Matsuura, Ikuo Shoji
Summary: Hepatitis B virus (HBV) infection induces oxidative stress and antioxidant enzyme expression. This study reveals that HBV X protein (HBx) is crucial for the HBV-induced antioxidant response. HBx activates Nrf2 protein, leading to suppression of HBV core promoter activity, and thus inhibiting viral replication.
JOURNAL OF VIROLOGY
(2023)
Article
Oncology
Wang Chaomin, Niu Wenhao, Hua Jialei, Zhao Ting, Feng Honglei, Hao Zhuang, Wang Yichao, Bai Changsen, Li Yueguo
Summary: HBx modulates the expression of SMAD4 spatially and temporally through both transcriptional activation and protein stabilization, shedding light on the molecular mechanism underlying HBx-induced hepatocarcinogenesis.
Review
Oncology
Xiaodong Zhang, Yufei Wang, Guang Yang
Summary: HBV infections are a global public health concern with the cccDNA template being a key factor in the replication cycle. Host factors involved in HBV cccDNA epigenetic modulation contribute to the development of HCC. The review discusses advances in research on HBV cccDNA, its modulation factors, and potential therapeutic strategies targeting cccDNA. The role of HBx in HBV cccDNA transcription and hepatocarcinogenesis is also highlighted.
CANCER BIOLOGY & MEDICINE
(2022)
Review
Immunology
Xueke Wang, Meisong Kang, Chun Liu, Ting Lin, Xiao Han, Xiwen Jiang
Summary: HCC, the most deadly malignant tumor globally, is closely associated with HBV, and lncRNA imbalance is a key factor in its development. Through studying the interaction between lncRNAs and DNA, RNA, or proteins, researchers can uncover crucial mechanisms in HCC progression. Dysfunctional lncRNAs in HBV-related HCC play significant roles in the regulation and potential molecular mechanisms of tumor occurrence and development.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2021)
Review
Oncology
Eun-Sook Park, Mehrangiz Dezhbord, Ah Ram Lee, Bo Bae Park, Kyun-Hwan Kim
Summary: This article summarizes the mechanisms of liver regeneration and the potential disruption by HBV infection, providing insights for the prevention and treatment of liver failure caused by defective regeneration.
Article
Oncology
Ling Dai, Xiang Gao, Zhihua Ye, Hanmin Li, Xin Yao, Dingbo Lu, Na Wu
Summary: The study aimed to explore the effect and mechanisms of traditional Chinese medicine treatment plan regulating liver regeneration in patients with HBV-related liver failure. After 8 weeks of treatment, the RLR group showed significantly lower mortality, improved liver function, and decreased jaundice levels compared to the control groups. The mechanism may be related to the influence of RLR treatment on cytokines associated with liver regeneration.
FRONTIERS OF MEDICINE
(2021)