Previously, we reported that coffee extract and its constituents, caffeic acid (CA) and p-coumaric acid, inhibit infection by the hepatitis C virus (HCV). In the present report, we identified another coffee-related compound, tannic acid (TA), which also inhibits HCV infection. We systematically evaluated which steps of the viral lifecycle were affected by CA and TA. TA substantially inhibits HCV RNA replication and egression, while CA does not. The infectivity of the HCV pretreated with CA or TA was almost lost. Cellular attachment of HCV particles and their interaction with apolipoprotein E, which is essential for HCV infectivity, were significantly reduced by CA. These results indicate that CA inhibits HCV entry via its direct effect on viral particles and TA inhibits HCV RNA replication and particle egression as well as entry into host cells. Taken together, our findings may provide insights into CA and TA as potential anti-HCV strategies.
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http://dx.doi.org/10.1248/bpb.b18-00970 | DOI Listing |
Life Sci
January 2025
School of Life Sciences, Tianjin University, Tianjin, China. Electronic address:
Lactoferrin (Lf) is a naturally occurring glycoprotein known for its antiviral and antibacterial properties and is present in various physiological fluids. Numerous studies have demonstrated its antiviral effectiveness against multiple viruses, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza virus (IFV), herpes simplex virus (HSV), hepatitis B virus (HBV), and human immunodeficiency virus (HIV). Lf, a vital component of the mucosal defense system, plays a crucial role in inhibiting viral infection by binding to both host cells and viral particles, such as the Hepatitis C virus (HCV).
View Article and Find Full Text PDFAdv Sci (Weinh)
November 2024
University of Chinese Academy of Sciences, Yuquan Road No. 19(A), Shijingshan District, Beijing, 100049, P. R. China.
Hepatitis C virus (HCV) is a major human pathogen causing liver diseases. Although direct-acting antiviral agents effectively inhibit HCV infection, cell-cell transmission remains a critical venue for HCV persistence in vivo. However, the underlying mechanism of how HCV spreads intercellularly remains elusive.
View Article and Find Full Text PDFFront Oncol
November 2024
Key Laboratory for Precision Diagnosis and Treatment of Pediatric Digestive System Diseases, Endoscopy Center and Gastroenterology Department, Shenzhen Children's Hospital, Shenzhen, China.
Arch Biochem Biophys
January 2025
Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University, Changsha, 410013, China. Electronic address:
Iron overload-dependent ferroptosis is believed to contribute to the brain injury of ischemia/reperfusion (I/R), whereas toll-like receptor 4 (TLR4) can exert pro-ferroptosis effect via inhibiting the glutathione peroxidase 4 (GPX4) level, but the mechanisms behind these phenomenon are not fully elucidated. Tumor necrosis factor receptor correlated factor 3-interaction Jun amino-terminal kinase [JNK]-activating modulator (T3JAM) can activate specific molecule and its downstream signaling pathways, including TLR4. This study aims to explore whether targeting T3JAM can reduce I/R-induced ferroptosis in brain via downregulating TLR4.
View Article and Find Full Text PDFUnlabelled: Cells under stress shift their proteome by repressing cap-dependent translation initiation. RNA elements called internal ribosome entry sites (IRES) can allow key cellular transcripts to remain efficiently translated to support an effective stress response. Well- characterized IRESes depend on RNA structures that reduce the protein requirements for translation initiation, thus circumventing translation inhibition.
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