Reactivation of Epstein-Barr virus (EBV) is associated with EBV-associated malignancies and is considered to be a benefit target for treatment. Andrographolide is claimed to have antiviral and anti-tumor activities. Therefore, this study aimed to investigate the effect of andrographolide on the inhibition of EBV lytic reactivation in EBV-positive cancer cells. The cytotoxicity of andrographolide was firstly evaluated in EBV-positive cancer cells; P3HR1, AGS-EBV and HONE1-EBV cells, using an MTT assay. Herein, the spontaneous expression of EBV lytic genes; BALF5, BRLF1 and BZLF1, was significantly inhibited in andrographolide-treated cells. Accordingly, andrographolide inhibited the expression of Zta and viral production in sodium butyrate (NaB)-induced EBV lytic reactivation. Additionally, proteomics and bioinformatics analysis revealed the differentially expressed proteins that inhibit EBV lytic reactivation in all treated cell lines were functionally related with the histone modifications and chromatin organization, such as histone H3-K9 modification and histone H3-K27 methylation. Taken together, andrographolide inhibits EBV reactivation in EBV-positive cancer cells by inhibiting EBV lytic genes, probably, through the histone modifications.
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http://dx.doi.org/10.3390/molecules27144666 | DOI Listing |
Folia Microbiol (Praha)
January 2025
Infection Bioengineering Group, POD 1B-602, Department of Biosciences and Biomedical Engineering, Indian Institute of Technology Indore, Indore, Madhya Pradesh, 453552, India.
The increasing prevalence of neurodegenerative diseases is a formidable task due to their multifactorial causation and treatments limited to disease maintenance and progression. Epstein-Barr virus (EBV) is reported to be involved with neuropathologies; previous studies from our group suggested the effective binding of epigallocatechin-3-gallate (EGCG) with EBV nuclear antigen 1 (EBNA1) and glycoprotein H (gH). Therefore, in the current study, we evaluated the anti-EBV effect of ECGG on the neuronal cells.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
Epstein-Barr virus (EBV) establishes persistent infection, causes infectious mononucleosis, is a major trigger for multiple sclerosis and contributes to multiple cancers. Yet, knowledge remains incomplete about how the virus remodels host B cells to support lytic replication. We previously identified that EBV lytic replication results in selective depletion of plasma membrane (PM) B cell receptor (BCR) complexes, composed of immunoglobulin and the CD79A and CD79B signaling chains.
View Article and Find Full Text PDFMicrobiol Immunol
December 2024
Department of Microbiology, Faculty of Medicine, Shimane University, Izumo, Shimane, Japan.
Upon infection with the virus, cells increase the expression of cytidine deaminase APOBEC3 family genes. This leads to the accumulation of C-to-T mutations in the replicating viral genome and suppresses viral propagation. In contrast, herpesviruses, including Epstein-Barr virus (EBV), express genes that counteract APOBEC3 during lytic infection.
View Article and Find Full Text PDFFront Microbiol
December 2024
School of Public Health and Emergency Management, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Epstein-Barr virus (EBV) infects more than 90% of the human population worldwide and establishes lifelong infection in hosts by switching between latent and lytic infection. EBV latency can be reactivated under appropriate conditions, leading to expression of the viral lytic genes and production of infectious progeny viruses. EBV reactivation involves crosstalk between various factors and signaling pathways, and the subsequent complicated virus-host interplays determine whether EBV continues to propagate.
View Article and Find Full Text PDFCurr Opin Virol
December 2024
German Cancer Research Center (DKFZ) Unit D400, Heidelberg, Germany; Institut National de la Santé et de la Recherche Médicale (INSERM) mixed Unit, Heidelberg, Germany. Electronic address:
Epidemiological studies have provided strong evidence that Epstein-Barr virus (EBV) lytic replication is linked to cancer development. Evidence of abortive lytic replication in some tumors and infections with recombinant viruses incapable of lytic replication in animal models have reinforced this view. Furthermore, multiple lytic proteins have been shown to induce genetic instability, a well-characterized precancerous state.
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