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KSHV hijacks the antiviral kinase IKKε to initiate lytic replication.
PLoS Pathog
January 2025
Institute of Pediatric Infection, Immunity, and Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
IKKε is a traditional antiviral kinase known for positively regulating the production of type I interferon (IFN) and the expression of IFN-stimulated genes (ISGs) during various virus infections. However, through an inhibitor screen targeting cellular kinases, we found that IKKε plays a crucial role in the lytic replication of Kaposi's sarcoma-associated herpesvirus (KSHV). Mechanistically, during KSHV lytic replication, IKKε undergoes significant SUMOylation at both Lys321 and Lys549 by the viral SUMO E3 ligase ORF45.
View Article and Find Full Text PDFUSP7 Inhibitors Destabilize EBNA1 and Suppress Epstein-Barr Virus Tumorigenesis.
J Med Virol
January 2025
The Wistar Institute, Philadelphia, Pennsylvania, USA.
Epstein-Barr virus (EBV) is a ubiquitous human ɣ-herpesvirus implicated in various malignancies, including Burkitt's lymphoma and gastric carcinomas. In most EBV-associated cancers, the viral genome is maintained as an extrachromosomal episome by the EBV nuclear antigen-1 (EBNA1). EBNA1 is considered to be a highly stable protein that interacts with the ubiquitin-specific protease 7 (USP7).
View Article and Find Full Text PDFKaposi's sarcoma-associated herpesvirus (KSHV) gB dictates a low-pH endocytotic entry pathway as revealed by a dual-fluorescent virus system and a rhesus monkey rhadinovirus expressing KSHV gB.
PLoS Pathog
January 2025
Junior Research Group Herpesviruses, Infection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, Göttingen, Germany.
Interaction with host cell receptors initiates internalization of Kaposi's sarcoma-associated herpesvirus (KSHV) particles. Fusion of viral and host cell membranes, which is followed by release of the viral capsid into the cytoplasm, is executed by the core fusion machinery composed of glycoproteins H (gH), L (gL), and B (gB), that is common to all herpesviruses. KSHV infection has been shown to be sensitive to inhibitors of vacuolar acidification, suggestive of low pH as a fusion trigger.
View Article and Find Full Text PDF[Expression of BTLA/HVEM axis in hematological and prospects for immune target therapy].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Hematology, Lanzhou University Second Hospital, Lanzhou 730000, China. *Corresponding authors, E-mail:
Article Synopsis
- BTLA is an inhibitory immune checkpoint that interacts with HVEM to regulate immune balance and maintain immune tolerance on the same cell, while also affecting different immune cells to suppress immune responses.
- Dysregulation of the BTLA/HVEM interaction can lead to impaired immune cell function, allowing tumor cells to evade immune detection and progress.
- Research indicates that BTLA and HVEM are often abnormally expressed in various tumors, making them potential targets for future immunotherapy approaches in treating hematologic malignancies.
Lactobacilli-Derived Postmetabolites Are Broad-Spectrum Inhibitors of Herpes Viruses In Vitro.
Int J Mol Sci
December 2024
Department of Virology, Stephan Angeloff Institute of Microbiology, Bulgarian Academy of Sciences, 26, Georgi Bonchev Str., 1113 Sofia, Bulgaria.
Herpes viruses are highly contagious agents affecting all classes of vertebrates, thus causing serious health, social, and economic losses. Within the One Health concept, novel therapeutics are extensively studied for both veterinary and human control and management of the infection, but the optimal strategy has not been invented yet. Lactic acid bacteria are key components of the microbiome that are known to play a protective role against pathogens as one of the proposed mechanisms involves compounds released from their metabolic activity.
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