We have found that not all Epstein-Barr viral (EBV) plasmids are duplicated each cell cycle. This inefficiency is intrinsic to EBV's mechanism of DNA synthesis in latently infected cells and necessarily leads to a loss of EBV plasmids from proliferating cells. If EBV provides its host cells advantages that allow those cells that retain EBV to outgrow those that lose it, then such proliferating populations will be EBV-positive. EBV-associated human tumors are EBV-positive. Thus, the presence of EBV plasmids in most cells of a tumor demonstrates that EBV sustains these tumors in vivo. The virus can provide multiple selective advantages to tumor cells, including promoting cell proliferation and inhibiting cell death. In the case of Burkitt's lymphomas (BL), most current evidence indicates that the tumor requires the virus minimally to block apoptosis.
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http://dx.doi.org/10.1016/j.semcancer.2009.07.006 | DOI Listing |
bioRxiv
January 2025
The Wistar Institute, Philadelphia, PA 19104, USA.
Chromatin structure plays a central role in the regulation of Epstein-Barr Virus (EBV) latency. The histone variant H2A.Z.
View Article and Find Full Text PDFViruses
January 2025
Program in Microbiology and Immunology, University of Pittsburgh, Pittsburgh, PA 15219, USA.
As a ubiquitous human pathogen, the Epstein-Barr virus (EBV) has established lifelong persistent infection in about 95% of the adult population. The EBV infection is associated with approximately 200,000 human cancer cases and 140,000 deaths per year. The presence of EBV in tumor cells provides a unique advantage in targeting the viral genome (also known as episome), to develop anti-cancer therapeutics.
View Article and Find Full Text PDFVirus Res
November 2024
University of Nevada, Reno School of Medicine, Department of Microbiology & Immunology, Reno, NV 89557, USA. Electronic address:
Kaposi's sarcoma-associated herpesvirus (KSHV) relies on many cellular proteins to complete replication and generate new virions. Paraspeckle nuclear bodies consisting of core ribonucleoproteins splicing factor proline/glutamine-rich (SFPQ), Non-POU domain-containing octamer-binding protein (NONO), and paraspeckle protein component 1 (PSPC1) along with the long non-coding RNA NEAT1, form a complex that has been speculated to play an important role in viral replication. Paraspeckle bodies are multifunctional and involved in various processes including gene expression, mRNA splicing, and anti-viral defenses.
View Article and Find Full Text PDFNat Commun
August 2024
Department of Microbiology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
G-quadruplex (G4) structures are found in eukaryotic cell replication origins, but their role in origin function remains unclear. In this study G4 motifs are found in the lytic DNA replication origin (oriLyt) of human cytomegalovirus (HCMV) and recombinant viruses show that a G4 motif in oriLyt essential region I (ER-I) is necessary for viral growth. Replication assays of oriLyt-containing plasmids and biochemical/biophysical analyses show that G4 formation in ER-I is crucial for viral DNA replication.
View Article and Find Full Text PDFJ Adv Res
August 2024
Department of Gynecologic Oncology, Women and Children's Hospital Affiliated to Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei, China; Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei, China; Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei, China; Hubei Cancer Clinical Study Center, Zhongnan Hospital of Wuhan University, Wuhan 430071, Hubei, China. Electronic address:
Introduction: CRISPR/Cas9 gene editing technology has significantly advanced gene therapy, with gene vectors being one of the key factors for its success. Poly (beta-amino ester) (PBAE), a distinguished non-viral cationic gene vector, is known to elevate intracellular reactive oxygen species (ROS) levels, which may cause cytotoxicity and, consequently, impact gene transfection efficacy (T.E.
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