Epstein-Barr virus lytic replication activates and is dependent upon MAPK-interacting kinase 1/2 in a cell-type dependent manner.

Epstein-Barr virus (EBV) is known to manipulate its cellular environment to enhance viral replication, which can lead to dysregulation of cellular machinery, setting the stage for potential future disease. Previous research showed that under rapamycin-mediated inhibition of mTORC1, EBV lytic protein production was altered in a cell-type specific manner, suggesting that EBV differentially activates or utilizes signaling pathways in B versus epithelial cells. Here we correlated activation of the mTORC1, ERK1/2, and p38 pathways in relation to EBV lytic replication and discovered that activation of MAPK-interacting kinase 1/2 (Mnk1/2) was strongly associated with EBV lytic replication.

BZLF1 transcript variants in Epstein-Barr virus-positive epithelial cell lines.

Epstein-Barr virus (EBV) is a widely prevalent pathogen currently infecting over 90% of the human population and is associated with various lymphomas and carcinomas. Lytic replication of EBV is regulated by the expression of the immediate-early genes BZLF1 and BRLF1. In B lymphocytes, BZLF1 transcripts have been shown to be processed to a fully spliced form, as well as zDelta, a spliced variant containing only the first and third exons.

Inhibition of mTORC1 inhibits lytic replication of Epstein-Barr virus in a cell-type specific manner.

Background: Epstein-Barr virus is a human herpesvirus that infects a majority of the human population. Primary infection of Epstein-Barr virus (EBV) causes the syndrome infectious mononucleosis. This virus is also associated with several cancers, including Burkitt's lymphoma, post-transplant lymphoproliferative disorder and nasopharyngeal carcinoma.

Glycolytic control of vacuolar-type ATPase activity: a mechanism to regulate influenza viral infection.

As new influenza virus strains emerge, finding new mechanisms to control infection is imperative. In this study, we found that we could control influenza infection of mammalian cells by altering the level of glucose given to cells. Higher glucose concentrations induced a dose-specific increase in influenza infection.

A Drosophila model for genetic analysis of influenza viral/host interactions.

Influenza viruses impose a constant threat to vertebrates susceptible to this family of viruses. We have developed a new tool to study virus-host interactions that play key roles in viral replication and to help identify novel anti-influenza drug targets. Via the UAS/Gal4 system we ectopically expressed the influenza virus M2 gene in Drosophila melanogaster and generated dose-sensitive phenotypes in the eye and wing.

Functional interactions between the Epstein-Barr virus BZLF1 protein and the promyelocytic leukemia protein.

The Epstein-Barr virus immediate-early protein BZLF1 (Z) has been shown to alter the cellular localization of the promyelocytic leukemia (PML) protein. PML has important implications for growth control, apoptosis, anti-viral effects and many more processes. Here we further examined the relationship between PML and the Epstein-Barr virus Z protein.

Mitochondrial transporters involved in oleic acid utilization and glutamate metabolism in yeast.

Utilization of fatty acids such as oleic acid as sole carbon source by the yeast Saccharomyces cerevisiae requires coordinated function of peroxisomes, where the fatty acids are degraded, and the mitochondria, where oxidation is completed. We identified two mitochondrial oxodicarboxylate transporters, Odc1p and Odc2p, as important in efficient utilization of oleic acid in yeast [Tibbetts et al., Arch.

Effects of SUMO-1 upon Epstein-Barr virus BZLF1 function and BMRF1 expression.

Epstein-Barr virus (EBV) is a human herpesvirus that has infected at least 90% of the world population. This very successful virus causes infectious mononucleosis and is associated with many different types of cancer. The EBV BZLF1 protein is a transcription factor that has also been shown to interact with many host cell proteins and pathways.

Modeling early Epstein-Barr virus infection in Drosophila melanogaster: the BZLF1 protein.

Epstein-Barr virus (EBV) is the causative agent of infectious mononucleosis and is associated with several forms of cancer, including lymphomas and nasopharyngeal carcinoma. The EBV immediate-early protein BZLF1 functions as a transcriptional activator of EBV early gene expression and is essential for the viral transition between latent and lytic replication. In addition to its role in the EBV life cycle, BZLF1 (Z) also has profound effects upon the host cellular environment, including disruption of cell cycle regulation, signal transduction pathways, and transcription.

Epstein-Barr virus immediate-early proteins BZLF1 and BRLF1 alter mitochondrial morphology during lytic replication.

Epstein-Barr virus (EBV) is a human DNA virus that is responsible for the syndrome infectious mononucleosis, and is associated with several forms of cancer. During both lytic and latent viral infection, viral proteins manipulate the host's cellular components to aid in viral replication and maintenance. Here, it is demonstrated that induction of EBV lytic replication results in a dramatic reorganization of mitochondria accompanied by a significant alteration of mitochondrial membrane potential and a rapid and transient increase in the microtubular cytoskeleton.

Epstein-Barr virus BZLF1 protein binds to mitotic chromosomes.

Epstein-Barr virus (EBV) is a human herpesvirus that causes infectious mononucleosis and is associated with several types of cancers, including nasopharyngeal carcinoma and Burkitt's lymphoma. An EBV protein that plays an integral role during lytic replication is the immediate-early protein BZLF1. Our laboratory has found that BZLF1 (Z) localizes to host chromosomes during mitosis.