Abstract
Epstein-Barr virus is a prevalent human herpesvirus, with about 95% of the world’s adult population positive for anti-EBV antigen antibodies. After the initial infection and production of new virus particles, the virus may enter a latent state within a subset of cells, and therefore can remain within the host indefinitely. Epstein-Barr virus contributes to a variety of diseases, including many types of cancers. We have created a model system in Drosophila melanogaster to study the effect of expression of the Epstein-Barr virus protein BZLF1, and to identify cellular proteins that mediate BZLF1 activity. Here we present the results of a genetic screen that determined that the Drosophila melanogaster CG9384 gene (an N-acetylglucosaminyl-transferase) is a significant modulator of BZLF1 activity and EBV early lytic replication.
Highlights
Epstein-Barr virus (EBV) is a widespread human herpesvirus, as nearly 95% of the world’s human adult population are positive for anti-EBV antigen antibodies [1]
Epstein-Barr virus is a prevalent human herpesvirus, with about 95% of the world’s adult population positive for anti-EBV antigen antibodies
We present the results of a genetic screen that determined that the Drosophila melanogaster CG9384 gene is a significant modulator of BZLF1 activity and EBV early lytic replication
Summary
Epstein-Barr virus (EBV) is a widespread human herpesvirus, as nearly 95% of the world’s human adult population are positive for anti-EBV antigen antibodies [1]. As EBV is so prevalent, and is associated with such a variety of cancers, it is important to understand how the virus contributes to pathogenesis and carcinogenesis. EBV replication is controlled by two different types of life cycles: lytic, which occurs upon infection of cells and leads to the production of infectious viral particles, and latent, which is the dormant phase in which the virus produces minimal viral proteins to maintain the viral genomes within immortalized B cells. Lytic replication, which occurs in epithelial cells as well as in B cells (before latency ensues) is broken down into three distinct phases of viral protein production: immediate-early, early and late. The immediate-early (IE) genes, BZLF1 and BRLF1, act like switches to activate lytic replication. The IE proteins are transcription factors that turn on the EBV early genes (which act to replicate the viral genome). The late genes encode virion structural elements [2]
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