Reactivation in B-cells is critical for the Epstein Barr virus (EBV) life cycle and it plays a role in amplifying viral titers in AIDS patients. The repertoire of EBV genes thought to be involved in viral replication consists primarily of approximately 80-90 protein-coding genes. These viral proteins play very diverse roles in virus production including roles in DNA replication, RNA transcription, molecular trafficking, virion assembly, viral egress, host shut-off etc. This is not to mention roles as viron components; both components that form the virus architecture as well as those that are involved in inducing the rapid signaling responses immediately following new infection. We hypothesize that in addition to this group of known protein coding genes, EBV encodes a previously unappreciated group of long non-coding transcripts that will ultimately be found to play an equally diverse set of functions in virus replication. Conceptually this would be important because it would change the texture and the details of how most of us visualize the reactivation process. From a practical standpoint, it would give us a new class of molecular targets that may offer the application of alternative therapeutic approaches against EBV.
The replication phase of the Epstein Barr virus results in the production of infectious virions and the spread of the virus within the host. In AIDS patients, virl proteins produced during the replication phase as well as oncogenic latency proteins are not as well targeted by the immune system, resulting in additional pathogenic consequences including lymphomas. Here we propose a new regulatory model for how EBV facilitates progression through the viral replication phase.
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