AI Article Synopsis
- The Epstein-Barr virus (EBV) can switch from a latent state in B lymphocytes to a lytic cycle, where it actively replicates and produces new virus particles.
- Researchers focused on the lytic gene BGLF3.5 and created mutants to study its function, discovering that a specific mutation led to a lack of BGLF4 protein and significantly hindered viral production.
- Further experiments revealed that BGLF3.5 is not crucial for the processes of viral replication and progeny production in HEK293 cells, contrasting with its functionality in a related virus, MHV-68.
Article Abstract
The Epstein-Barr virus (EBV) predominantly establishes a latent infection in B lymphocytes, but a small percentage of infected cells switch from the latent state to the lytic cycle, leading to potent viral DNA replication and progeny viruses production. We here focused on a lytic gene BGLF3.5, and first established BGLF3.5 mutants by marker cassette insertion. Unexpectedly, this insertion mutant failed to produce BGLF4 protein and thus progeny production was severely inhibited. Then we carefully made two point mutant viruses (stop codon insertion or frame-shift mutation) and found that BGLF3.5 is not essential for EBV lytic replication processes, such as viral gene expression, DNA replication, or progeny production in the HEK293 cells although its homolog in murine gammaherpesvirus 68 (MHV-68) was reported to be essential. In addition, we examined the roles of two short, upstream open reading frames within the 5'UTR of BGLF3.5 gene in translation of BGLF4.
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| http://dx.doi.org/10.1016/j.virol.2015.04.007 | DOI Listing |
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