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.
| Original language | English |
|---|---|
| Pages (from-to) | 44-53 |
| Number of pages | 10 |
| Journal | Virology |
| Volume | 483 |
| DOIs | |
| Publication status | Published - 01-09-2015 |
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All Science Journal Classification (ASJC) codes
- Virology
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Roles of Epstein-Barr virus BGLF3.5 gene and two upstream open reading frames in lytic viral replication in HEK293 cells. / Watanabe, Takahiro; Fuse, Kenshiro; Takano, Takahiro; Narita, Yohei; Goshima, Fumi; Kimura, Hiroshi; Murata, Takayuki.
In: Virology, Vol. 483, 01.09.2015, p. 44-53.Research output: Contribution to journal › Article
TY - JOUR
T1 - Roles of Epstein-Barr virus BGLF3.5 gene and two upstream open reading frames in lytic viral replication in HEK293 cells
AU - Watanabe, Takahiro
AU - Fuse, Kenshiro
AU - Takano, Takahiro
AU - Narita, Yohei
AU - Goshima, Fumi
AU - Kimura, Hiroshi
AU - Murata, Takayuki
PY - 2015/9/1
Y1 - 2015/9/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84928978836&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84928978836&partnerID=8YFLogxK
U2 - 10.1016/j.virol.2015.04.007
DO - 10.1016/j.virol.2015.04.007
M3 - Article
C2 - 25965794
AN - SCOPUS:84928978836
VL - 483
SP - 44
EP - 53
JO - Virology
JF - Virology
SN - 0042-6822
ER -