In:
Journal of General Virology, Microbiology Society, Vol. 88, No. 5 ( 2007-05-01), p. 1454-1459
Abstract:
Epstein–Barr virus (EBV) latent membrane protein 2A (LMP2A) blocks B-cell receptor (BCR) signalling after BCR cross-linking to inhibit activation of lytic EBV, and ectopically expressed LMP2B negatively regulates LMP2A. Here, it is demonstrated that silencing of LMP2B in EBV-harbouring Burkitt's lymphoma Akata cells results in reduced expression of EBV immediate-early lytic BZLF1 gene mRNA and late lytic gp350/220 protein upon BCR cross-linking. Similarly, reduction of lytic EBV activation was observed in Akata cells overexpressing LMP2A. In contrast, silencing of LMP2A expression resulted in higher lytic EBV mRNA and protein expression in BCR cross-linked Akata cells. These observations indicate a role for LMP2B distinct from that of LMP2A in regulation of lytic EBV activation in the host cell and support the hypothesis that LMP2B exhibits a negative-regulatory effect on the ability of LMP2A to maintain EBV latency by preventing the switch to lytic replication.
Type of Medium:
Online Resource
ISSN:
0022-1317
,
1465-2099
DOI:
10.1099/vir.0.82790-0
Language:
English
Publisher:
Microbiology Society
Publication Date:
2007
detail.hit.zdb_id:
2007065-2
SSG:
12
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