PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter.

PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter.
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PARP1 通过结合 BZLF1 启动子来限制 Epstein Barr 病毒裂解再激活。

DOI:
10.1016/j.virol.2017.04.006
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发表时间:
2017-07
期刊:
影响因子:
3.7
通讯作者:
Tempera I
Tempera I
中科院分区:
医学3区
文献类型:
--
作者:
Lupey-Green LN;Moquin SA;Martin KA;McDevitt SM;Hulse M;Caruso LB;Pomerantz RT;Miranda JL;Tempera I

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The Epstein Barr virus (EBV) genome persists in infected host cells as a chromatinized episome and is subject to chromatin-mediated regulation. Binding of the host insulator protein CTCF to the EBV genome has an established role in maintaining viral latency type, and in other herpesviruses, loss of CTCF binding at specific regions correlates with viral reactivation. Here, we demonstrate that binding of PARP1, an important cofactor of CTCF, at the BZLF1 lytic switch promoter restricts EBV reactivation. Knockdown of PARP1 in the Akata-EBV cell line significantly increases viral copy number and lytic protein expression. Interestingly, CTCF knockdown has no effect on viral reactivation, and CTCF binding across the EBV genome is largely unchanged following reactivation. Moreover, EBV reactivation attenuates PARP activity, and Zta expression alone is sufficient to decrease PARP activity. Here we demonstrate a restrictive function of PARP1 in EBV lytic reactivation.
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