Role of the vaccinia virus E3L and K3L gene products in rescue of VSV and EMCV from the effects of IFN-alpha.

Role of the vaccinia virus E3L and K3L gene products in rescue of VSV and EMCV from the effects of IFN-alpha.
复制标题

痘苗病毒 E3L 和 K3L 基因产物在拯救 VSV 和 EMCV 免受 IFN-α 影响中的作用。

DOI:
10.1089/jir.1998.18.721
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发表时间:
1998
期刊:
Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research.
影响因子:
--
通讯作者:
Jacobs,BL
Jacobs,BL
中科院分区:
--
文献类型:
--
作者:
Shors,ST;Beattie,E;Paoletti,E;Tartaglia,J;Jacobs,BL

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相似文献

牛痘病毒 (VV) 已被证明对干扰素-α (IFN-α) 的抗病毒作用具有相对抵抗力,并且可以从 IFN 的抗病毒作用中拯救 IFN 敏感病毒的复制,例如脑心肌炎病毒 (EMCV) 和水泡性口炎病毒 (VSV)。 E3L 和 K3L 基因产物与 VV 的 IFN 抗性有关。我们研究了这些 VV 编码功能在拯救 VSV 和 EMCV 免受 IFN 影响中所发挥的作用。 E3L开放阅读框(ORF)的瞬时表达足以将VSV从IFN诱导的抗病毒状态中拯救出来,但不能拯救EMCV。 E3L 突变体对 VSV 的拯救与突变 E3L 基因产物结合 dsRNA 的能力相关。相反,K3L ORF 的瞬时表达足以部分拯救 EMCV,但不能拯救 VSV 免受 IFN 的影响。删除 K3L 或 E3L ORF 的 VV 的结果与通过这些基因瞬时表达获得的结果一致。这些结果表明,VV E3L 基因产物可能负责 VV 介导的 VSV 免受 IFN 影响的拯救,而 K3L 基因产物可能至少部分负责 EMCV 的拯救。
Vaccinia virus (VV) has been shown to be relatively resistant to the antiviral effects of interferon-α (IFN-α) and to rescue replication of IFN-sensitive viruses, such as encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV), from the antiviral effects of IFN. The E3L and K3L gene products have been implicated in the IFN resistance of VV. We have investigated the role that these VV-encoded functions play in the rescue of VSV and EMCV from the effects of IFN. Transient expression of the E3L open reading frame (ORF) was sufficient to rescue VSV but not EMCV from the IFN-induced antiviral state. Rescue of VSV by mutants of E3L correlated with the ability of the mutated E3L gene products to bind dsRNA. Conversely, transient expression of the K3L ORF was sufficient to partially rescue EMCV but not VSV from the effects of IFN. Results with VV deleted of either the K3L or E3L ORFs were consistent with results obtained by transient expression of these genes. These results demonstrate that the VV E3L gene products are likely responsible for the VV-mediated rescue of VSV from the effects of IFN and the K3L gene product is likely at least partly responsible for rescue of EMCV.