Implication of TRIM alpha and TRIMCyp in interferon-induced anti-retroviral restriction activities.
Implication of TRIM alpha and TRIMCyp in interferon-induced anti-retroviral restriction activities.
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DOI：
10.1186/1742-4690-5-59
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发表时间：
2008-07-09
期刊：
影响因子：
3.3
通讯作者：
Nisole S
中科院分区：
文献类型：
--
作者：
Carthagena L;Parise MC;Ringeard M;Chelbi-Alix MK;Hazan U;Nisole S
TRIM5α是一种限制因子，在灵长类细胞中以物种特异性的方式干扰逆转录病毒感染。尽管TRIM5α是结构性表达的，但它的表达被证明是由I型干扰素上调的。在灵长类动物中，猫头鹰猴子细胞中存在一个特殊的病例，这种细胞表达TRIM5和亲环素A之间的融合蛋白，即TRIMCyp，专门干扰HIV-1感染。到目前为止，还没有关于干扰素可能诱导TrIMCyp的研究。我们研究了干扰素治疗对不同灵长类细胞中逆转录病毒限制的影响，并评估了TRIM5、α或TRIMCyp在干扰素诱导的抗逆转录病毒活性中的意义。首先，我们发现人I型干扰素可以增强人、非洲绿猴和猕猴细胞中TRIM5α的表达，以及在OWL猴细胞中TRIMCyp的表达。在表达α的灵长类细胞系中，I型干扰素对HIV-1感染几乎没有影响，而在人和非洲绿猴细胞中对N-MLV具有很强的抑制活性。相比之下，OWL猴细胞经I型干扰素处理后，对HIV-1的限制性大大增强，对MLV的非嗜毒性限制性也显著增强。我们证明了α是干扰素诱导的人和非洲绿猴细胞中抗N-MLV活性的主要介体，而TRIMCyp则介导了干扰素诱导的猫头鹰细胞中HIV-1的限制性增强。相反，I型干扰素在OWL猴细胞中诱导的抗MLV限制不依赖于TRIMCyp的表达。总之，我们的观察表明，TRIM5α和TRIMCyp都参与了干扰素诱导的灵长类细胞的抗逆转录病毒反应。此外，我们还发现，I型干扰素在猫头鹰猴细胞中也诱导了对MLV的TRIMCyp不依赖的限制活性。
TRIM5α is a restriction factor that interferes with retroviral infections in a species-specific manner in primate cells. Although TRIM5α is constitutively expressed, its expression has been shown to be up-regulated by type I interferon (IFN). Among primates, a particular case exists in owl monkey cells, which express a fusion protein between TRIM5 and cyclophilin A, TRIMCyp, specifically interfering with HIV-1 infection. No studies have been conducted so far concerning the possible induction of TRIMCyp by IFN. We investigated the consequences of IFN treatment on retroviral restriction in diverse primate cells and evaluated the implication of TRIM5α or TRIMCyp in IFN-induced anti-retroviral activities. First, we show that human type I IFN can enhance TRIM5α expression in human, African green monkey and macaque cells, as well as TRIMCyp expression in owl monkey cells. In TRIM5α-expressing primate cell lines, type I IFN has little or no effect on HIV-1 infection, whereas it potentates restriction activity against N-MLV in human and African green monkey cells. In contrast, type I IFN treatment of owl monkey cells induces a great enhancement of HIV-1 restriction, as well as a strain-tropism independent restriction of MLV. We were able to demonstrate that TRIM5α is the main mediator of the IFN-induced activity against N-MLV in human and African green monkey cells, whereas TRIMCyp mediates the IFN-induced HIV-1 restriction enhancement in owl monkey cells. In contrast, the type I IFN-induced anti-MLV restriction in owl monkey cells is independent of TRIMCyp expression. Together, our observations indicate that both TRIM5α and TRIMCyp are implicated in IFN-induced anti-retroviral response in primate cells. Furthermore, we found that type I IFN also induces a TRIMCyp-independent restriction activity specific to MLV in owl monkey cells.
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影响因子：
3.3
作者：
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通讯作者：
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影响因子：
6.7
作者：
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DOI：
10.1073/pnas.0403364101
发表时间：
2004-08-10
影响因子：
11.1
作者：
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