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APOBEC3G and HIV-1:Strike and Counterstrike.

机译:APOBEC3G和HIV-1:打击和反打击。

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摘要

APOBEC3G (A3G), a deoxycytidine deaminase, is a powerful host antiretroviral factor that can restrict HIV-1 infection. This restriction is counteracted by the HIV-1 virion infectivity factor (Vif) protein, whose activity culminates in depletion of A3G from infected cells. In the absence of Vif, viruses encapsidate A3G, which acts in part to mutate viral DNA formed during reverse transcription upon subsequent infection of a new cell. Cellular A3G also functions as a post-entry restriction factor for HIV in resting CD4 T cells, where it resides in a low molecular mass form. Unfortunately, this barrier is forfeited when CD4 T cells are activated because A3G is recruited into inactive high molecular mass ribonucleoprotein complexes. In addition to restricting HIV, A3G and related deaminases may counter other retroviruses and protect the cell from endogenous mobile retroelements. Understanding A3G complex assembly and its interplay with HIV Vif may make possible future development of a new class of HIV therapeutic agents.
机译:APOBEC3G(A3G)是一种脱氧胞苷脱氨酶,是一种强大的宿主抗逆转录病毒因子,可以限制HIV-1感染。 HIV-1病毒体感染因子(Vif)蛋白抵消了这种限制,该蛋白的活性最终导致被感染细胞中的A3G耗尽。在没有Vif的情况下,病毒会包围A3G,A3G的部分作用是突变随后感染新细胞后在逆转录过程中形成的病毒DNA。细胞A3G还作为静息CD4 T细胞中HIV进入后的限制因子,它以低分子量形式存在。不幸的是,由于A3G被募集到无活性的高分子量核糖核蛋白复合物中,当CD4 T细胞被激活时,这种屏障就消失了。除了限制HIV外,A3G和相关的脱氨酶还可以对抗其他逆转录病毒,并保护细胞免受内源性移动逆转录因子的侵害。了解A3G复杂装配及其与HIV Vif的相互作用可能使新型HIV治疗剂的未来开发成为可能。

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