The Susceptibility of Primate Lentiviruses to Nucleosides and Vpx during Infection of Dendritic Cells Is Regulated by CA
The Susceptibility of Primate Lentiviruses to Nucleosides and Vpx during Infection of Dendritic Cells Is Regulated by CA
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DOI：
10.1128/jvi.03315-14
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发表时间：
2015-04-01
影响因子：
5.4
通讯作者：
Cimarelli, Andrea
中科院分区：
文献类型：
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作者：
Barateau, Veronique;Xuan-Nhi Nguyen;Cimarelli, Andrea
阻断人类免疫缺陷病毒1型（HIV-1）对树突状细胞（DC）的感染可以通过Vpx（病毒蛋白X）来缓解，Vpx降解无菌α基序-羟化酶结构域1（SAMHD 1）或通过外源添加的脱氧核苷（dNs）来缓解，从而支持SAMHD 1通过限制脱氧核苷三磷酸（dNTPs）起作用的假设。然而，这一概念受到质疑。我们发现，虽然dNs和Vpx增加了HIV-1的感染性，只有后者恢复了猕猴变异的猴免疫缺陷病毒SIVMAC Delta Vpx病毒的感染性。这种独特的行为似乎映射到CA，表明物种特异性CA相互作用调节DC的感染。
The block toward human immunodeficiency virus type 1 (HIV-1) infection of dendritic cells (DCs) can be relieved by Vpx (viral protein X), which degrades sterile alpha motif-hydroxylase domain 1 (SAMHD1) or by exogenously added deoxynucleosides (dNs), lending support to the hypothesis that SAMHD1 acts by limiting deoxynucleoside triphosphates (dNTPs). This notion has, however, been questioned. We show that while dNs and Vpx increase the infectivity of HIV-1, only the latter restores the infectivity of a simian immunodeficiency virus of macaques variant, SIVMAC Delta Vpx virus. This distinct behavior seems to map to CA, suggesting that species-specific CA interactors modulate infection of DCs.