Barateau Véronique, Nguyen Xuan-Nhi, Bourguillault Fanny, Berger Grégory, Cordeil Stéphanie, Cimarelli Andrea
Centre International de Recherche en Infectiologie (CIRI), Lyon, France INSERM, U1111, Lyon, France Ecole Normale Supérieure de Lyon, Lyon, France CNRS, UMR5308, Lyon, France University of Lyon, Lyon I, UMS3444/US8 BioSciences Gerland, Lyon, France.
Centre International de Recherche en Infectiologie (CIRI), Lyon, France INSERM, U1111, Lyon, France Ecole Normale Supérieure de Lyon, Lyon, France CNRS, UMR5308, Lyon, France University of Lyon, Lyon I, UMS3444/US8 BioSciences Gerland, Lyon, France
J Virol. 2015 Apr;89(7):4030-4. doi: 10.1128/JVI.03315-14. Epub 2015 Jan 21.
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, SIVMACΔVpx virus. This distinct behavior seems to map to CA, suggesting that species-specific CA interactors modulate infection of DCs.
树突状细胞（DCs）对1型人类免疫缺陷病毒（HIV-1）感染的阻滞可通过Vpx（病毒蛋白X，其可降解无菌α基序-羟化酶结构域1，即SAMHD1）或外源性添加的脱氧核苷（dNs）来解除，这支持了SAMHD1通过限制三磷酸脱氧核苷（dNTPs）发挥作用的假说。然而，这一观点受到了质疑。我们发现，虽然dNs和Vpx可增加HIV-1的感染性，但只有后者能恢复猕猴猿免疫缺陷病毒变体SIVMACΔVpx病毒的感染性。这种不同的行为似乎与衣壳蛋白（CA）有关，表明物种特异性的CA相互作用分子可调节DCs的感染。
