Plasmalemmal vesicle associated protein (PV1) modulates SV40 virus infectivity in CV-1 cells.

Plasmalemmal vesicle associated protein (PV1) modulates SV40 virus infectivity in CV-1 cells.
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DOI:
10.1016/j.bbrc.2011.07.063
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发表时间:
2011-08-26
影响因子:
3.1
通讯作者:
Stan, Radu V.
Stan, Radu V.
中科院分区:
生物学4区
文献类型:
--
作者:
Tse, Dan;Armstrong, David A.;Oppenheim, Ariella;Kuksin, Dmitry;Norkin, Leonard;Stan, Radu V.

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质膜小泡相关蛋白(Plvap/PV 1)是气孔膜形成所必需的结构蛋白。小窝是与SV 40病毒进入灵长类细胞有关的质膜内陷。在这里,我们表明,在CV-1绿色猴上皮细胞中的从头Plvap/PV 1表达显着降低了SV 40病毒建立生产性感染的能力,当细胞与低浓度的病毒孵育。然而,在存在高病毒滴度的情况下,PV 1对SV 40病毒感染性没有影响。从机制上讲,PV 1表达不会降低已知的SV 40受体如GM 1神经节苷脂和MHC I类蛋白的细胞表面表达。此外,PV 1不减少由SV 40 VP 1蛋白产生的病毒样颗粒与CV-1细胞表面的结合,并且当细胞与高或低VLP浓度孵育时不影响它们的内化。这些结果表明,PV 1蛋白能够阻断SV 40感染性在低,但不是在高病毒浓度,通过干扰感染性内化途径在细胞表面或在后内化步骤。
Plasmalemmal vesicle associated protein (Plvap/PV1) is a structural protein required for the formation of the stomatal diaphragms of caveolae. Caveolae are plasma membrane invaginations that were implicated in SV40 virus entry in primate cells. Here we show that de novo Plvap/PV1 expression in CV-1 green monkey epithelial cells significantly reduces the ability of SV40 virus to establish productive infection, when cells are incubated with low concentrations of the virus. However, in presence of high viral titers PV1 has no effect on SV40 virus infectivity. Mechanistically, PV1 expression does not reduce the cell surface expression of known SV40 receptors such as GM1 ganglioside and MHC class I proteins. Furthermore, PV1 does not reduce the binding of virus-like particles made by SV40 VP1 protein to the CV-1 cell surface and does not impact their internalization when cells are incubated with either high or low VLP concentrations. These results suggest that PV1 protein is able to block SV40 infectivity at low but not at high viral concentration either by interfering with the infective internalization pathway at the cell surface or at a post internalization step.
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