Carbon Dots' Antiviral Functions Against Noroviruses.
Carbon Dots' Antiviral Functions Against Noroviruses.
复制标题
DOI：
10.1038/s41598-017-00675-x
复制
发表时间：
2017-03-31
影响因子：
4.6
通讯作者：
Yang L
中科院分区：
文献类型：
--
作者：
Dong X;Moyer MM;Yang F;Sun YP;Yang L
本研究首次评估了碳量子点（CDots）对人类诺如病毒样颗粒（VLP）、GI. 1和GII. 4 VLP的抗病毒活性。合成并评价了具有不同表面钝化分子的CDots，2，2 ′-（乙二氧基）双（乙胺）（EDA）-CDots和3-乙氧基丙胺（EPA）-CDots。结果表明，在5 μg/mL的CDot浓度下，EDA-和EPA-CDot均高度有效地抑制两种VLP菌株与人细胞上的组织血型抗原（HBGA）受体的结合，其中EDA-CDot实现100%抑制，EPA CDot实现85-99%抑制。在低CDot浓度（2 μg/mL）下，带正电荷的EDA-CDot表现出比不带电荷的EPA-CDot（~60%）更高的抑制效果（~82%），表明CDot的表面电荷状态在CDot与带负电荷的VLP之间的相互作用中起作用。这两种类型的CDot也表现出对VLP与其各自抗体结合的抑制作用，但比对HBGA结合的抑制作用小得多。在CDot处理后，VLP保持完整，并且在VLP的衣壳蛋白上没有观察到降解。总之，观察到的CDot对诺如病毒的抗病毒作用主要是通过有效抑制VLP与HBGA受体的结合和适度抑制VLP与其抗体的结合，而不影响病毒衣壳蛋白和病毒颗粒的完整性。
This study reported the first assessment of carbon dots’ (CDots) antiviral activity to human norovirus virus-like-particles (VLPs), GI.1 and GII.4 VLPs. CDots with different surface passivation molecules, 2,2′-(ethylenedioxy)bis(ethylamine) (EDA)-CDots and 3-ethoxypropylamine (EPA)-CDots, were synthesized and evaluated. The results indicated both EDA- and EPA- CDots were highly effective to inhibit both strains of VLPs’ bindings to histo-blood group antigens (HBGA) receptors on human cells at CDots concentration of 5 µg/mL, with EDA-CDots achieving 100% inhibition and EPA CDots achieving 85–99% inhibition. At low CDots concentration (2 µg/mL), positively charged EDA-CDots exhibited higher inhibitory effect (~82%) than non-charged EPA-CDots (~60%), suggesting the surface charge status of CDots played a role in the interactions between CDots and the negatively charged VLPs. Both types of CDots also exhibited inhibitory effect on VLP’s binding to their respective antibodies, but much less effective than those to HBGA binding. After CDots treatments, VLPs remained intact, and no degradation was observed on VLPs’ capsid proteins. Taken together, the observed antiviral effects of CDots on noroviruses were mainly through the effective inhibition of VLPs’ binding to HBGA receptors and moderate inhibition of VLPs’ binding to their antibodies, without affecting the integrity of viral capsid protein and the viral particle.