La Colombe Health Center, Fokoue P.O. Box 02, Cameroon.
Molecules. 2022 Mar 17;27(6):1947. doi: 10.3390/molecules27061947.
This article discusses the importance of D-xylose for fighting viruses (especially SARS-CoV-2) that use core proteins as receptors at the cell surface, by providing additional supporting facts that these viruses probably bind at HS/CS attachment sites (i.e., the hydroxyl groups of Ser/Thr residues of the core proteins intended to receive the D-xylose molecules to initiate the HS/CS chains). Essentially, the additional supporting facts, are: some anterior studies on the binding sites of exogenous heparin and soluble HS on the core proteins, the inhibition of the viral entry by pre-incubation of cells with heparin, and additionally, corroborating studies about the mechanism leading to type 2 diabetes during viral infection. We then discuss the mechanism by which serine protease inhibitors inhibit SARS-CoV-2 entry. The biosynthesis of heparan sulfate (HS), chondroitin sulfate (CS), dermatan sulfate (DS), and heparin (Hep) is initiated not only by D-xylose derived from uridine diphosphate (UDP)-xylose, but also bioactive D-xylose molecules, even in situations where cells were previously treated with GAG inhibitors. This property of D-xylose shown by previous anterior studies helped in the explanation of the mechanism leading to type 2 diabetes during SARS-CoV-2 infection. This explanation is completed here by a preliminary estimation of xyloside GAGs (HS/CS/DS/Hep) in the body, and with other previous studies helping to corroborate the mechanism by which the D-xylose exhibits its antiglycaemic properties and the mechanism leading to type 2 diabetes during SARS-CoV-2 infection. This paper also discusses the confirmatory studies of regarding the correlation between D-xylose and COVID-19 severity.
本文讨论了 D-木糖在与核心蛋白作为细胞表面受体的病毒（尤其是 SARS-CoV-2）作斗争中的重要性，提供了额外的支持性事实，表明这些病毒可能结合在 HS/CS 附着位点上（即，核心蛋白中 Ser/Thr 残基的羟基，旨在接收 D-木糖分子以启动 HS/CS 链）。从本质上讲，额外的支持性事实是：一些关于外源性肝素和可溶性 HS 与核心蛋白结合位点的前期研究，细胞与肝素预孵育可抑制病毒进入，此外，还有关于病毒感染期间导致 2 型糖尿病的机制的佐证研究。然后，我们讨论了丝氨酸蛋白酶抑制剂抑制 SARS-CoV-2 进入的机制。肝素硫酸盐 (HS)、软骨素硫酸盐 (CS)、硫酸皮肤素 (DS) 和肝素 (Hep) 的生物合成不仅由来自尿苷二磷酸 (UDP)-木糖的 D-木糖启动，而且还由生物活性 D-木糖分子启动，即使在细胞先前用 GAG 抑制剂处理的情况下也是如此。先前的前期研究表明 D-木糖具有这种性质，有助于解释 SARS-CoV-2 感染期间导致 2 型糖尿病的机制。通过对体内木糖苷 GAG（HS/CS/DS/Hep）的初步估计以及其他先前的研究，有助于证实 D-木糖发挥其抗高血糖特性和 SARS-CoV-2 感染期间导致 2 型糖尿病的机制。本文还讨论了关于 D-木糖与 COVID-19 严重程度之间相关性的确认性研究。
