Ixilka Biotech S.L, Bizkaia, Spain.
Ixilka Biotech S.L, Bizkaia, Spain.
Biomed J. 2024 Jun;47(3):100650. doi: 10.1016/j.bj.2023.100650. Epub 2023 Aug 19.
Epigenetics and clinical observations referring to Betacoronavirus lead to the conjecture that Sarbecovirus may have the ability to infect lymphocytes using a different way than the spike protein. In addition to inducing the death of lymphocytes, thus drastically reducing their population and causing a serious immune deficiency, allows it to remain hidden for long periods of latency using them as a viral reservoir in what is named Long-Covid Disease. Exploring possibilities, the hypothesis is focused on that N protein may be the key of infecting lymphocytes.
The present article exhibits a computational assay for the latest complete sequences reported to GISAID, correlating N genotypes with an enhancement in the affinity of the complex that causes immune deficiency in order to determine a good docking with the N protein and some receptors in lymphocytes.
A novel high-interaction coupling of N-RBD and CD147 is presented as the main way of infecting lymphocytes, allowing to define those genotypes involved in their affinity enhancement.
The hypothesis is consistent with the mutagenic deriving observed on the in-silico assay, which reveals that genotypes N/120 and N/152 are determinant to reduce the Immune Response of the host infecting lymphocytes, allowing the virus persists indefinitely and causing an Acquire Immune Deficiency Syndrome.
表观遗传学和针对β冠状病毒的临床观察促使人们推测，沙贝科病毒可能具有使用不同于刺突蛋白的方式感染淋巴细胞的能力。除了诱导淋巴细胞死亡，从而大幅减少其数量并导致严重的免疫缺陷外，它还可以利用它们作为潜伏期间的病毒储库，即所谓的长新冠疾病，从而长时间保持隐藏状态。为了探索这种可能性，该假说集中在 N 蛋白可能是感染淋巴细胞的关键。
本文展示了针对 GISAID 报告的最新完整序列的计算分析，将 N 基因型与导致免疫缺陷的复合物的亲和力增强相关联，以确定与 N 蛋白和淋巴细胞中的某些受体的良好对接。
提出了一种 N-RBD 和 CD147 的新型高相互作用偶联作为感染淋巴细胞的主要方式，从而能够确定那些参与其亲和力增强的基因型。
该假说与在计算机模拟分析中观察到的诱变结果一致，该结果表明，N/120 和 N/152 基因型是决定感染淋巴细胞的宿主免疫反应降低的决定因素，允许病毒无限期持续存在并导致获得性免疫缺陷综合征。
