{"title":"获得性免疫缺陷综合症与 SARS-CoV-2 N 基因型的相关性。","authors":"","doi":"10.1016/j.bj.2023.100650","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>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.</p></div><div><h3>Method</h3><p>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.</p></div><div><h3>Results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>","PeriodicalId":8934,"journal":{"name":"Biomedical Journal","volume":"47 3","pages":"Article 100650"},"PeriodicalIF":4.1000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2319417023000872/pdfft?md5=1edaaac170d38d8c21d14f03478af8b3&pid=1-s2.0-S2319417023000872-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes\",\"authors\":\"\",\"doi\":\"10.1016/j.bj.2023.100650\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>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.</p></div><div><h3>Method</h3><p>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.</p></div><div><h3>Results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>\",\"PeriodicalId\":8934,\"journal\":{\"name\":\"Biomedical Journal\",\"volume\":\"47 3\",\"pages\":\"Article 100650\"},\"PeriodicalIF\":4.1000,\"publicationDate\":\"2024-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2319417023000872/pdfft?md5=1edaaac170d38d8c21d14f03478af8b3&pid=1-s2.0-S2319417023000872-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biomedical Journal\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2319417023000872\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical Journal","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2319417023000872","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
背景:根据表观遗传学和对 Betacoronavirus 的临床观察,我们推测 Sarbecovirus 可能有能力以不同于尖峰蛋白的方式感染淋巴细胞。除了诱导淋巴细胞死亡,从而使淋巴细胞数量急剧下降并导致严重的免疫缺陷外,它还能利用淋巴细胞作为病毒库长期潜伏,这就是所谓的 "长病毒病"。在探索各种可能性的过程中,假设的重点是 N 蛋白可能是感染淋巴细胞的关键:本文展示了对 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亲和力增强联系起来,以确定 N 蛋白与淋巴细胞中某些受体的良好对接:结果:N-RBD和CD147的新型高相互作用耦合被认为是感染淋巴细胞的主要方式,从而确定了参与亲和力增强的基因型:结论:该假说与在微观分析中观察到的诱变衍生一致,揭示了基因型 N/120 和 N/152 是降低宿主感染淋巴细胞免疫反应的决定性因素,从而使病毒无限期存在并导致获得性免疫缺陷综合症。
Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes
Background
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.
Method
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.
Results
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.
Conclusion
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.
期刊介绍:
Biomedical Journal publishes 6 peer-reviewed issues per year in all fields of clinical and biomedical sciences for an internationally diverse authorship. Unlike most open access journals, which are free to readers but not authors, Biomedical Journal does not charge for subscription, submission, processing or publication of manuscripts, nor for color reproduction of photographs.
Clinical studies, accounts of clinical trials, biomarker studies, and characterization of human pathogens are within the scope of the journal, as well as basic studies in model species such as Escherichia coli, Caenorhabditis elegans, Drosophila melanogaster, and Mus musculus revealing the function of molecules, cells, and tissues relevant for human health. However, articles on other species can be published if they contribute to our understanding of basic mechanisms of biology.
A highly-cited international editorial board assures timely publication of manuscripts. Reviews on recent progress in biomedical sciences are commissioned by the editors.