Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Tanta University, Tanta, Egypt. Electronic address: https://scholar.google.com/citations?user=9zbm6t4AAAAJ&hl=ar.
Faculty of Medicine, Tanta University, Tanta, Egypt.
J Mol Graph Model. 2021 Jun;105:107836. doi: 10.1016/j.jmgm.2021.107836. Epub 2021 Feb 4.
Autoimmune response after the infection of SARS-COV-2 is evident as more cases of Guillain Barre syndrome and Kawasaki disease are diagnosed. In this study, we aim to investigate a possible mechanism of autoimmune lung injury.
We extracted the peptide sequences of surface proteins of the SARS-COV-2 from the NCBI data protein. We used Blastp to assess the homologous sequences between the human proteins in the UNIPROT database that are associated with respiratory distress. Then, we filtered the homologous sequences to those selectively expressed in the lung and homologous to surface viral proteins. We then assessed the epitope sequences for MHC-I and MHC-II using recommended settings and reference MHC in the IEDB database.
Homeobox protein 2.1 (NKX2-1) and ATP-binding cassette sub-family A member 3 (ABCA3) showed homologous sequence to both surface glycoproteins and envelope proteins. The HLA-DR and HLA-DQ had a similar binding pattern to ABCA3 as surface glycoproteins and envelope proteins, respectively. Other HLA molecules that had a similar binding pattern to SARS-COV-2 as human proteins were HLA-A and HLA-DP.
Our study indicates that there is a possible autoimmune mechanism underlying the acute respiratory distress syndrome in SARS-COV-2.
SARS-CoV-2 感染后会发生自身免疫反应，越来越多的格林-巴利综合征和川崎病病例被诊断出来。在这项研究中，我们旨在研究一种潜在的自身免疫性肺损伤机制。
我们从 NCBI 蛋白质数据库中提取了 SARS-CoV-2 表面蛋白的肽序列。我们使用 Blastp 评估了与呼吸窘迫相关的 UNIPROT 数据库中人类蛋白质之间的同源序列。然后，我们筛选出与表面病毒蛋白选择性表达且同源的同源序列。然后，我们使用 IEDB 数据库中推荐的设置和参考 MHC 来评估 MHC-I 和 MHC-II 的表位序列。
Homeobox protein 2.1 (NKX2-1) 和 ATP-binding cassette sub-family A member 3 (ABCA3) 与表面糖蛋白和包膜蛋白均显示出同源序列。HLA-DR 和 HLA-DQ 与 ABCA3 的结合模式与表面糖蛋白和包膜蛋白分别相似。其他与 SARS-CoV-2 具有相似结合模式的 HLA 分子是 HLA-A 和 HLA-DP。
我们的研究表明，SARS-CoV-2 急性呼吸窘迫综合征可能存在自身免疫机制。
