Sun Shipeng, Wang Tao, Pang Bo, Wei Huamin, Liu Guijian
Clinical Laboratories, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, No. 5 Bei Xian Ge St., Xi Cheng District, Beijing, 100053, People's Republic of China,
Theory Biosci. 2014 Jun;133(2):79-89. doi: 10.1007/s12064-013-0196-1. Epub 2013 Dec 22.
Molecular mimicry and arthritogenic peptides form the basis of hypotheses that attempt to explain the pathogenesis of HLA-B27-positive ankylosing spondylitis (AS). We propose, therefore, that certain human viruses may possess peptide sequences that mimic HLA-B27-binding human 'self' peptides which might induce or play a significant role in AS. In the present study, we performed bioinformatic analysis, using BLASTP, of the human virus proteome and HLA-B27-binding human 'self' peptides including peptides derived from arthritogenic sequences. We identified that some HLA-B27-binding peptides, particularly those present in proteins of the cartilage and bone, are highly similar to those present in viruses known to cause chronic infection. We suggest that the identical short amino acid sequences shared between human viruses and HLA-B27 peptides may play a role in the pathogenesis of AS.
分子模拟和致关节炎肽构成了试图解释 HLA - B27 阳性强直性脊柱炎(AS)发病机制的假说基础。因此,我们提出某些人类病毒可能拥有与 HLA - B27 结合的人类“自身”肽序列相似的肽序列,这些序列可能在 AS 中诱发或起重要作用。在本研究中,我们使用 BLASTP 对人类病毒蛋白质组和 HLA - B27 结合的人类“自身”肽(包括源自致关节炎序列的肽)进行了生物信息学分析。我们发现一些 HLA - B27 结合肽,特别是那些存在于软骨和骨蛋白质中的肽,与已知会引起慢性感染的病毒中的肽高度相似。我们认为人类病毒和 HLA - B27 肽之间共享的相同短氨基酸序列可能在 AS 的发病机制中起作用。