Role of CD26 molecule in the infection of MERS(Middle East respiratory syndrome) virus and development of new therapy

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670486
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Infectious disease medicine
• Research Institution: Juntendo University
• Principal Investigator: MORIMOTO CHIKAO 順天堂大学, 医学(系)研究科(研究院), 客員教授 (30119028)
• Co-Investigator(Kenkyū-buntansha): IWATA Satoshi 順天堂大学, 医学部, 非常勤講師 (00396871) ; OHNUMA Kei 順天堂大学, 医学部, 准教授 (10396872)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: MERS感染症 / コロナウイルス / CD26/DPPⅣ / 重症呼吸器感染症 / ヒト化CD26抗体 / CD26単クローン抗体 / アポトーシス / エピトープ

Outline of Final Research Achievements

We identified the domains of CD26 involved in the binding of Middle East respiratory syndrome coronavirus using distinct clones of anti-CD26 monoclonal antibodies (MAbs). One clone, named 2F9, almost completely inhibited viral entry. The humanized anti-CD26 MAb also significantly inhibited infection. These findings indicate that both 2F9 and humanized Mab are potential therapeutic agents for MERS infection.
MERS infects human bronchial epithelial Calu-3 cells as well as CD26 Jurkat T lymphocyte cells. Unlike severe acute respiratory syndrome (SARS)-CoV, which exclusively infects and releases through the apical route, this virus can do so through either side of polarized Calu-3 cells. Infection results in profound apoptosis irrespective of its production of titers that are lower than those of SARS-CoV. Together, our results provide new insights into the dissemination and pathogenesis of MERS-CoV and may cause in immune defects since it infected in human CD26 T cells.

Free Research Field

医歯薬学