Peck Kayla M, Cockrell Adam S, Yount Boyd L, Scobey Trevor, Baric Ralph S, Heise Mark T
Department of Biology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.
Genetics, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.
J Virol. 2015 Apr;89(8):4696-9. doi: 10.1128/JVI.03445-14. Epub 2015 Feb 4.
Middle East respiratory syndrome coronavirus (MERS-CoV) utilizes dipeptidyl peptidase 4 (DPP4) as an entry receptor. Mouse DPP4 (mDPP4) does not support MERS-CoV entry; however, changes at positions 288 and 330 can confer permissivity. Position 330 changes the charge and glycosylation state of mDPP4. We show that glycosylation is a major factor impacting DPP4 receptor function. These results provide insight into DPP4 species-specific differences impacting MERS-CoV host range and may inform MERS-CoV mouse model development.
中东呼吸综合征冠状病毒（MERS-CoV）利用二肽基肽酶4（DPP4）作为进入受体。小鼠DPP4（mDPP4）不支持MERS-CoV进入；然而，第288位和第330位的变化可赋予其易感性。第330位改变了mDPP4的电荷和糖基化状态。我们表明，糖基化是影响DPP4受体功能的主要因素。这些结果为影响MERS-CoV宿主范围的DPP4物种特异性差异提供了见解，并可能为MERS-CoV小鼠模型的开发提供参考。
