Glycosylation of Mouse DPP4 Plays a Role in Inhibiting Middle East Respiratory Syndrome Coronavirus Infection

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  • Peck, Kayla M.
    • Affiliation: University of North Carolina at Chapel Hill
    • Other Affiliation: Biology Department
  • Cockrell, Adam S.
    • Affiliation: University of North Carolina at Chapel Hill
    • Other Affiliation: Department of Genetics
  • Yount, Boyd L.
    • Affiliation: University of North Carolina at Chapel Hill
    • Other Affiliation: Department of Epidemiology
  • Scobey, Trevor
    • Affiliation: University of North Carolina at Chapel Hill
    • Other Affiliation: Department of Epidemiology
  • Baric, Ralph S.
    • Affiliation: University of North Carolina at Chapel Hill
    • Other Affiliation: Departments of Microbiology and Immunology
  • Heise, Mark T.
    • Affiliation: University of North Carolina at Chapel Hill
    • Other Affiliation: Departments of Genetics and Microbiology and Immunology
Abstract
  • 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.
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  • Article
Rights statement
  • In Copyright
Journal title
  • Journal of Virology
Journal volume
  • 89
Journal issue
  • 8
Page start
  • 4696
Page end
  • 4699
Language
  • English
ISSN
  • 1098-5514
  • 1070-6321
  • 0022-538X
Location
  • Chapel Hill, North Carolina, United States
Publisher
  • American Society for Microbiology

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