SNX27-mediated endocytic recycling of GLUT1 is suppressed by SARS-CoV-2 spike, possibly explaining neuromuscular disorders in patients with COVID-19 - 06/09/22
Doi : 10.1016/j.jinf.2022.06.021
Yongwen Ren a, b, c, 1, Yihan Liu a, b, c, 1, Zhiwen Zhang b, c, Yuwen Liu b, c, Kangxin Li b, c, Leiliang Zhang a, b, c, ⁎ 
a Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China
b Department of Pathogen Biology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China
c Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China
⁎Corresponding author at: Department of Pathogen Biology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.Department of Pathogen Biology, School of Clinical and Basic Medical SciencesShandong First Medical University & Shandong Academy of Medical SciencesJinanShandongChina
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Highlights |
• | SARS-CoV-2 S inhibits the interaction between SNX27 and its cargo GLUT1. |
• | SARS-CoV-2 S disrupts the interaction between SNX27 and retromer component Vps26A. |
• | Endocytic recycling of GLUT1 mediated by SNX27 is suppressed by SARS-CoV-2 S. |
• | GLUT1 deficiency by S could explain neuromuscular disorders in long COVID patients. |
© 2022
Publié par Elsevier Masson SAS.
Vol 85 - N° 4
P. e116-e118 - octobre 2022 Retour au numéro
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