The uncoating of EV71 in mature late endosomes requires CD-M6PR.

Seii Ohka, Soon Hao Tan, Eri Ishiyama, Katsutoshi Ogasawara, Tomohito Hanasaka, Kinji Ishida, Kyoji Hagiwara, Chia-Chyi Liu, Pele Choi-Sing Chong, Ken-Ichi Hanaki, Giampietro Schiavo

Biology open 2022 Sep 15

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Enterovirus 71 (EV71) is one of the causative agents of hand-foot-and-mouth disease, which in some circumstances could lead to severe neurological diseases. Despite of its importance for human health, little is known about the early stages of EV71 infection. EV71 starts uncoating with its receptor, human scavenger receptor B2 (hSCARB2), at low pH. We show that EV71 was not targeted to lysosomes in human rhabdomyosarcoma cells overexpressing hSCARB2 and that the autophagic pathway is not essential for EV71 productive uncoating. Instead, EV71 was efficiently uncoated 30 min after infection in late endosomes (LEs) containing hSCARB2, mannose-6-phosphate receptor (M6PR), RAB9, bis(monoacylglycero)phosphate and lysosomal associated membrane protein 2 (LAMP2). Furthering the notion that mature LEs are crucial for EV71 uncoating, cation-dependent (CD)-M6PR knockdown impairs EV71 infection. Since hSCARB2 interacts with cation-independent (CI)-M6PR through M6P-binding sites and CD-M6PR also harbor a M6P-binding site, CD-M6PR is likely to play important roles in EV71 uncoating in LEs. © 2022. Published by The Company of Biologists Ltd.

Citation

Seii Ohka, Soon Hao Tan, Eri Ishiyama, Katsutoshi Ogasawara, Tomohito Hanasaka, Kinji Ishida, Kyoji Hagiwara, Chia-Chyi Liu, Pele Choi-Sing Chong, Ken-Ichi Hanaki, Giampietro Schiavo. The uncoating of EV71 in mature late endosomes requires CD-M6PR. Biology open. 2022 Sep 15;11(9)