Title: | A Sialylated Voltage-Dependent Ca2+ Channel Binds Hemagglutinin and Mediates Influenza A Virus Entry into Mammalian Cells |
Authors: | Fujioka, Yoichiro Browse this author |
Nishide, Shinya Browse this author →KAKEN DB |
Ose, Toyoyuki Browse this author →KAKEN DB |
Suzuki, Tadaki Browse this author →KAKEN DB |
Kato, Izumi Browse this author |
Fukuhara, Hideo Browse this author |
Fujioka, Mari Browse this author |
Horiuchi, Kosui Browse this author |
Satoh, Aya O. Browse this author |
Nepal, Prabha Browse this author |
Kashiwagi, Sayaka Browse this author |
Wang, Jing Browse this author |
Horiguchi, Mika Browse this author |
Sato, Yuko Browse this author |
Paudel, Sarad Browse this author |
Nanbo, Asuka Browse this author →KAKEN DB |
Miyazaki, Tadaaki Browse this author →KAKEN DB |
Hasegawa, Hideki Browse this author |
Maenaka, Katsumi Browse this author →KAKEN DB |
Ohba, Yusuke Browse this author →KAKEN DB |
Keywords: | influenza A virus |
virus entry |
calcium ion |
calcium channel |
calcium channel blockers |
hemagglutinin |
sialylation |
virus-host cell interaction |
Issue Date: | 13-Jun-2018 |
Publisher: | Cell Press |
Journal Title: | Cell host & microbe |
Volume: | 23 |
Issue: | 6 |
Start Page: | 809 |
End Page: | 818 |
Publisher DOI: | 10.1016/j.chom.2018.04.015 |
Abstract: | Influenza A virus (IAV) infection is initiated by the attachment of the viral glycoprotein hemagglutinin (HA) to sialic acid on the host cell surface. However, the sialic acid-containing receptor crucial for IAV infection has remained unidentified. Here, we show that HA binds to the voltage-dependent Ca2+ channel Cav1.2 to trigger intracellular Ca2+ oscillations and subsequent IAV entry and replication. IAV entry was inhibited by Ca2+ channel blockers (CCBs) or by knockdown of Cav1.2. The CCB diltiazem also inhibited virus replication in vivo. Reintroduction of wild-type but not the glycosylation-deficient mutants of Cav1.2 restored Ca2+ oscillations and virus infection in Cav1.2-depleted cells, demonstrating the significance of Cav1.2 sialylation. Taken together, we identify Cav1.2 as a sialylated host cell surface receptor that binds HA and is critical for IAV entry. |
Rights: | © 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ |
http://creativecommons.org/licenses/by-nc-nd/4.0/ |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/74619 |
Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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