A Ca2+-dependent signalling circuit regulates influenza A virus internalization and infection

Yoichiro Fujioka, Masumi Tsuda, Asuka Nanbo, Tomoe Hattori, Junko Sasaki, Takehiko Sasaki, Tadaaki Miyazaki and Yusuke Ohba ()
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Yoichiro Fujioka: Hokkaido University Graduate School of Medicine, N15W7, Sapporo 060-8638, Japan
Masumi Tsuda: Hokkaido University Graduate School of Medicine, N15W7, Sapporo 060-8638, Japan
Asuka Nanbo: Hokkaido University Graduate School of Medicine, N15W7, Sapporo 060-8638, Japan
Tomoe Hattori: Hokkaido University Research Centre for Zoonosis Control, N20W10, Sapporo 060-0020, Japan
Junko Sasaki: Akita University Graduate School of Medicine
Takehiko Sasaki: Akita University Graduate School of Medicine
Tadaaki Miyazaki: Hokkaido University Research Centre for Zoonosis Control, N20W10, Sapporo 060-0020, Japan
Yusuke Ohba: Hokkaido University Graduate School of Medicine, N15W7, Sapporo 060-8638, Japan

Nature Communications, 2013, vol. 4, issue 1, 1-13

Abstract: Abstract Various viruses enter host cells via endocytosis, but the molecular mechanisms underlying the specific internalization pathways remain unclear. Here we show that influenza A viruses (IAVs) enter cells via redundant pathways of clathrin-mediated and clathrin-independent endocytosis, with intracellular Ca2+ having a central role in regulation of both pathways by activating a signalling axis comprising RhoA, Rho-kinase, phosphatidylinositol 4-phosphate 5-kinase (PIP5K) and phospholipase C (PLC). IAV infection induces oscillations in the cytosolic Ca2+ concentration of host cells, the prevention of which markedly attenuates virus internalization and infection. The small GTPase RhoA is found both to function downstream of the virus-induced Ca2+ response and itself to induce Ca2+ oscillations in a manner dependent on Rho-kinase and subsequent PIP5K-PLC signalling. This signalling circuit regulates both clathrin-mediated and clathrin-independent endocytosis during virus infection and seems to constitute a key mechanism for regulation of IAV internalization and infection.

Date: 2013
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DOI: 10.1038/ncomms3763

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