The mechanism of influenza virus internalization into host cells via calcium signaling-mediated endocytosis

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860254
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Experimental pathology
• Research Institution: Hokkaido University
• Principal Investigator: Fujioka Yoichiro 北海道大学, 医学(系)研究科(研究院), 助教 (70597492)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: エンドサイトーシス / インフルエンザウイルス / イメージング / シグナル伝達

Outline of Final Research Achievements

We have reported that Ras-PI3K signaling mediates endocytosis, and influenza viruses exploit this pathway to expedite their efficient incorporation into cells. Moreover, calcium signaling, triggered by the viruses, has been identified as an upstream regulator of Ras-PI3K signaling. In this study, we explored in detail the mechanism by which calcium signaling is activated upon the viral infection. First, we performed high-speed imaging experiments with fluorescently labeled virus particles to gain further insight into the spatiotemporal dynamics of Ca2+ responses upon virus entry. Immediately after infection, localized and modest Ca2+ elevations, prior to the aforementioned robust Ca2+ release from endoplasmic reticulum, were detected in the regions where the labeled particles were adsorbed. Moreover, we identified the membrane protein, which is involved in the Ca2+ elevation by the viruses.

Free Research Field

細胞生物学