Further analysis of phosphorylationin events in herpes simplex virus infection

2017 Fiscal Year Final Research Report

• Project/Area Number: 26460548
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Virology
• Research Institution: The University of Tokyo
• Principal Investigator: Akihisa Kato 東京大学, 医科学研究所, 助教 (40581187)
• Co-Investigator(Kenkyū-buntansha): 川口 寧 東京大学, 医科学研究所, 教授 (60292984)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: HSV / VP26 / Us8A / 神経病原性 / 神経侵襲性 / リン酸化プロテオーム解析

Outline of Final Research Achievements

Herpes simplex virus type (HSV) causes a range of human diseases. HSV has evolved mechanisms to utilize the phosphorylation system for the regulation of their own viral proteins and to establish a cellular environment for efficient viral replication and virulence. However, our knowledge of them remains to be limited and fragmented. In this study, we identified novel phosphorylation sites of small capsid protein VP26 and putative membrane protein Us8A by mass spectrometry-based phosphoproteomic analysis of HSV-infected cells. Our study showed that (i) the phosphorylation of VP26 Thr-111 is required for both efficient HSV-1 replication and cell-cell spread in SK-N-SH cells and HSV-1 neurovirulence in mice by regulating localazaton of VP26 and its binding partner, the major capsid protein VP5, (ii) the Us3-mediated phosphorylation of Us8A Ser-61 regulates Us8A function for viral invasion into the CNS from peripheral sites.

Free Research Field

ウイルス学