• Role of Ezrin Phosphorylation in HIV-1 Replication

Kamiyama, Haruka

Izumida, Mai

Umemura, Yuria

Hayashi, Hideki

Matsuyama, Toshifumi

Kubo, Yoshinao

    • ©2018 Kamiyama, Izumida, Umemura, Hayashi, Matsuyama and Kubo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
  • Other Ezri
  • Other HIV-1
  • Other Viral assembly
  • Other Viral budding
  • Other Viral entry
  • Host-cell expression of the ezrin protein is required for CXCR4 (X4)-tropic HIV-1 infection. Ezrin function is regulated by phosphorylation at threonine-567. This study investigates the role of ezrin phosphorylation in HIV-1 infection and virion release. We analyzed the effects of ezrin mutations involving substitution of threonine-567 by alanine (EZ-TA), a constitutively inactive mutant, or by
    aspartic acid (EZ-TD), which mimics phosphorylated threonine. We also investigated the effects of ezrin silencing on HIV-1 virion release using a specific siRNA. We observed that X4-tropic HIV-1
    vector infection was inhibited by expression of the EZ-TA mutant but increased by expression of the EZ-TD mutant, suggesting that ezrin phosphorylation in target cells is required for efficient HIV-1 entry. Expression of a dominant-negative mutant of ezrin (EZ-N) and ezrin silencing in HIV-1 vector-producing cells significantly reduced the infectivity of released virions without affecting virion production. This result indicates that endogenous ezrin expression is required for virion infectivity. The EZ-TD but not the EZ-TA inhibited virion release from HIV-1 vector-producing cells.
    Taken together, these findings suggest that ezrin phosphorylation in target cells is required for efficient HIV-1 entry but inhibits virion release from HIV-1 vector-producing cells.
  • identifier:Frontiers in Microbiology, 9,; 2018
  • identifier:1664-302X
PublisherFrontiers Media S.A.
Date Issued 2018-08-27
NIItypejournal article
Identifier URI
  • isIdenticalTo DOI
    • ISSN 1664-302X
    • Frontiers in Microbiology
    9, 1912