Heat Shock Protein 90 Ensures the Integrity of Rubella Virus p150 Protein and Supports Viral Replication.


Journal

Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724

Informations de publication

Date de publication:
15 11 2019
Historique:
received: 13 07 2019
accepted: 21 08 2019
pubmed: 6 9 2019
medline: 21 7 2020
entrez: 6 9 2019
Statut: epublish

Résumé

Two viral nonstructural proteins, p150 and p90, are expressed in rubella virus (RUBV)-infected cells and mediate viral genome replication, presumably using various host machineries. Molecular chaperones are critical host factors for the maintenance of cellular proteostasis, and certain viral proteins use this chaperone system. The RUBV p150 and p90 proteins are generated from a precursor polyprotein, p200, via processing by the protease activity of its p150 region. This processing is essential for RUBV genome replication. Here we show that heat shock protein 90 (HSP90), a molecular chaperone, is an important host factor for RUBV genome replication. The treatment of RUBV-infected cells with the HSP90 inhibitors 17-allylamino-17-desmethoxygeldanamycin (17-AAG) and ganetespib suppressed RUBV genome replication. HSP90α physically interacted with p150, but not p90. Further analyses into the mechanism of action of the HSP90 inhibitors revealed that HSP90 activity contributes to p150 functional integrity and promotes p200 processing. Collectively, our data demonstrate that RUBV p150 is a client of the HSP90 molecular chaperone and that HSP90 functions as a key host factor for RUBV replication.

Identifiants

pubmed: 31484751
pii: JVI.01142-19
doi: 10.1128/JVI.01142-19
pmc: PMC6819934
pii:
doi:

Substances chimiques

HSP90 Heat-Shock Proteins 0
Molecular Chaperones 0
RNA, Viral 0
Viral Nonstructural Proteins 0
RNA-Dependent RNA Polymerase EC 2.7.7.48

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2019 American Society for Microbiology.

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Auteurs

Masafumi Sakata (M)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan msakata@nih.go.jp.

Hiroshi Katoh (H)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan.

Noriyuki Otsuki (N)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan.

Kiyoko Okamoto (K)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan.

Yuichiro Nakatsu (Y)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan.

Chang-Kweng Lim (CK)

Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan.

Masayuki Saijo (M)

Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan.

Makoto Takeda (M)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan.

Yoshio Mori (Y)

Department of Virology 3, National Institute of Infectious Diseases, Tokyo, Japan.

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Classifications MeSH