Measles virus induces persistent infection by autoregulation of viral replication

Natural infection with measles virus (MV) establishes lifelong immunity. Persistent infection with MV is likely involved in this phenomenon, as non-replicating protein antigens never induce such long-term immunity. Although MV establishes stable persistent infection in vitro and possibly in vivo, th...

Full description

Bibliographic Details
Main Authors:	Doi, Tomomitsu, Kwon, Hyun-Jeong, Honda, Tomoyuki, Sato, Hiroki, Yoneda, Misako, Kai, Chieko
Format:	Online
Language:	English
Published:	Nature Publishing Group 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121633/

id	pubmed-5121633
recordtype	oai_dc
spelling	pubmed-51216332016-11-28 Measles virus induces persistent infection by autoregulation of viral replication Doi, Tomomitsu Kwon, Hyun-Jeong Honda, Tomoyuki Sato, Hiroki Yoneda, Misako Kai, Chieko Article Natural infection with measles virus (MV) establishes lifelong immunity. Persistent infection with MV is likely involved in this phenomenon, as non-replicating protein antigens never induce such long-term immunity. Although MV establishes stable persistent infection in vitro and possibly in vivo, the mechanism by which this occurs is largely unknown. Here, we demonstrate that MV changes the infection mode from lytic to non-lytic and evades the innate immune response to establish persistent infection without viral genome mutation. We found that, in the persistent phase, the viral RNA level declined with the termination of interferon production and cell death. Our analysis of viral protein dynamics shows that during the establishment of persistent infection, the nucleoprotein level was sustained while the phosphoprotein and large protein levels declined. The ectopic expression of nucleoprotein suppressed viral replication, indicating that viral replication is self-regulated by nucleoprotein accumulation during persistent infection. The persistently infected cells were able to produce interferon in response to poly I:C stimulation, suggesting that MV does not interfere with host interferon responses in persistent infection. Our results may provide mechanistic insight into the persistent infection of this cytopathic RNA virus that induces lifelong immunity. Nature Publishing Group 2016-11-24 /pmc/articles/PMC5121633/ /pubmed/27883010 http://dx.doi.org/10.1038/srep37163 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Doi, Tomomitsu Kwon, Hyun-Jeong Honda, Tomoyuki Sato, Hiroki Yoneda, Misako Kai, Chieko
spellingShingle	Doi, Tomomitsu Kwon, Hyun-Jeong Honda, Tomoyuki Sato, Hiroki Yoneda, Misako Kai, Chieko Measles virus induces persistent infection by autoregulation of viral replication
author_facet	Doi, Tomomitsu Kwon, Hyun-Jeong Honda, Tomoyuki Sato, Hiroki Yoneda, Misako Kai, Chieko
author_sort	Doi, Tomomitsu
title	Measles virus induces persistent infection by autoregulation of viral replication
title_short	Measles virus induces persistent infection by autoregulation of viral replication
title_full	Measles virus induces persistent infection by autoregulation of viral replication
title_fullStr	Measles virus induces persistent infection by autoregulation of viral replication
title_full_unstemmed	Measles virus induces persistent infection by autoregulation of viral replication
title_sort	measles virus induces persistent infection by autoregulation of viral replication
description	Natural infection with measles virus (MV) establishes lifelong immunity. Persistent infection with MV is likely involved in this phenomenon, as non-replicating protein antigens never induce such long-term immunity. Although MV establishes stable persistent infection in vitro and possibly in vivo, the mechanism by which this occurs is largely unknown. Here, we demonstrate that MV changes the infection mode from lytic to non-lytic and evades the innate immune response to establish persistent infection without viral genome mutation. We found that, in the persistent phase, the viral RNA level declined with the termination of interferon production and cell death. Our analysis of viral protein dynamics shows that during the establishment of persistent infection, the nucleoprotein level was sustained while the phosphoprotein and large protein levels declined. The ectopic expression of nucleoprotein suppressed viral replication, indicating that viral replication is self-regulated by nucleoprotein accumulation during persistent infection. The persistently infected cells were able to produce interferon in response to poly I:C stimulation, suggesting that MV does not interfere with host interferon responses in persistent infection. Our results may provide mechanistic insight into the persistent infection of this cytopathic RNA virus that induces lifelong immunity.
publisher	Nature Publishing Group
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121633/
_version_	1613739574585982976

Measles virus induces persistent infection by autoregulation of viral replication

Similar Items