Measles virus induces persistent infection by autoregulation of viral replication

Tomomitsu Doi, Hyun Jeong Kwon, Tomoyuki Honda, Hiroki Sato, Misako Yoneda, Chieko Kai

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


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.

Original languageEnglish
Article number37163
JournalScientific reports
Publication statusPublished - Nov 24 2016
Externally publishedYes

ASJC Scopus subject areas

  • General


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