Measles virus induces persistent infection by autoregulation of viral replication
| Autor: | Tomomitsu Doi, Tomoyuki Honda, Hiroki Sato, Hyun Jeong Kwon, Misako Yoneda, Chieko Kai |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Viral protein viruses 030106 microbiology Genome Viral Virus Replication medicine.disease_cause Article Cell Line Measles virus Viral Proteins 03 medical and health sciences Viral entry Immunity Interferon medicine Homeostasis Signaling Lymphocytic Activation Molecule Associated Protein Multidisciplinary Innate immune system biology Interferon-beta Nucleocapsid Proteins biology.organism_classification Virology Immunity Innate Nucleoproteins 030104 developmental biology Viral replication Lytic cycle Mutation RNA Viral Interferons Measles medicine.drug |
| Zdroj: | Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/srep37163 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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