Rabies virus nucleoprotein functions to evade activation of the RIG-I-mediated antiviral response
| Autor: | Hiroyuki Koyama, Tatsunori Masatani, Yoshiharu Sawaki, Makoto Sugiyama, Yuki Ito, Keisuke Nakagawa, Kenta Shimizu, Naoto Ito |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Virulence Factors
Immunology Active Transport Cell Nucleus Cellular Response to Infection medicine.disease_cause Microbiology Virus Cell Line DEAD-box RNA Helicases Viral Proteins Interferon Virology medicine CXCL10 Humans Receptors Immunologic Mononegavirales Lyssavirus Chemokine CCL5 Oligonucleotide Array Sequence Analysis Neurons biology RIG-I Gene Expression Profiling Rabies virus Interferon-beta Rhabdoviridae biology.organism_classification Molecular biology Chemokine CXCL10 Nucleoproteins Insect Science DEAD Box Protein 58 Interferon Regulatory Factor-3 medicine.drug |
| Zdroj: | Journal of virology. 84(8) |
| ISSN: | 1098-5514 |
| Popis: | The rabies virus Ni-CE strain causes nonlethal infection in adult mice after intracerebral inoculation, whereas the parental Nishigahara (Ni) strain kills mice. We previously reported that the chimeric CE(NiN) strain with the N gene from the Ni strain in the genetic background of the Ni-CE strain kills adult mice, indicating that the N gene is related to the different pathogenicities of Ni and Ni-CE strains. In the present study, to obtain an insight into the mechanism by which the N gene determines viral pathogenicity, we compared the effects of Ni, Ni-CE, and CE(NiN) infections on host gene expressions using a human neuroblastoma cell line. Microarray analysis of these infected cells revealed that the expression levels of particular genes in Ni- and CE(NiN)-infected cells, including beta interferon (IFN-β) and chemokine genes (i.e., CXCL10 and CCL5) were lower than those in Ni-CE-infected cells. We also demonstrated that Ni-CE infection activated the interferon regulatory factor 3 (IRF-3)-dependent IFN-β promoter and induced IRF-3 nuclear translocation more efficiently than did Ni or CE(NiN) infection. Furthermore, we showed that Ni-CE infection, but not Ni or CE(NiN) infection, strongly activates the IRF-3 pathway through activation of RIG-I, which is known as a cellular sensor of virus infection. These findings indicate that the N protein of rabies virus (Ni strain) has a function to evade the activation of RIG-I. To our knowledge, this is the first report that the Mononegavirales N protein functions to evade induction of host IFN and chemokines. |
| Databáze: | OpenAIRE |
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