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Journal of General Virology (2002), 83, 2109-2116.
© 2002 Society for General Microbiology

Animal: RNA Viruses

Olfactory receptor neurons prevent dissemination of neurovirulent influenza A virus into the brain by undergoing virus-induced apoptosis

Isamu Mori1,2,3, Fumi Goshima3, Yoshinori Imai4, Shinichi Kohsaka4, Tsuyoshi Sugiyama2, Tomoaki Yoshida2, Takashi Yokochi2, Yukihiro Nishiyama3 and Yoshinobu Kimura1

Department of Microbiology, Fukui Medical University School of Medicine, 23-3 Matsuoka-cho, Yoshida-gun, Fukui 910-1193, Japan1
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan2
Laboratory of Virology, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Aichi, Japan3
Department of Neurochemistry, National Institute of Neuroscience, Tokyo, Japan4

Author for correspondence: Yoshinobu Kimura. Fax +81 776 61 8104. e-mail ykimura{at}fmsrsa.fukui-med.ac.jp

Olfactory receptor neurons (ORNs) were infected upon intranasal inoculation with the R404BP strain of neurovirulent influenza A virus. Virus-infected neurons and a small fraction of neighbouring uninfected neurons displayed apoptotic neurodegeneration substantiated by the immunohistochemistry for activated caspase-3 molecules and the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling method. However, virus infection was restricted within the peripheral neuroepithelium and all mice survived the infection. Virus-infected ORNs revealed upregulated expression of the Fas ligand molecules, activating the c-Jun N-terminal kinase signal transduction pathway. In addition, Iba1-expressing activated microglia/macrophages appeared to partake in phagocytic activities, eventually clearing apoptotic bodies. These results raise the possibility that induction of apoptosis in olfactory receptor neurons at an early stage of infection may provide protective effects against invasion of the neurovirulent virus from the peripheral to the CNS.




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