[Pathophysiological events in the central nervous system of mice during neurovirulent influenza A virus infection].
Influenza A/WSN/33 virus inoculated into the olfactory bulb of C57BL/6 mice selectively infects the anterior olfactory nucleus, habenular, paraventricular thalamic, and brainstem monoaminergic neurons. Infected neurons died by day 12 with perforin-mediated neuroapoptosis, that appears significant to exterminate the intracellular pathogen in the early stage of infection. In perforin-deficient mice virus infection continued for a longer period of 35 days. Activated microglial cells with overexpression of the Iba1 appeared widespread in the brain, participating in the protection, maintenance, and repair of infection-spared neurons. Macrophages accumulated in virus-infected areas to expedite the resolution of the virus infection.
Kimura
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Department of Microbiology, Fukui Medical University School of Medicine.
D000818:Animals; D001927:Brain Diseases / Q000209:etiology*; D008562:Membrane Glycoproteins / Q000172:deficiency; D051379:Mice; D008810:Mice, Inbred C57BL; D009976:Orthomyxoviridae Infections / Q000150:complications*; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins
D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D054353:Perforin