2007 Fiscal Year Final Research Report Summary
Research on the pathogenesis, clinical features, diagnostic methods and treatment of acute encephalitis/encephalopathy.
| Project/Area Number |
17209037
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Okayama University |
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Principal Investigator |
MORISHIMA Tsuneo Okayama University, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Professor (90157892)
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| Co-Investigator(Kenkyū-buntansha) |
OKABE Nobuhiko Okayama University, Infectious Disease, Surveillance Center, National Institute of Infectious Diseases, Director (10057028)
NUNOI Hiroyuki University of Miyazaki, Faculty of Medicine, Professor (50218260)
MIZUGUCHI Masashi the University of Tokyo, Graduate School of Medicine, Professor (20209753)
KIMURA Hiroshi Nagoya University, Graduate School of Medicine, Assistant Professor (30303621)
ICHIYAMA Takashi Yamaguchi University, Graduate School of Medicine, Lecture (20263767)
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| Project Period (FY) |
2005 – 2007
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| Keywords | acute encephalitis / acute encephalopathy / influenza / HHV-6 / rotavirus / pathogenesis |
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| Research Abstract |
The annual incidence of acute encephalitis/encephalopathy among children younger than 15 years old is approximately 1,000 cases and 25% of them are influenza-associated encephalopathy, followed by encephalopathy/encephalitis caused by HHV-6 or 7 (12%), mumps and rotavirus CNS encephalitis/encephalopathy (4-5%). Although the pathogenesis of influenza-associated encephalopathy is still unclear, several reports have suggested that the pathogenesis involves cytokines such as soluble tumor necrosis factor (sTNF) receptor-1, interleukin-1β (IL-1β), IL-6, TNF-a, IL-8, and IL-10. It has been suggested that neurons and hepatocytes are induced to undergo apoptosis in influenza-associated encephalopathy as a consequence of hypercytokinemia. In contrast, the pathogenesis of other viral encephalitis/encephalopathy is still unclear. In rotavirus encephalopathy, the virus replication could not be found in the brain, while severe brain and lung edema was found associated with hyper cytokinemia. Therefore, not only in influenza but in other virus infections, brain damage may occur due to hyper cytokinemia without virus replication. These findings might be important for the management of the illness. In addition, we could develop multiplex PCR system for the early diagnosis of HSV encephalitis, HHV-6 encephalopathy and EBV CNS infections.
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