2009 Fiscal Year Final Research Report
Studies on receptor-independent infection of coronaviruses and its implication in the pathogenesis
| Project/Area Number |
19390135
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
TAGUCHI Fumihiro National Institute of Infectious Diseases, 獣医学部, 准教授 (30107429)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Rihito (30129746)
SHIRATO Kazuya (40415477)
HIRAI Asuka (50450557)
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| Project Period (FY) |
2007 – 2009
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| Keywords | 病原性 |
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| Research Abstract |
Murine coronavirus wild type (wt) JHM strain infects in a receptor-independent fashion (receptor independent infection, RII in short), while a mutant isolated from wild type wt JHM, called srr7, lacks this activity, when examined at 24 hours after infection of mixed neural cell culture. However, variant viruses with RII activity were isolated from srr7 infected mixed cells, when infection was maintained for 3 days. Wt JHM with RII activity showed high neurovirulence for mice, killing those mice within 2-3 days after infection. Srr7 also killed mice when higher dose was inoculated after longer survival time compared with that of wt JHM. Wt JHM antigen was detected in a variety of neural cells, which may be attributed to the RII in mouse brain. However, srr7 antigen was not widely distributed. These results suggest the possibility that high virulence of JHM is attributed to the RII activity. We also tried to obtain porcine coronavirus that grows and shows the virulence for mice to see whether coronaviruses other than JHM display RII activity. After passage of Vero-cell adapted porcine epidemic diarrhea virus (PEDV) through suckling mouse brain, we obtained variant with higher virulence for mice, which shows enhanced cell-cell fusion activity compared with original, non-adapted virus. The mutant showed 4 amino acids mutation in the S protein which is believed to be critical for cell-cell fusion. However, it is not understood whether those mutations in the S could be responsible for higher virulence. In order to pursue this issue, we have to establish the reverse genetics system of PEDV
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Research Products
(19 results)
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[Journal Article] Role of mouse hepatitis virus (MHV) receptor mCEACAM1 in the resistance of mice to MHV infection: Studies on mice with chimeric mCEACAM1a and 1b.2010
Author(s)
Hirai A, Ohtsuka N, Ikeda T, Taniguchi R, Blau D, Nakagaki K, Miura HS, Ami Y, Yamada YK, Itohara S, Holmes KV, Taguchi F
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