2003 Fiscal Year Final Research Report Summary
Studies on natural infection with human parainfulenza virus type 3 in Japanese SPF rats colonies.
| Project/Area Number |
14580803
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
MIYATA Hironori University of Occupational and Environmental Health, Faculty of Medicine, Associate professor, 医学部, 助教授 (70174191)
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| Project Period (FY) |
2002 – 2003
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| Keywords | experimental rat / parainfluenza virus type 3 / pneumonia |
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| Research Abstract |
The parainfulenza virus type 3 (PIV3) naturally infected in rats, which serologically identified its prevalence, was focused on in this study. The lung homogenate of seronegative rat which housed in seropositive rat colonies was inoculated into vero cell to isolate the virus. After twice blind passage, the culture supernatant turned to 1st RT-PCR positive, and vero cell line after 3rd blind passage represented partially giant cells and cytopathic effects lately. The direct immunofluorecent assay with anti human PIV3 antibody showed specific fluorecence in cytoplasm in affected vero cell. HN viral genome of this strain named No.24 was composed of 1,716 bases, capable of coding 572 amino acids. No additional and deletional sequences in No.24 strain were observed, comparing with previously reported human and bovine type PIV3 HN genomes. The phylogenic tree analysis based on the HN viral genome demonstrated that No.24 strain belongs to a blanch of human PIV3 group, but not a bovine type. SD rats and ICR mice were experimentally infected with this strain to clarify the pathogenesis. The virus was recovered from the lung homogenate of infected rats at 3 and 5 days post infection (dpi), which represented the viral replication. The pathological lesions were observed the degeneration, ablatio, and apoptosis of bronchial epitheliocytes, eosionophilic inclusion bodies in same cell at 5-7 dpi. But, after 10 dpi, no patholigical lesions were observed in any infected rats. The infected rats seroconvered at 7 dpi and showed continuously seropositive until 21 dpi. These results including slight pathological change suggested that the PIV3 derived from rat has transient and slight pathogenesis to experimental SD rats. On the other hand, none of infected mice with No.24 had pathological lesion in lung. But, HI and IFA antibody against PIV3 was observed from 7 dpi to 21 dpi. These results showed that the rat PIV3 pathogenesis against mice need not to take into consideration.
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