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J Gen Virol 86 (2005), 733-741; DOI 10.1099/vir.0.80666-0

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© 2005 Society for General Microbiology

Contamination of a specific-pathogen-free rat breeding colony with Human parainfluenzavirus type 3

Hironori Miyata1, Tamotsu Kanazawa2, Kazumoto Shibuya3 and Shigeo Hino4

1 Animal Research Center, University of Occupational and Environmental Health, 1-1 Iseigaoka Yahatanishi, Kitakyushu 807-8555, Japan
2 Department of Parasitology and Tropical Public Health, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka Yahatanishi, Kitakyushu 807-8555, Japan
3 Nippon Institute for Biological Science, Shin-machi, Ome, Tokyo 198-0024, Japan
4 Division of Virology, Faculty of Medicine, Tottori University, Yonago 683-8503, Japan

Correspondence
Hironori Miyata
h-miyata{at}med.uoeh-u.ac.jp

Routine antibody surveillance for Sendai virus in a breeding colony suggested viral invasion into laboratory rats. A more specific haemagglutination-inhibition test implied that the agent was related closely to Human parainfluenza virus type 3 (hPIV3), rather than Sendai virus. To isolate this virus, Vero cells were inoculated with lung homogenates of 30 young animals from the colony. One of the cultures became positive at the second passage by RT-PCR directed to the hPIV3 NP and L genes. Cytopathic effect with cell fusion was observed at the third passage. The HN gene of this virus (KK24) had >93 % similarity to those of other hPIV3 isolates, suggesting a human origin of KK24. Experimental intranasal inoculation of KK24 into SD rats showed virus replication in the lungs at 3–5 days post-infection (p.i.). Pathological examination of the lungs at day 5 p.i. indicated a moderate detachment, degradation and apoptosis of bronchial epitheliocytes with peribronchial mononuclear infiltrations. At day 7 p.i., these changes became less prominent, and no lesions were apparent at day 10 p.i. or later. The infected rats seroconverted at day 7 p.i. On the contrary, none of the 30 experimentally infected ICR mice showed any pathological lesions in their lungs, despite seroconversion at 7 days p.i. These results suggest that hPIV3 can invade rat colonies and has a moderate and transient pathogenicity in rats. This is the first report of non-experimental hPIV3 infection in laboratory rats, unexpectedly detected by antibody screening for Sendai virus.

The GenBank/EMBL/DDBJ accession numbers for the hPIV3 sequences reported in this paper are AB195612 for B12 NP, AB189962 for KK24 NP, AB195610 for KK24 L, AB189960 for KK24 HN, AB195613 for BRD NP, AB195611 for BRD L and AB189961 for BRD HN.







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