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Clinical and Diagnostic Laboratory Immunology, January 2003, p. 185-188, Vol. 10, No. 1
1071-412X/03/$08.00+0 DOI: 10.1128/CDLI.10.1.185-188.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Yasuhiro Ikeda,1,
Eiji Sato,1,3 Yorihiro Nishimura,1,2 Yasuo Inoshima,1,4 Masayuki Shimojima,1 Yukinobu Tohya,1 Takeshi Mikami,1,4 and Takayuki Miyazawa1,2,3*
Department of Veterinary Microbiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, and Host and Defence, PRESTO, Japan Science and Technology Corporation, Tachikawa, Tokyo,1 Research Center for Emerging Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka,2 ,3 Laboratory of Veterinary Public Health, Department of Veterinary Medicine, College of Bioresource, Nihon University, Fujisawa, Kanagawa, Japan4
Received 23 July 2002/ Returned for modification 4 September 2002/ Accepted 9 October 2002
Four of six specific pathogen-free cats were infected after intravaginal exposure to molecularly cloned lymphotropic but non-Crandell feline kidney (CRFK)-tropic feline immunodeficiency virus strain TM2 and its AP-1 deletion mutant. The sequences of the env V3-to-V5 region which defines the CRFK tropism were unchanged in the infected cats through the infection. These data suggest that the strain was transmitted across the mucosal epithelium without a broadening of cell tropism.
Present address: Pasturing Disease Section, Shichinohe Research Unit, National Institute of Animal Health, Kamikitagun, Aomori, Japan.
Present address: Department of Immunology, The Windeyer Institute, University College London, London, United Kingdom.
Present address: Department of Pathobiology, College of Veterinary Medicine, University of Florida, Gainesville, Florida.
¶ Present address: Viral Pathogenicity Section, Department of Exotic Diseases, National Institute of Animal Health, Kodaira, Tokyo, Japan.
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