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Viral and Mycoplasmal of Laboratory Rodents
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3-13. 19. Traub, E. (1953). A filterable virus recovered from white mice. Science 81: 298-299. 20. M. T. (1949). A murine virus (JHM) causing disseminated encephalomyelitis with extensive destruction of myelin. I. Isolation and biological properties of the virus. J. Exp. Med. 90: 181-194. 21. A. and Smith. G. (1936). The visceral lesions produced in mice by the salivary gland virus of mice. J. Exp. Med. 63: 303-310. 22. J. (1936). Some possible effects of nursing on the mammary gland tumor incidence in mice.
III. PATH0GENESIS Naturally transmitted Sendai virus replicates primarily in respiratory epithelium. This localization occurs despite widely distributed susceptible tissues that express the 42 David G. Brownstein appropriate viral receptors (35,36). One attractive explanation for the respiratory tropism for Sendai virus and other parainfluenza viruses is the availability of fusionactivating proteases in respiratory tissues. Tashiro and Homma have shown that mouse lungs contain a specific trypsin-like enzyme which efficiently cleaves F Q to F\ and F2 when infected with wild-type Sendai virus (37,38).
II. Isolation of ectromelia virus from a vaccine strain. Acta Path. Microbiol. Scand. 24: 375-378. CHAPTER 6 SENDAI VIRUS David G. Brownstein Section of Comparative Medicine Yale University School of Medicine New Haven, Connecticut I. INTRODUCTION Sendai virus emerged as a spontaneous contaminant of laboratory rodent colonies a little over 30 years ago during attempts to recover human respiratory viruses in mice at Tokohu University Hospital in Sendai, Japan (1). The attendant confusion over the original host for this parainfluenza 1 virus has yet to be resolved.