SIGNS AND LESIONS OF EXPERIMENTAL SENDAI VIRUS-INFECTION IN 2 GENETICALLY DISTINCT STRAINS OF SCID BEIGE MICE/

The pathogenesis of Sendai virus infection was studied in genetically immunodeficient mice of genotype scid/scid.bg/bg (SCID-beige) using C. B-17 SCID-beige mice, a BALB/c-related strain that expresses the same major histocompatibility complex as the Sendai virus-susceptible DBA/2 (H-2(d)). Mice were inoculated intranasally with isolate 771076 of Se ndai virus, then killed at 2-day intervals beginning on day 4 postinoc ulation. Clinical signs were evident beginning at 8 to 10 days post-in oculation, and all animals remaining were killed in extremis by 14 to 17 days post-inoculation. Lesions in inoculated mice were confined to the respiratory tract. In the nasal passages, a nonresolving rhinitis, with epithelial hyperplasia/metaplasia occurred. Cranioventral bronch opneumonitis was characterized by marked hyperplasia and necrosis of e pithelial cells lining airways and with leukocytic infiltration. At th e alveolar level, there was marked hypertrophy and hyperplasia of type II pneumocytes, mobilization of alveolar macrophages, and obliteratio n of the normal architecture in severely affected areas. Viral antigen was evident beginning at 4 days post-inoculation and persisted in aff ected areas throughout the duration of the study. Because immunocompet ent C57BL/6 mice are known to be genetically resistant to Sendai virus , the susceptibility of C57BL/6 SCID-beige to Sendai virus was then co mpared to that of C.B-17 SCID-beige mice. In age-matched animals of th e two strains, there was no evidence of natural resistance to Sendai v irus infection in the immunodeficient C57BL/6 strain compared to the C .B-17 mice. These studies indicate that the genetic differences in sus ceptibility of two strains of immunocompetent mice to Sendai virus inf ection are eliminated by expression of the mutations scid and beige.