Signs and Lesions of Experimental Sendai Virus Infection in Two Genetically Distinct Strains of SCID/Beige Mice
| Autor: | B. A. Croy, D. C. Auger, D. H. Percy |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Male
0301 basic medicine Time Factors Necrosis 040301 veterinary sciences viruses Mice SCID Biology 0403 veterinary science Pathogenesis Mice 03 medical and health sciences Species Specificity Antigen Metaplasia medicine Animals Antigens Viral Lung Paramyxoviridae Infections General Veterinary 04 agricultural and veterinary sciences Hyperplasia biology.organism_classification medicine.disease Virology Sendai virus Parainfluenza Virus 1 Human Mice Inbred C57BL Trachea 030104 developmental biology medicine.anatomical_structure Female Disease Susceptibility medicine.symptom Respiratory tract |
| Zdroj: | Veterinary Pathology. 31:67-73 |
| ISSN: | 1544-2217 0300-9858 |
| DOI: | 10.1177/030098589403100109 |
| Popis: | 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-24). Mice were inoculated intranasals with isolate 771076 of Sendai virus, then killed at 2-day intervals beginning on day 4 post-inoculation. Clinical signs were evident beginning at 8 to 10 days post-inoculation, 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 bronchopneumonitis was characterized by marked hyperplasia and necrosis of epithelial cells lining airways and with leukocytic infiltration. At the alveolar level, there was marked hypertrophy and hyperplasia of type II pneumocytes, mobilization of alveolar macrophages, and obliteration of the normal architecture in severely affected areas. Viral antigen was evident beginning at 4 days post-inoculation and persisted in affected areas throughout the duration of the study. Because immunocompetent C57BL/6 mice are known to be genetically resistant to Sendai virus, the susceptibility of C57B/6 SCID-beige to Sendai virus was then compared to that of C.B-17 SCID-beige mice. In age-matched animals of the two strains, there was no evidence of natural resistance to Sendai virus infection in the immunodeficient C57BL/6 strain compared to the C.B-17 mice. These studies indicate that the genetic differences in susceptibility of two strains of immunocompetent mice to Sendai virus infection are eliminated by expression of the mutations scid and beige. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|