Reinfection of mice with respiratory syncytial virus
✍ Scribed by Barney S. Graham; Lori A. Bunion; Peter F. Wright; David T. Karzon
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- English
- Weight
- 825 KB
- Volume
- 34
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
A BALB/c model of respiratory syncytial virus infection has been developed in which hightitered replication occurs in lung, immunological infiltrates in lung can be detected histologically, and illness can be consistently reproduced. The immunodeterminants of RSV reinfection in this system were investigated by rechallenging mice with RSV early (less than 2 months after primary infection) and late (16 to 21 months after primary infection) and correlating illness and titer of RSV isolated from lungs and noses with RSV‐specific serological responses and lung histology. After early rechallenge, RSV was cleared within 24 hours from both nose and lung. After late rechallenge, RSV was isolated at 72 hours from nose in 21/24 mice, but from lung in only 5/24 mice. Isolation of RSV from lung after rechallenge was associated with low RSV‐specific antibody titers measured by ELISA and plaque‐reduction neutralization. The presence of lymphocyte aggregates around the bronchovascular bundles was associated with inability to isolate RSV from lung and lack of illness. The basophilic lymphocytes were small and uniform in size with dense nuclei and a small amount of cytoplasm. These studies demonstrate that nasal and pulmonary reinfection with RSV is possible in mice after late rechallenge. The studies also indicate the potential importance of RSV‐specific antibody in protecting lung from reinfection.
📜 SIMILAR VOLUMES
## Abstract Differences in the severity of respiratory syncytial virus (RSV)‐induced lower respiratory disease in infants have been attributed to multiple environmental and genetic factors. To identify the genetic factor(s) influencing RSV susceptibility, we examined RSV infection in eight inbred m
In mice, respiratory syncytial virus (RSV) infection during allergic provocation aggravates the allergic Th2 immune response, characterised by production of interleukin (IL)-4, IL-5, and IL-13, and eosinophilic inflammation. This enhancement of the Th2 response occurs simultaneously with a strong RS
## Abstract __Pseudomonas aeruginosa__ causes opportunistic infections in immunocompromised individuals and patients ventilated mechanically and is the major pathogen in patients with cystic fibrosis, in which it causes chronic infections. Epidemiological, in vitro and animal data suggest a role fo
## Abstract Based on the concept of a common mucosal immune system, the murine gastrointestinal tract was inoculated (oral) with three doses (5, 20, and 40 μg) of UV‐inactivated respiratory syncytial virus (RSV) in order to elicit a virus‐specific immune response in the respiratory tract. Only the
We describe two infants suffering from severe pneumonia caused by respiratory syncytial virus (RSV) infection and needing mechanical ventilation with both high ventilator settings and a high fraction of inspired oxygen. The severity of the respiratory failure and the possibility of decreased and/or