Further studies on subacute encephalitis and hydrocephalus in hamsters caused by measles virus from persistently infected cell cultures
✍ Scribed by Erling Norrby; Peggy Swoveland; Kenneth P. Johnson; Krister Kristensson
- Publisher
- John Wiley and Sons
- Year
- 1980
- Tongue
- English
- Weight
- 1005 KB
- Volume
- 5
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Newborn hamsters were inoculated intracerebrally (IC) with disrupted measles carrier Lu 106 cells. No acute neurological disease developed, but limited, persistent neural infection was identified by immune fluorescence and by virus isolation. By ten days after inoculation, virus could be recovered only by co cultivation of explant cultures of central nervous system (CNS) tissue and Vero cells. Virus was still demonstrable in CNS by both techniques 50 days after inoculation, the latest sample collected. Animals inoculated as newborns developed a poor hem agglutination‐inhibiting (HI) antibody response.
In three‐week‐old hamsters inoculated IC no detectable replication of carrier virus occurred. The serum HI antibody response was more than 20 times higher than that in animals inoculated as newborns.
Hydrocephalus developed in a fraction of animals inoculated at birth or at the age of three weeks. Both infectious and heat‐inactivated disrupted virus carrier material, but not control material of Lu 106 cells, gave hydrocephalus. The precise mechanism leading to hydrocephalus is unclear. Carrier virus material may produce a meningeal irritation causing disturbances of the extraventricular flow or resorption of cerebrospinal fluid, leading to communicating hydrocephalus. Infectious carrier virus may replicate in and destroy ependymal cells, further contributing to hydrocephalus.