VIRUS LOAD AND NEUROPATHOLOGY IN THE FIV MODEL

Citation
D. Boche et al., VIRUS LOAD AND NEUROPATHOLOGY IN THE FIV MODEL, Journal of neurovirology, 2(6), 1996, pp. 377-387
Citations number
67
Categorie Soggetti
Neurosciences,Virology
Journal title
ISSN journal
13550284
Volume
2
Issue
6
Year of publication
1996
Pages
377 - 387
Database
ISI
SICI code
1355-0284(1996)2:6<377:VLANIT>2.0.ZU;2-N
Abstract
The FIV (feline immunodeficiency virus) induces in cats brain changes presenting similarities with those observed in human immunodeficiency virus infection. This FIV model was used to study the relationship bet ween viral load in brain, in lymphoid organs and central nervous syste m (CNS) changes during the early and late stages of infection. Early b rain changes were analyzed in animals experimentally infected with two different FIV isolates and sacrificed at 7 and 15 days, 1, 2, 6, and 12 months past inoculation (p.i.). Late CNS abnormalities were analyze d in naturally FIV-infected cats referred to the Veterinary School of Nantes. For each animal, one cerebral hemisphere was fixed and examine d using routine techniques. The characterization of FIV replicating ce lls by in situ hybridization was performed an the other half frozen he misphere an sections performed in the anterior and the median regions of the brain. During the early stages of infection, moderate gliosis w ith glial nodules and sometimes white matter pallor and meningitis wer e associated with few infected cells scattered in the brain. Infection was an early event as infected cells could be detected in brain at 7 p.i. For each cat, these findings were found identic al in the two ana lyzed areas. During the late stages, brain lesions and the number of v irus replicating cells increased especially in animals with perivascul ar infiltrates. The multinucleated giant cells encephalitis was never observed and the number of FIV replicating cells scattered in the whol e brain was always low. This discrepancy between the number of replica ting cells and the brain lesions, corroborates the hypotheses suggesti ng that brain injuries may be mediated via diffusive factors and ampli fication processes through cytokine cascades and cell activations.