Long-lasting astrocyte reaction to persistent Junin virus infection of rat cortical neurons

• Published in: Journal of Neural Transmission Vol. 110; no. 8; pp. 847 - 857
• Main Authors: CACCURI, R. L, IACONO, R. F, WEISSENBACHER, M. C, AVILA, M. M, BERRIA, M. I
• Format: Journal Article
• Language: English
• Published: Wien Springer 01.08.2003; New York, NY Springer Nature B.V
• Subjects: Animals; Animals, Newborn; Arenaviridae Infections - immunology; Arenaviridae Infections - pathology; Arenaviridae Infections - physiopathology; Astrocytes - immunology; Astrocytes - pathology; Astrocytes - virology; Biological and medical sciences; Cerebral Cortex - immunology; Cerebral Cortex - pathology; Cerebral Cortex - virology; Chronic Disease; Fundamental and applied biological sciences. Psychology; Glial Fibrillary Acidic Protein - metabolism; Gliosis - immunology; Gliosis - pathology; Gliosis - virology; Hyperplasia - immunology; Hyperplasia - pathology; Hyperplasia - virology; Immunohistochemistry; Junin virus - immunology; Junin virus - pathogenicity; Neurons - immunology; Neurons - pathology; Neurons - virology; Rats; Rats, Wistar; Vertebrates: nervous system and sense organs; Rat; neuronal infection; Immunocytochemistry; Chronic neurological disease; Neuroglia; Rodentia; Astrocyte; Junin virus; astrocyte activation; Infection; Vertebrata; Chronic; histocytomorphometry; Mammalia; Neuron; Animal; Viral disease
• ISSN: 0300-9564; 1435-1463
• DOI: 10.1007/s00702-003-0010-1

Immunoperoxidase labeling was performed in histological sections from rat brain harvested during acute (10-30 days), clinically inapparent (90-270 days) and late (450-540 days) stages of Junin virus-induced neurological disease. In frontoparietal cortex, count of viral antigen (+) neurons peaked during the acute period (27.7+/-6.8), dropped within the intermediate (4.8+/-4.0 to 1.4+/-1.1) and increased (7.6+/-4.3) at the onset of the late neurological syndrome. In infected vs. control rats, the number of GFAP (+) astrocytes maximized during the acute stage (19+/-4 vs. 11+/-5), and from the end of the intermediate (27+/-5 vs. 21+/-5) up to the late (37+/-7 vs. 26+/-6) periods. In turn, surface density of GFAP (+) material in infected samples peaked at 0.196+/-0.066, while it failed to exceed 0.090+/-0.043 in controls. Both astrocyte hypertrophy relapsing into chronicity, as depicted by surface density, and astrocyte hyperplasia preceding the onset of the late neurological syndrome, support their pathogenic contribution to disease expression.