Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
Serial pathogenesis study of SIV brain infection.
Symp Nonhum Primate Models AIDS. 1990 Nov 28-30;8:36 (abstract no. 20). Unique Identifier : AIDSLINE PRIM8/900020 Sharer LR; Michaels J; Murphey-Corb M; HU FS; Kuebler DJ; Baskin GB; New Jersey Medical School, Newark, NJ
Abstract:
In order to determine the early sequence of events in the central nervous system (CNS) following experimental SIV infection, in situ hybridization (ISH) using a radiolabeled RNA probe of SIV/Delta D915 was performed on snap frozen brain tissue from 24 juvenile rhesus macaques. Twenty animals (nursery reared and CMV free) were inoculated at 8 months of age with SIV/Delta B670; there were 4 age matched controls. Four infected animals were sacrificed at each time interval: 2, 4, 8, and 24 weeks post inoculation; four became moribund and were sacrificed at 10, 11 1/2, 20 and 23 weeks. Brain tissue from at least three different anatomic sites was probed in each animal. In addition, formalin fixed tissue was evaluated for histopathology and for the presence of SIV antigen by immunocytochemistry (IC), using both a rabbit polyclonal antiserum to SIV and a mouse monoclonal antibody to p26 core antigen of SIV. ISH for SIV nucleic acid sequences on frozen sections proved to be the most sensitive of the techniques employed to detect the presence of virus, although it tended to confirm the histopathological and IC findings from the fixed tissues. Only one animal had positive signal at 2 weeks, in rare cells in leptomeninges (LM). An animal with parenchymal lesions at 4 weeks had abundant signal in LM and parenchyma, while 2 others had signal in LM only. Positive signal was first detected in choroid plexus stroma at 8 weeks but could not be confirmed at earlier time points, despite the presence of inflammation and possible antigen staining at this site. The 2 moribund animals at 10 and 11 1/2 weeks had the most severe lesions and also had the greatest amount of parenchymal signal. Positive ISH for SIV in brain parenchyma was chiefly located in perivascular inflammatory infiltrates in white matter, with a smaller number of perivascular lesions in gray matter; occasional positive cells could however be detected away from vessels in the cerebral cortex. A rare cell on the luminal side of blood vessels exhibited signal, but this was always seen in association with positive inflammatory cells in and around the vessel wall. No positive endothelial cells were detected in uninflamed vessels. Morphologically identified nerve cells were uniformly negative. The first appearance of SIV nucleic acid sequences in the CNS was in LM, followed by detection in the parenchyma about blood vessels. The severity of CNS disease correlated with the severity and rapidity of systemic disease, rather than with the duration of the SIV infection.
Keywords: Animal Antibodies, Monoclonal/IMMUNOLOGY Antigens, Viral/ANALYSIS Base Sequence Central Nervous System Diseases/*MICROBIOLOGY/PATHOLOGY Cerebral Cortex/BLOOD SUPPLY/MICROBIOLOGY Choroid Plexus/MICROBIOLOGY Macaca mulatta Myelin Sheath/MICROBIOLOGY RNA Probes Sensitivity and Specificity Simian Acquired Immunodeficiency Syndrome/*COMPLICATIONS/ PATHOLOGY Staining SIV/IMMUNOLOGY/*PHYSIOLOGY ABSTRACT 910730
M9170974
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
