NATURE AND SEQUENCE OF SIMIAN IMMUNODEFICIENCY VIRUS-INDUCED CENTRAL-NERVOUS-SYSTEM LESIONS - A KINETIC-STUDY

Citation
S. Czub et al., NATURE AND SEQUENCE OF SIMIAN IMMUNODEFICIENCY VIRUS-INDUCED CENTRAL-NERVOUS-SYSTEM LESIONS - A KINETIC-STUDY, Acta Neuropathologica, 92(5), 1996, pp. 487-498
Citations number
41
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
Journal title
ISSN journal
00016322
Volume
92
Issue
5
Year of publication
1996
Pages
487 - 498
Database
ISI
SICI code
0001-6322(1996)92:5<487:NASOSI>2.0.ZU;2-7
Abstract
To determine the onsets and specificities of neuropathological feature s observed after simian immunodeficiency Virus (SIV) infection of maca ques, brains of 19 clinically unaffected rhesus monkeys (group A) were examined after intervals ranging from 1 to 48 weeks postinfection and compared to 8 animals with AIDS (group B) as well as to 8 uninfected controls. Based on morphological and virological parameters, seven pat terns specific for SIV infection of the central nervous system (CNS) w ere discerned. In both groups of infected but not control animals, we found mononuclear aggregates in meninges, perivascular space, and chor oid plexus stroma (designated pattern 1), isolated infected cells with in CNS parenchyma (pattern 2), axonal degeneration (pattern 3), spongy change (pattern 4), microglial proliferation (pattern 5), and small v essel proliferation (pattern 6). SIV encephalitis (pattern 7) was only evident in animals with clinically evident disease. Changes character istic of patterns 3, 5 and 6 appeared to be chronic and non-progressiv e, whereas lesions of patterns 1, 2 and 4 appeared to have progressed in animals with AIDS. The main component of mononuclear aggregates in animals of group A were lymphocytes, in contrast to animals of group B , in which macrophages dominated the inflammatory infiltrates. Altoget her, our results demonstrate that subtle leukoencephalopathy was a spe cific feature of clinically silent as well as clinically evident phase s of SIV infection. This might explain the neurological impairment of HIV-positive non-AIDS individuals.