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
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.