Journal of Virology, May 2001, p. 4448-4452, Vol. 75, No. 9
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.9.4448-4452.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Division of Comparative Pathology, New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772
Received 20 October 2000/Accepted 24 January 2001
The influence of host cytokine response on viral load, disease
progression, and neurologic lesions was investigated in the simian
immunodeficiency virus (SIV)-infected macaque model of AIDS. Cytokine
gene expression (interleukin-1
[IL-1
], IL-2, IL-6, IL-10, gamma
interferon [IFN-
], and tumor necrosis factor alpha [TNF-
])
and viral loads were evaluated by semiquantitative reverse
transcription-PCR in lymph nodes of 5 control animals and 28 animals
infected with SIVmac251 at the terminal stages of AIDS. Infected
animals showed higher expression of IFN-
, IL-6, and IL-10 mRNAs
compared with controls. Levels of all cytokines were comparable between
animals with rapid (survival, <200 days) or slow/normal (survival,
>200 days) disease progression. However, among rapid progressors, the
eight animals with SIV encephalitis had a unique cytokine profile
(increased IL-2, IL-6, and IFN-
) that was associated with higher
viral loads. These observations provide evidence that host cytokine
responses may influence SIV neuropathogenesis independent of disease progression.
Present address: Beth Israel Deaconess Medical Center, Boston, MA 02215.
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