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. 2001 May;75(9):4448-52.
doi: 10.1128/JVI.75.9.4448-4452.2001.

Macaques with rapid disease progression and simian immunodeficiency virus encephalitis have a unique cytokine profile in peripheral lymphoid tissues

M S Orandle  1 , K C Williams, A G MacLean, S V Westmoreland, A A Lackner
Affiliations

Macaques with rapid disease progression and simian immunodeficiency virus encephalitis have a unique cytokine profile in peripheral lymphoid tissues

M S Orandle et al. J Virol. 2001 May.

Abstract

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-1beta [IL-1beta], IL-2, IL-6, IL-10, gamma interferon [IFN-gamma], and tumor necrosis factor alpha [TNF-alpha]) 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-gamma, 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-gamma) that was associated with higher viral loads. These observations provide evidence that host cytokine responses may influence SIV neuropathogenesis independent of disease progression.

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Figures

FIG. 1
FIG. 1
Representative histologic lesion in the CNS of an SIV-infected macaque with SIVE. (A) Hematoxylin and eosin-stained section of brain demonstrating a typical lesion of SIVE consisting of perivascular accumulations of mononuclear cells and multinucleated giant cells. (B) RNA in situ hybridization for SIV transcripts demonstrating abundant viral replication within mononuclear cells and multinucleated giant cells within a lesion. Original magnification, ×400.
FIG. 2
FIG. 2
Cytokine gene expression in axillary lymph nodes of macaques infected with SIVmac251 and sacrificed at the terminal stages of disease. Bars represent mean values +/− standard error of the mean for uninfected control animals (Uninfected; n = 5) and SIV-infected animals (Infected; n = 28). Results are expressed as a ratio of cytokine mRNA/β-actin mRNA. ∗, P < 0.05.
FIG. 3
FIG. 3
Evaluation of cytokine gene expression in axillary lymph nodes of SIV-infected macaques grouped by disease progression. Animals with a survival period of ≤200 dpi were grouped together as rapid progressors (Rapid; n = 16; mean survival, 155 days) and animals with a survival period of ≥200 dpi were grouped together as slow progressors (Slow; n = 12; mean survival, 567 days). Bars denote mean values +/− standard error of the mean. Results are expressed as a ratio of cytokine mRNA/β-actin mRNA.
FIG. 4
FIG. 4
Evaluation of cytokine gene expression in axillary lymph nodes of SIV-infected macaques grouped by disease progression and pathologic outcome. Animals with a survival period of ≤200 dpi were first grouped together as rapid progressors and then subgrouped into those with SIV encephalitis (Rapid SIVE; n = 8) and those without SIV encephalitis (Rapid no SIVE; n = 8). Animals with a survival period of ≥200 dpi were grouped together as slow progressors (Slow; n = 12), and the fourth group was uninfected controls (Controls; n = 5). Bars denote mean values +/− standard error of the mean. Results are expressed as a ratio of cytokine mRNA/β-actin mRNA. ∗, P < 0.05, Rapid no SIVE versus Rapid SIVE.
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