期刊
JOURNAL OF VIROLOGY
卷 76, 期 11, 页码 5797-5802出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.76.11.5797-5802.2002
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资金
- NCRR NIH HHS [P51 RR000168, RR000168, P51 RR000164, K26 RR000168, RR000164] Funding Source: Medline
- NIMH NIH HHS [MH61192, R01 MH061192] Funding Source: Medline
- NINDS NIH HHS [R01 NS030769, NS30769, NS35732] Funding Source: Medline
Inflammatory cytokines are believed to play an important role in the pathogenesis of human immunodeficiency virus type 1-associated encephalitis. To examine this in the simian immunodeficiency virus (SIV)infected macaque model of neuroAIDS, inflammatory cytokine gene expression was evaluated in the brains of macaques infected with pathogenic SIVmac251 by reverse transcriptase PCR. Interleukin-1 beta was readily detected in the brains of all animals evaluated, regardless of infection status or duration of infection. Tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) transcripts were undetectable in the brains of uninfected control animals but were upregulated at 7 and 14 days postinoculation. At the terminal stage of infection, TNF-alpha and IFN-gamma transcripts were coexpressed in the brains of four of five animals with SIV encephalitis (SIVE). Within an encephalitic brain, TNF-alpha and IFN-gamma transcripts were detected in six of seven regions with histologic evidence of SIVE, suggesting a direct relationship between neuropathology and altered cytokine gene expression. With combined fluorescent in situ hybridization and immunofluorescence, TNF-alpha-expressing cells were frequently identified as CD68-positive macrophages within perivascular lesions. These observations provide evidence that cytokines produced by activated inflammatory macrophages are an important element in the pathogenesis of SIVE.
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