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本文引用的文献

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Quantitation of human immunodeficiency virus, immune activation factors, and quinolinic acid in AIDS brains.
J Clin Invest. 1993 Jun;91(6):2769-75. doi: 10.1172/JCI116518.
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HIV infection is active and progressive in lymphoid tissue during the clinically latent stage of disease.在疾病的临床潜伏期,HIV感染在淋巴组织中活跃且呈进行性发展。
Nature. 1993 Mar 25;362(6418):355-8. doi: 10.1038/362355a0.
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Apoptosis induced by tumor necrosis factor in cells chronically infected with feline immunodeficiency virus.肿瘤坏死因子在慢性感染猫免疫缺陷病毒的细胞中诱导的细胞凋亡。
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Kinetics of human immunodeficiency virus type 1 (HIV-1) DNA and RNA synthesis during primary HIV-1 infection.人类免疫缺陷病毒1型(HIV-1)初次感染期间HIV-1 DNA和RNA合成的动力学
Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6405-9. doi: 10.1073/pnas.90.14.6405.
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Detection and localization of HIV RNA and TNF mRNA in rectal biopsies from patients with AIDS.艾滋病患者直肠活检组织中HIV RNA和TNF mRNA的检测与定位
Cytokine. 1993 Jul;5(4):305-8. doi: 10.1016/1043-4666(93)90061-9.
6
Induction of apoptosis in a T lymphoblastoid cell line infected with feline immunodeficiency virus.感染猫免疫缺陷病毒的T淋巴母细胞系中细胞凋亡的诱导
Arch Virol. 1994;135(1-2):153-8. doi: 10.1007/BF01309772.
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Primary stage of feline immunodeficiency virus infection: viral dissemination and cellular targets.猫免疫缺陷病毒感染的初期阶段:病毒传播及细胞靶点
J Virol. 1994 May;68(5):3080-91. doi: 10.1128/JVI.68.5.3080-3091.1994.
8
Massive covert infection of helper T lymphocytes and macrophages by HIV during the incubation period of AIDS.在艾滋病潜伏期,人类免疫缺陷病毒对辅助性T淋巴细胞和巨噬细胞进行大量隐匿性感染。
Nature. 1993 Mar 25;362(6418):359-62. doi: 10.1038/362359a0.
9
The immunopathogenesis of human immunodeficiency virus infection.人类免疫缺陷病毒感染的免疫发病机制。
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10
An experimental study of primary feline immunodeficiency virus infection in cats and a historical comparison to acute simian and human immunodeficiency virus diseases.猫原发性猫免疫缺陷病毒感染的实验研究以及与急性猿猴和人类免疫缺陷病毒疾病的历史比较。
Vet Immunol Immunopathol. 1994 Nov;43(4):337-55. doi: 10.1016/0165-2427(94)90156-2.

肿瘤坏死因子α与猫免疫缺陷病毒表达之间的关系。

Relationship between tumor necrosis factor alpha and feline immunodeficiency virus expressions.

作者信息

Kraus L A, Bradley W G, Engelman R W, Brown K M, Good R A, Day N K

机构信息

Department of Medical Microbiology and Immunology, University of South Florida, Tampa 33612, USA.

出版信息

J Virol. 1996 Jan;70(1):566-9. doi: 10.1128/JVI.70.1.566-569.1996.

DOI:10.1128/JVI.70.1.566-569.1996
PMID:8523571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC189845/
Abstract

The presence of feline immunodeficiency virus (FIV) proviral DNA, expression of FIV p26 core protein, and production of tumor necrosis factor alpha (TNF-alpha) were assessed in sequential biopsies of spleen and lymph node sections, of mononuclear cells of the peripheral blood, and of the serum of specific-pathogen-free cats during the acute phase of FIV infection. A temporal relationship between TNF-alpha production and FIV p26 expression was noted. Two months following FIV infection, and preceding the detection of FIV viremia, levels of TNF-alpha in serum increased significantly (P = 0.04), and they remained elevated during FIV viremia in the third month postinfection. Immunoprecipitates representing expression of TNF-alpha and of FIV p26 were localized in common foci of lymph nodes of FIV-infected cats during this period of active viremia. With the advent of anti-FIV antibodies, circulating levels of TNF-alpha and p26 antigen and expression of TNF-alpha and p26 in the lymph nodes decreased during the fifth month postinfection, and p26 production became undetectable. With clearance of viremia, burden of proviral DNA in peripheral blood mononuclear cells became reduced (P = 0.041), with provirus remaining integrated principally within lymph nodes (P = 0.046). During aviremia, p26 expression was undetectable in any tissue but remained inducible in vitro. During acute FIV infection, TNF-alpha production and p26 expression are intimately linked.

摘要

在猫免疫缺陷病毒(FIV)感染急性期,对无特定病原体猫的脾脏和淋巴结切片、外周血单个核细胞及血清进行连续活检,评估FIV前病毒DNA的存在、FIV p26核心蛋白的表达以及肿瘤坏死因子α(TNF-α)的产生。发现TNF-α产生与FIV p26表达之间存在时间关系。FIV感染两个月后,在检测到FIV病毒血症之前,血清中TNF-α水平显著升高(P = 0.04),且在感染后第三个月FIV病毒血症期间一直维持在较高水平。在此活跃病毒血症期间,代表TNF-α和FIV p26表达的免疫沉淀物定位于FIV感染猫淋巴结的共同病灶中。随着抗FIV抗体的出现,感染后第五个月,TNF-α和p26抗原的循环水平以及淋巴结中TNF-α和p26的表达下降,且无法检测到p26的产生。随着病毒血症的清除,外周血单个核细胞中前病毒DNA的负荷降低(P = 0.041),前病毒主要仍整合在淋巴结内(P = 0.046)。在无病毒血症期间,任何组织中均未检测到p26表达,但在体外仍可诱导表达。在急性FIV感染期间,TNF-α产生与p26表达密切相关。