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Expression of CCR5 increases during monocyte differentiation and directly mediates macrophage susceptibility to infection by human immunodeficiency virus type 1.CCR5的表达在单核细胞分化过程中增加,并直接介导巨噬细胞对1型人类免疫缺陷病毒感染的易感性。
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Immunopathologic changes in the thymus during the acute stage of experimentally induced feline immunodeficiency virus infection in juvenile cats.幼猫实验性诱导感染猫免疫缺陷病毒急性期胸腺的免疫病理变化。
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A single amino acid substitution in the transmembrane envelope glycoprotein of feline immunodeficiency virus alters cellular tropism.猫免疫缺陷病毒跨膜包膜糖蛋白中的单个氨基酸取代改变了细胞嗜性。
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Shared usage of the chemokine receptor CXCR4 by the feline and human immunodeficiency viruses.猫免疫缺陷病毒和人类免疫缺陷病毒对趋化因子受体CXCR4的共同利用。
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猫免疫缺陷病毒分子克隆在体内的细胞嗜性差异

Differential cell tropism of feline immunodeficiency virus molecular clones in vivo.

作者信息

Dean G A, Himathongkham S, Sparger E E

机构信息

Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27606, USA.

出版信息

J Virol. 1999 Apr;73(4):2596-603. doi: 10.1128/JVI.73.4.2596-2603.1999.

DOI:10.1128/JVI.73.4.2596-2603.1999
PMID:10074104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC104014/
Abstract

Independent studies have demonstrated different cell tropisms for molecular clones of feline immunodeficiency virus (FIV). In this report, we examined three clones, FIV-pF34, FIV-14, and FIV-pPPR, for replication in Crandell feline kidney (CrFK) cells, feline peripheral blood mononuclear cells (PBMC), and feline macrophage cultures. Importantly, cell tropism for these three clones was also examined in vivo. FIV-pF34 replication was efficient in CrFK cells but severely restricted in PBMC, whereas replication of FIV-pPPR was vigorous in PBMC but severely restricted in CrFK cells. FIV-14 replication was productive in both CrFK cells and PBMC. Interestingly, all three molecular clones replicated with similar efficiencies in primary feline monocyte-derived macrophages. In vivo, FIV-pF34 proved least efficient for establishing persistent infection, and proviral DNA when detectable, was localized predominately to nonlymphoid cell populations (macrophages). FIV-pPPR proved most efficient for induction of a persistent viremia in vivo, and proviral DNA was localized predominately in CD4(+) and CD8(+) lymphocyte subsets. FIV-14 inoculation of cats resulted in an infection characterized by seroconversion and localization of proviral DNA in CD4(+) lymphocytes only. Results of this study on diverse FIV molecular clones revealed that in vitro replication efficiency of an FIV isolate in PBMC directly correlated with replication efficiency in vivo, whereas proficiency for replication in macrophages in vitro was not predictive for replication potential in vivo. Also, infection of both CD4(+) and CD8(+) lymphocyte subsets was associated with higher virus load in vivo. Results of the studies on these three FIV clones, which exhibited differential cell tropism, indicated a correlation between in vitro and in vivo cell tropism and virus replication.

摘要

独立研究已证明猫免疫缺陷病毒(FIV)分子克隆具有不同的细胞嗜性。在本报告中,我们检测了三个克隆FIV-pF34、FIV-14和FIV-pPPR在克兰德尔猫肾(CrFK)细胞、猫外周血单核细胞(PBMC)和猫巨噬细胞培养物中的复制情况。重要的是,还在体内检测了这三个克隆的细胞嗜性。FIV-pF34在CrFK细胞中复制高效,但在PBMC中受到严重限制,而FIV-pPPR在PBMC中复制活跃,但在CrFK细胞中受到严重限制。FIV-14在CrFK细胞和PBMC中均能有效复制。有趣的是,所有三个分子克隆在原代猫单核细胞衍生的巨噬细胞中复制效率相似。在体内,FIV-pF34被证明建立持续感染的效率最低,可检测到的前病毒DNA主要定位于非淋巴细胞群体(巨噬细胞)。FIV-pPPR被证明在体内诱导持续病毒血症的效率最高,前病毒DNA主要定位于CD4(+)和CD8(+)淋巴细胞亚群。给猫接种FIV-14导致感染,其特征为血清转化且前病毒DNA仅定位于CD4(+)淋巴细胞。对不同FIV分子克隆的这项研究结果表明,FIV分离株在PBMC中的体外复制效率与体内复制效率直接相关,而在体外巨噬细胞中的复制能力并不能预测其在体内的复制潜力。此外,CD4(+)和CD8(+)淋巴细胞亚群的感染与体内较高的病毒载量相关。对这三个表现出不同细胞嗜性的FIV克隆的研究结果表明,体外和体内细胞嗜性与病毒复制之间存在相关性。