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拉沙病毒对人树突状细胞和巨噬细胞的感染具有增殖性,但无法激活这些细胞。

Lassa virus infection of human dendritic cells and macrophages is productive but fails to activate cells.

作者信息

Baize Sylvain, Kaplon Jérôme, Faure Caroline, Pannetier Delphine, Georges-Courbot Marie-Claude, Deubel Vincent

机构信息

Unité de Biologie des Infections Virales Emergentes, Centre de Recherche Mérieux-Pasteur à Lyon, Laboratoire P4-Jean Mérieux, Lyon, France.

出版信息

J Immunol. 2004 Mar 1;172(5):2861-9. doi: 10.4049/jimmunol.172.5.2861.

DOI:10.4049/jimmunol.172.5.2861
PMID:14978087
Abstract

Lassa fever is a hemorrhagic fever caused by Lassa virus (LV), an old-world Arenavirus. Little is known about the immune responses that occur during the disease, but protection seems to be linked to the induction of cellular responses specific for viral glycoproteins. Conversely, severe Lassa fever may be associated with immunosuppression. We studied the infection of human dendritic cells (DC) and macrophages (MP) by LV. Both these cell types are susceptible to LV infection. Viral nucleoprotein was detected in DC and MP, and high and moderate viral titers were obtained with culture supernatants of DC and MP, respectively. LV did not induce apoptosis in DC and MP. These cells were not activated by LV infection. No change was observed in the expression of surface molecules involved in activation, costimulation, adhesion, and Ag presentation following LV infection, or in the functional properties of DC. Inflammatory cytokine production was not detected at the mRNA or protein level after LV infection of DC and MP. Thus, MP, and particularly DC, are crucial targets for LV and are probably involved in the early replication of LV from the initial site of infection. The lack of activation and maturation of cells following infection may be associated with the immunosuppression observed in severe LV infection.

摘要

拉沙热是一种由拉沙病毒(LV)引起的出血热,拉沙病毒是一种旧大陆沙粒病毒。对于该疾病期间发生的免疫反应知之甚少,但保护作用似乎与诱导针对病毒糖蛋白的细胞反应有关。相反,严重的拉沙热可能与免疫抑制有关。我们研究了拉沙病毒对人树突状细胞(DC)和巨噬细胞(MP)的感染情况。这两种细胞类型均易受拉沙病毒感染。在DC和MP中检测到病毒核蛋白,并且分别从DC和MP的培养上清液中获得了高和中等的病毒滴度。拉沙病毒未诱导DC和MP凋亡。这些细胞未因拉沙病毒感染而被激活。拉沙病毒感染后,参与激活、共刺激、黏附和抗原呈递的表面分子的表达,或DC的功能特性均未观察到变化。DC和MP感染拉沙病毒后,在mRNA或蛋白质水平均未检测到炎性细胞因子的产生。因此,MP,尤其是DC,是拉沙病毒的关键靶标,可能参与了拉沙病毒从感染初始部位的早期复制。感染后细胞缺乏激活和成熟可能与严重拉沙病毒感染中观察到的免疫抑制有关。

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