Role of interferons in the control of Lassa virus replication in human dendritic cells and macrophages

被引：62

作者：

Baize, S ^{[1
]}

Pannetier, D ^{[1
]}

Faure, C ^{[1
]}

Marianneau, P ^{[1
]}

Marendat, I ^{[1
]}

Georges-Courbot, MC ^{[1
]}

Deubel, V ^{[1
]}

机构：

[1] Inst Pasteur, Unite Biol Infect Virales Emergentes, Lab Jean Merieux P4, F-69365 Lyon 07, France

来源：

MICROBES AND INFECTION | 2006年 / 8卷 / 05期

关键词：

antigen-presenting cell; arenavirus; human; innate immunity;

D O I：

10.1016/j.micinf.2006.02.002

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Lassa fever is a hemorrhagic fever caused by Lassa virus (LV), which primarily targets human dendritic cells (DC) and macrophages (MP). Massive numbers of viral particles are released with no effect on the viability, activation or maturation of these cells. LV does not inhibit the activation of cells induced by sCD40L or LPS. We report here the consequences of exogenous activation of LV-infected human DC and MP for viral replication. The activation of cells with lipopolysaccharide or exogenous poly(I-C) and the transfection of cells with poly(I-C) strongly inhibited LV replication, at least partly by inducing type I interferon (IFN) synthesis. In contrast, cell stimulation with sCD40L did not induce type I IFN responses or inhibit LV release. Recombinant type I IFNs strongly inhibited LV replication in both cell types, whereas IFN gamma and IFN lambda, did not. The modest type I IFN production observed in LV-infected MP, but not in DC, was involved in controlling LV replication in MP. These results provide an explanation for the slower replication of LV in MP than in DC, and suggest that type I IFNs are crucial in the control of LV. (c) 2006 Elsevier SAS. All rights reserved.

引用

页码：1194 / 1202

页数：9

共 39 条

[1] Inhibition of different lassa virus strains by alpha and gamma interferons and comparison with a less pathogenic arenavirus [J].