African swine fever virus infects macrophages, the natural host cells, via clathrin- and cholesterol-dependent endocytosis

被引：77

作者：

Galindo, Inmaculada ^{[1
]}

Angel Cuesta-Geijo, Miguel ^{[1
]}

Hlavova, Karolina ^{[1
]}

Munoz-Moreno, Raquel ^{[1
]}

Barrado-Gil, Lucia ^{[1
]}

Dominguez, Javier ^{[1
]}

Alonso, Covadonga ^{[1
]}

机构：

[1] Inst Nacl Invest & Tecnol Agr & Alimentaria INIA, Dept Biotechnol, Madrid, Spain

来源：

VIRUS RESEARCH | 2015年 / 200卷

关键词：

African swine fever virus; Virus entry; Endocytosis; Macrophages; African swine fever and vaccinia virus entry; Natural host cell; MONOCLONAL-ANTIBODIES; VERO CELLS; ENTRY; MACROPINOCYTOSIS; DYNAMIN; MONOCYTES/MACROPHAGES; INTERNALIZATION; EXPRESSION; RECEPTORS; TITRATION;

D O I：

10.1016/j.virusres.2015.01.022

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The main cellular target for African swine fever virus (ASFV) is the porcine macrophage. However, existing data about the early phases of infection were previously characterized in non-leukocyte cells such as Vero cells. Here, we report that ASFV enters the natural host cell using dynamin-dependent and clathrin-mediated endocytosis. This pathway is strongly pH-dependent during the first steps of infection in porcine macrophages. We investigated the effect of drugs inhibiting several endocytic pathways in macrophages and compared ASFV with vaccinia virus (VV), which apparently involves different entry pathways. The presence of cholesterol in cellular membranes was found to be essential for a productive ASFV infection while actin-dependent endocytosis and the participation of phosphoinositide-3-kinase (PI3K) activity were other cellular factors required in the process of viral entry. These findings improved our understanding of the ASFV interactions with macrophages that allow for successful viral replication. (C) 2015 Elsevier B.V. All rights reserved.

引用

页码：45 / 55

页数：11

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