Survival of parvovirus B19-infected cells by cellular autophagy

被引:64
作者
Nakashima, Akitoshi
Tanaka, Nobuyuki
Tamai, Keiichi
Kyuuma, Masanao
Ishikawa, Yoshinori
Sato, Hiroyuki
Yoshimori, Tamotsu
Saito, Shigeru
Sugamura, Kazuo
机构
[1] Tohoku Univ, Grad Sch Med, Dept Microbiol & Immunol, Aoba Ku, Sendai, Miyagi 9808575, Japan
[2] Fukuoka Red Cross Blood Ctr, Fukuoka 8188588, Japan
[3] Natl Inst Genet, Dept Cell Genet, Mishima, Shizuoka 4118540, Japan
[4] Toyama Med & Pharmaceut Univ, Sch Med, Dept Obstet & Gynecol, Toyama 9300194, Japan
基金
日本学术振兴会;
关键词
parvovirus B19; autophagy; LC3; 3-MA;
D O I
10.1016/j.virol.2006.03.029
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Human parvovirus B19 (B19) is a well-known pathogenic agent which causes apoptosis in erythrocyte lineage cells Here, we provide the first evidence that mitochondrial autophagy is specifically found in the B19-infected cells. The protein expression ratio for LC3-II/LC3-I increased significantly in infected cells, indicating possible involvement of cellular autophagy in the infection process. Immunofluorescence confocal microscopy analyses revealed that B19 infection induced an intracellular autophagosome as judged by endogenous LC3 staining. Moreover, inhibition of autophagy by 3-MA significantly facilitated B19-infection-mediated cell death. These results suggest a novel mechanism by which B19-infected cells survive by cellular autophagy. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:254 / 263
页数:10
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