DC-SIGN and DC-SIGNR interact with the glycoprotein of Marburg virus and the S protein of severe acute respiratory syndrome coronavirus

被引:293
作者
Marzi, A
Gramberg, T
Simmons, G
Moller, P
Rennekamp, AJ
Krumbiegel, M
Geier, M
Eisemann, J
Turza, N
Saunier, B
Steinkasserer, A
Becker, S
Bates, P
Hofmann, H
Pöhlmann, S
机构
[1] Univ Erlangen Nurnberg, Nikolaus Fiebiger Ctr, D-91054 Erlangen, Germany
[2] Univ Erlangen Nurnberg, Inst Clin & Mol Virol, D-91054 Erlangen, Germany
[3] Univ Erlangen Nurnberg, Dept Dermatol, D-91054 Erlangen, Germany
[4] Univ Marburg, Inst Virol, D-3550 Marburg, Germany
[5] Univ Penn, Dept Microbiol, Philadelphia, PA 19104 USA
[6] Ohio Univ, Coll Osteopath Med, Athens, OH 45701 USA
[7] Ohio Univ, Edison Biotechnol Inst, Athens, OH 45701 USA
关键词
D O I
10.1128/JVI.78.21.12090-12095.2004
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The lectins DC-SIGN and DC-SIGNR can augment viral infection; however, the range of pathogens interacting with these attachment factors is incompletely defined. Here we show that DC-SIGN and DC-SIGNR enhance infection mediated by the glycoprotein (GP) of Marburg virus (MARV) and the S protein of severe acute respiratory syndrome coronavirus and might promote viral dissemination. SIGNR1, a murine DC-SIGN homologue, also enhanced infection driven by MARV and Ebola virus GP and could be targeted to assess the role of attachment factors in filovirus infection in vivo.
引用
收藏
页码:12090 / 12095
页数:6
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