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

来源：

JOURNAL OF VIROLOGY | 2004年 / 78卷 / 21期

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

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页码：12090 / 12095

页数：6

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