Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis

Sha Mi, Xinhua Lee, Xiang-ping Li, Geertruida M. Veldman, Heather Finnerty, Lisa Racie, Edward LaVallie, Xiang-Yang Tang, Philippe Edouard, Steve Howes, James C. Keith and John M. McCoy ()
Additional contact information
Sha Mi: Genetics Institute, Inc.
Xinhua Lee: Genetics Institute, Inc.
Xiang-ping Li: Genetics Institute, Inc.
Geertruida M. Veldman: Genetics Institute, Inc.
Heather Finnerty: Genetics Institute, Inc.
Lisa Racie: Genetics Institute, Inc.
Edward LaVallie: Genetics Institute, Inc.
Xiang-Yang Tang: Genetics Institute, Inc.
Philippe Edouard: Genetics Institute, Inc.
Steve Howes: Genetics Institute, Inc.
James C. Keith: Genetics Institute, Inc.
John M. McCoy: Genetics Institute, Inc.

Nature, 2000, vol. 403, issue 6771, 785-789

Abstract: Abstract Many mammalian viruses have acquired genes from their hosts during their evolution1. The rationale for these acquisitions is usually quite clear: the captured genes are subverted to provide a selective advantage to the virus. Here we describe the opposite situation, where a viral gene has been sequestered to serve an important function in the physiology of a mammalian host. This gene, encoding a protein that we have called syncytin, is the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W2. We find that the major sites of syncytin expression are placental syncytiotrophoblasts, multinucleated cells that originate from fetal trophoblasts. We show that expression of recombinant syncytin in a wide variety of cell types induces the formation of giant syncytia, and that fusion of a human trophoblastic cell line expressing endogenous syncytin can be inhibited by an anti-syncytin antiserum. Our data indicate that syncytin may mediate placental cytotrophoblast fusion in vivo, and thus may be important in human placental morphogenesis.

Date: 2000
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DOI: 10.1038/35001608

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