HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chisaka, H. Articles by Sugamura, K. Search for Related Content PubMed PubMed Citation Articles by Chisaka, H. Articles by Sugamura, K. Agricola Articles by Chisaka, H. Articles by Sugamura, K.

A transgenic mouse model for non-immune hydrops fetalis induced by the NS1 gene of human parvovirus B19

Department of Microbiology and Immunology¹ and Department of Obstetrics and Gynecology², Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan
CREST Program of the Japan Science and Technology Corporation, Sendai 980-8575, Japan³

Author for correspondence: Kazuo Sugamura. Fax +81 22 717 8097. e-mail sugamura{at}mail.cc.tohoku.ac.jp

Human parvovirus B19 (B19) infection during pregnancy is associated with the adverse foetal outcome known as non-immune hydrops fetalis (NIHF). Although B19 is known to infect erythroid-lineage cells in vivo as well as in vitro, the mechanism leading to the occurrence of NIHF is not clear. To investigate the possible involvement of the B19 non-structural protein NS1 in NIHF, three independent lines of transgenic mice were generated that expressed NS1 under the control of the Cre-loxP system and the GATA1 promoter. Two of the three lines expressed NS1 in erythroid-lineage cells. Most of the transgenic mice died at the embryonic stage, some of which developed hydropic changes caused by severe anaemia at embryonic day 15·5 (E15·5). Histological examination of embryos at E15·5 showed significantly fewer erythropoietic islands in the liver parenchyma, whereas their hearts showed no abnormal signs, such as cardiomegaly and apoptotic cells. The NS1-transgenic mouse lines established here provide an animal model for human NIHF and suggest that NS1 plays a crucial role in the adverse outcome associated with intrauterine B19 infection in humans.

This article has been cited by other articles:

				L. Abdel-Latif, B. K. Murray, R. L. Renberg, K. L. O'Neill, H. Porter, J. B. Jensen, and F. B. Johnson Cell death in bovine parvovirus-infected embryonic bovine tracheal cells is mediated by necrosis rather than apoptosis J. Gen. Virol., September 1, 2006; 87(9): 2539 - 2548. [Abstract] [Full Text] [PDF]

				R. T. Dackor, K. Fritz-Six, W. P. Dunworth, C. L. Gibbons, O. Smithies, and K. M. Caron Hydrops Fetalis, Cardiovascular Defects, and Embryonic Lethality in Mice Lacking the Calcitonin Receptor-Like Receptor Gene Mol. Cell. Biol., April 1, 2006; 26(7): 2511 - 2518. [Abstract] [Full Text] [PDF]

				N. Takasawa, Y. Munakata, K. K. Ishii, Y. Takahashi, M. Takahashi, Y. Fu, T. Ishii, H. Fujii, T. Saito, H. Takano, et al. Human Parvovirus B19 Transgenic Mice Become Susceptible to Polyarthritis J. Immunol., October 1, 2004; 173(7): 4675 - 4683. [Abstract] [Full Text] [PDF]

				E. Morita, A. Nakashima, H. Asao, H. Sato, and K. Sugamura Human Parvovirus B19 Nonstructural Protein (NS1) Induces Cell Cycle Arrest at G1 Phase J. Virol., March 1, 2003; 77(5): 2915 - 2921. [Abstract] [Full Text] [PDF]