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Inhibition of bovine sperm–zona binding by bovine herpesvirus-1

¹ Departments of Reproduction, Obstetrics and Herd Health and ² Physiology, Biochemistry and Biometry, Faculty of Veterinary Medicine, University of Ghent, Salisburylaan 133, 9820 Merelbeke, Belgium, ³ Department of Virology, Veterinary and Agrochemical Research Center, 1180 Brussels, Belgium, ⁴ Veterinary Virology, Faculty of Veterinary Medicine, University of Liege, 4000 Liege, Belgium, ⁵ Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada, ⁶ Department of Molecular Biotechnology, Faculty of Agricultural and Applied Biological Sciences, University of Ghent, 9000 Ghent, Belgium, ⁷ Laboratory of Virology, Department of Virology, Parasitology and Immunology, Faculty of Veterinary Medicine, University of Ghent, 9820 Merelbeke, Belgium

Correspondence should be addressed to A Van Soom; Email: ann.vansoom{at}UGent.be

The purpose of the present study was to identify a potential interference of bovine herpesvirus-1 (BoHV-1) with sperm–oocyte interactions during bovine in vitro fertilization. An inhibition of almost 70% of sperm–zona binding was observed when bovine cumulus-denuded oocytes were inseminated in the presence of 10⁷ 50% tissue culture infective dose/ml BoHV-1. The inhibitory effect of BoHV-1 on sperm–zona binding was mediated by an interaction of the virus with spermatozoa, but not with oocytes. Treatment of spermatozoa with BoHV-1, however, did not affect sperm motility and acrosomal status. Antiserum against BoHV-1 prevented the virus-induced inhibition of sperm–zona binding, indicating that BoHV-1 itself affects the fertilization process. In order to investigate which BoHV-1 glycoprotein(s) are responsible for the virus–sperm interaction, BoHV-1 was treated with monoclonal antibodies against the viral glycoproteins gB, gC, gD and gH prior to insemination. Anti-gC completely prevented the inhibitory effect of BoHV-1 on sperm–zona binding, while anti-gD caused a reduction of this inhibition. Further evidence for the involvement of gC and gD in the virus–sperm interaction was provided by the fact that purified gC and gD decreased sperm–zona binding in a dose-dependent way with gC being more effective than gD. These results indicated that BoHV-1 inhibits bovine sperm–zona binding by interacting with spermatozoa. The binding of BoHV-1 to a spermatozoon is mediated by the viral glycoproteins gC and gD, and therefore seems to be comparable with the mechanisms of BoHV-1 attachment to its natural host cell.