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Journal of Virology, April 2004, p. 3872-3879, Vol. 78, No. 8
0022-538X/04/$08.00+0 DOI: 10.1128/JVI.78.8.3872-3879.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Infectious and Parasitic Diseases, Virology, and Immunology,1 Laboratory of General Pathology, Department of Morphology and Pathology, Faculty of Veterinary Medicine, University of Liège, B-4000 Liège,4 Division of Animal Virology, CER, B-6900 Marloie, Belgium,2 Institute of Molecular Biology, Friedrich Loeffler Institutes, Federal Research Centre for Virus Diseases of Animals, 17493 Greifswald-Insel Riems, Germany3
Received 30 September 2003/ Accepted 24 December 2003
Homologous recombination between strains of the same alphaherpesvirus species occurs frequently both in vitro and in vivo. This process has been described between strains of herpes simplex virus type 1, herpes simplex virus type 2, pseudorabies virus, feline herpesvirus 1, varicella-zoster virus, and bovine herpesvirus 1 (BoHV-1). In vivo, the rise of recombinant viruses can be modulated by different factors, such as the dose of the inoculated viruses, the distance between inoculation sites, the time interval between inoculation of the first and the second virus, and the genes in which the mutations are located. The effect of the time interval between infections with two distinguishable BoHV-1 on recombination was studied in three ways: (i) recombination at the level of progeny viruses, (ii) interference induced by the first virus infection on ß-galactosidase gene expression of a superinfecting virus, and (iii) recombination at the level of concatemeric DNA. A time interval of 2 to 8 h between two successive infections allows the establishment of a barrier, which reduces or prevents any successful superinfection needed to generate recombinant viruses. The dramatic effect of the time interval on the rise of recombinant viruses is particularly important for the risk assessment of recombination between glycoprotein E-negative marker vaccine and field strains that could threaten BoHV-1 control and eradication programs.
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