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1 Institute for Medical Microbiology, Infectious and Epidemic Diseases, Ludwig-Maximilians-Universität München, Veterinärstr. 13, D-80539 Munich, Germany
2 Institute for Comparative Tropical Medicine and Parasitology, Ludwig-Maximilians-Universität München, Leopoldstraße 5, D-80802 Munich, Germany
3 Boehringer Ingelheim Vetmedica GmbH, D-55216 Ingelheim, Germany
Correspondence
Antonie Neubauer
toni.neubauer{at}micro.vetmed.uni-muenchen.de
To analyse the function of the equid herpesvirus 4 (EHV-4) glycoprotein M homologue (gM), two different mutated viruses (E4
gM-GFP and E4
gM-w) were generated. Both gM-negative EHV-4-mutants were characterized on complementing and on non-complementing cells and compared with E4RgM, a virus where gM-expression had been repaired. It was demonstrated in virus growth kinetics that deleting gM had a more dramatic influence on EHV-4 replication than expected. Extracellular infectivity was detected 912 h later than in EHV-4-infected Vero cells and titres were reduced up to 2000-fold. In addition, mean maximal diameters of plaques were less than 20 % of diameters of wild-type plaques. These results are in contrast to most other alphaherpesviruses, including the closely related equid herpesvirus type 1, where deletion of gM only marginally influences the ability of viruses to replicate in cell culture. Nevertheless, analysis of infected cells by electron microscopy did not reveal a specific defect for deleting gM. It was concluded that EHV-4 gM is important for more than one step in virus replication in cell culture, influencing both efficient virus egress and cell-to-cell spread.
Present address: MSD Sharp&Dohme GmbH; D-85440 Haar, Germany.
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