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Short Communication |
1 Institute of Diagnostic Virology, Friedrich-Loeffler-Institut, Suedufer 10, 17493 Greifswald, Germany
2 Institute of Infectology, Friedrich-Loeffler-Institut, Suedufer 10, 17493 Greifswald, Germany
3 Institute for Medical Microbiology, Infectious and Epidemic Diseases, Faculty of Veterinary Medicine, Ludwig Maximilians University Munich, Germany
Correspondence
Martin Beer
martin.beer{at}fli.bund.de
The role of the UL49 gene product, VP22, of bovine herpesvirus type 1 (BoHV-1) in virus replication was characterized with respect to a putative functional interaction of VP22 with the viral glycoprotein E (gE) during BoHV-1 cell-to-cell spread. Deletion of the open reading frames of UL49 and/or gE from an infectious BoHV-1 bacterial artificial chromosome clone did not severely impair the production of viral progeny in single-step growth experiments. However, plaque sizes induced by a VP22-negative BoHV-1 were reduced by 52 %, whilst for the gE/VP22-negative double-deletion mutant a reduction of 83 % could be observed in comparison with parental and revertant viruses, which was consistent with a marked reduction in multi-step growth experiments at early time points. These results suggest that gE and VP22 are important for BoHV-1 cell-to-cell spread, and that both are likely to act independently of each other in a critical pathway for virus cell-to-cell spread.
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