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Avian polyomavirus mutants with deletions in the VP4-encoding region show deficiencies in capsid assembly and virus release, and have reduced infectivity in chicken

Reimar Johne^1,

¹ Institute for Virology, Faculty of Veterinary Medicine, University of Leipzig, An den Tierkliniken 29, D-04103 Leipzig, Germany
² Intervet International, Wim de Körverstraat 35, 5830 AA Boxmeer, The Netherlands
³ Department of Anatomy, Histology and Embryology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany
⁴ Institute for Avian Diseases, Ludwig Maximilians University Munich, Sonnenstraße 18, D-85764 Oberschleißheim, Germany

Correspondence
Reimar Johne
Reimar.Johne{at}bfr.bund.de

Avian polyomavirus (APV) is the causative agent of an acute fatal disease in psittacine and some non-psittacine birds. In contrast to mammalian polyomaviruses, the APV genome encodes the additional capsid protein VP4 and its variant VP4, truncated by an internal deletion. Both proteins induce apoptosis. Mutation of their common initiation codon prevents virus replication. Here, the generation of replication competent deletion mutants expressing either VP4 or VP4 is reported. In contrast to infection with wild-type virus, chicken embryo cells showed no cytopathic changes after infection with the mutants, and induction of apoptosis as well as virus release from the infected cells were delayed. Electron microscopy revealed the presence of a high proportion of small particles and tubules in preparations of the VP4 deletion mutant, indicating a scaffolding function for VP4. Wild-type and mutant viruses elicited neutralizing antibodies against APV after intramuscular and intraperitoneal infection of chicken; however, VP4-specific antibodies were only detected after infection with wild-type virus. Using the oculonasal route of infection, seroconversion was only observed in chickens infected with the wild-type virus, indicating a strongly reduced infectivity of the mutants. Based on the biological properties of the deletion mutants, they could be considered as candidates for APV marker vaccines.

Present address: Federal Institute for Risk Assessment, Diedersdorfer Weg 1, D-12277 Berlin, Germany.

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