Avian Polyomavirus: An Overview

Ritchie, Branson W.; Niagro, Frank D.; Latimer, Kenneth S.; Davis, Richard A.; Pesti, Denise; Lukert, P. D.

doi:10.2307/27671041

Cited by 26 publications

(22 citation statements)

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“…There is a great diversity in cell types concerned by these inclusions, but they are never totally absent in avian hosts (15). Various examinations performed previously (1,18) and during this work failed to identify such inclusions in birds diagnosed with HNEG.…”

Section: Discussionmentioning

confidence: 81%

“…An acute nature is therefore highly unusual in the Polyomavirus genus (5). Only BFDVs were shown to be associated with fulminant diseases in psittacines, finches, and falconides, with a clinical evolution, lesions, and epidemiologic features that are dramatically different among susceptible species (6,9,15). Clinical signs and gross lesions associated with these infections show an amazing likeness with descriptions of HNEG: the most reliable features are an acute death with poor or no premonitory signs and lesions, including ascites, subcutaneous edema, nephritis, and intestinal hemorrhages (1,15,19).…”

Section: Discussionmentioning

confidence: 98%

“…At the cellular level, GHPV probably actively replicates in B cells, as suggested by the medullar lympholysis observed in the bursa of Fabricius. This elective replication in B cells is described in other polyomavirus infections such as BK virus, JC virus, and BFDV infections (6,15,20). In addition, histopathology suggests that GHPV shows a wide tropism for various cell types, like all APVs (15).…”

Section: Discussionmentioning

confidence: 99%

“…This elective replication in B cells is described in other polyomavirus infections such as BK virus, JC virus, and BFDV infections (6,15,20). In addition, histopathology suggests that GHPV shows a wide tropism for various cell types, like all APVs (15). In contrast, most mammalian polyomaviruses display a restricted tropism for a few cell types (12).…”

Section: Discussionmentioning

confidence: 99%

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A Novel Polyomavirus (Goose Hemorrhagic Polyomavirus) Is the Agent of Hemorrhagic Nephritis Enteritis of Geese

Guérin

Gelfi

Dubois

et al. 2000

J Virol

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We have identified the etiological agent of hemorrhagic nephritis enteritis of geese (HNEG), a fatal disease of European geese. HNEG has been recognized in almost all goose breeding areas, with an epizootic pattern, and up to now, the infectious agent has remained unknown. In order to identify the causative agent, infected tissues from HNEG-affected geese were inoculated to 1-day-old goslings, which then developed clinical signs typical of HNEG. Tissue homogenates from these birds were subjected to Freon extraction followed by sucrose density gradient ultracentrifugation. The resulting main band was examined by electron microscopy and consisted of spherical, naked, papovavirus-like particles approximately 45 nm in diameter. The virus was isolated and propagated in goose kidney cell primary culture. Tissue-or culture-purified virus allowed the experimental reproduction of the disease in goslings. Random PCR amplification of viral nucleic acid produced a 1,175-bp fragment which was shown to be associated with field samples collected from geese affected by HNEG on commercial farms in France. Sequence analysis of the PCR product revealed a unique open reading frame, showing 63 to 72% amino acid similarity with the major capsid protein (VP1) of several polyomaviruses. Finally, based on phylogenetic analysis, we conclude that the causative agent of HNEG is closely related to but clearly distinct from other polyomaviruses; we thus have named this newly identified virus Goose hemorrhagic polyomavirus.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A Novel Polyomavirus (Goose Hemorrhagic Polyomavirus) Is the Agent of Hemorrhagic Nephritis Enteritis of Geese

Guérin

Gelfi

Dubois

et al. 2000

J Virol

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“…In budgerigars, APV causes enlarged clear basophilic or amphophilic nuclear inclusions in liver, kidney and spleen (Ritchie et al, 1991) although inclusions may also be found in many other tissues such as skin, feather, feather follicle, uropygial gland, crop, lung, heart, bone marrow and brain. Ultrastructurally, viral particles first appear in swollen nuclei and they may subsequently be found in the cytoplasm of more senescent cells (Dykstra & Bozeman, 1982).…”

Section: Introductionmentioning

confidence: 99%

A concurrent outbreak of psittacine beak and feather disease virus, and avian polyomavirus infection in budgerigars(Melopsittacus undulatus)

Ramis¹,

Latimer

Gibert³

et al. 1998

Avian Pathology

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A dual natural infection with psittacine beak and feather disease virus and budgerigar fledgling disease virus in a breeding aviary of budgerigars (Melopsittacus undulatus) is described. One-hundred per cent of newly-hatched birds were affected and mortality was high (85%). Most surviving birds had diarrhoea, feather alterations and 30% mortality after a 5-to 10-week period. Necropsies of 1-week-old and 2-month-old birds demonstrated non-specific lesions, but histologically nuclear inclusions suggestive of viral infection (adenovirus, herpesvirus, polyomavirus) and also cytoplasmic inclusions suggestive of beak and feather disease were seen in integument and internal organs. Staining of tissues with viral specific DNA probes for psittacine beak and feather disease virus and for avian polyomavirus demonstrated simultaneous presence of viral DNA from both viruses in some birds. This is the first description of a concurrent outbreak of psittacine beak and feather disease virus and avian polyomavirus infection in a breeding aviary.

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