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. 2012 Feb;18(2):234-41.
doi: 10.3201/eid1802.111525.

Pathogenesis of avian bornavirus in experimentally infected cockatiels

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Pathogenesis of avian bornavirus in experimentally infected cockatiels

Anne K Piepenbring et al. Emerg Infect Dis. 2012 Feb.

Abstract

Avian bornavirus (ABV) is the presumed causative agent of proventricular dilatation disease (PDD), a major fatal disease in psittacines. However, the influencing factors and pathogenesis of PDD are not known and natural ABV infection exhibits remarkable variability. We investigated the course of infection in 18 cockatiels that were intracerebrally and intravenously inoculated with ABV. A persistent ABV infection developed in all 18 cockatiels, but, as in natural infection, clinical disease patterns varied. Over 33 weeks, we simultaneously studied seroconversion, presence of viral RNA and antigens, infectious virus, histopathologic alterations, and clinical signs of infection in the ABV-infected birds. Our study results further confirm the etiologic role of ABV in the development of PDD, and they provide basis for further investigations of the pathogenetic mechanisms and disease-inducing factors for the development of PDD.

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Figures

Figure 1
Figure 1
Timing of the first detection of avian bornavirus (ABV) RNA in cockatiels that had been intracerebrally or intravenously inoculated with ABV. ABV RNA was amplified significantly earlier in samples from intracerebrally inoculated birds compared with intravenously inoculated birds (α = 0.005 by using the Wilcoxon-Mann-Whitney test). A noninoculated sentinel bird, which was housed with the intracerebrally inoculated group of cockatiels, was the last bird to shed ABV RNA.
Figure 2
Figure 2
Timing of the first detection of antibodies against avian bornavirus (ABV) in cockatiels that had been intracerebrally or intravenously inoculated with ABV. The time of ABV antibody detection did not differ substantially between the 2 inoculation groups.
Figure 3
Figure 3
Avian bornavirus antibody in cockatiels inoculated intracerebrally (A) and intravenously (B) with avian bornavirus. In both groups, an exponential rise in antibody titers was detected within the first 12 weeks after inoculation and was followed by a plateau of high antibody titers (<20,480).
Figure 4
Figure 4
Detection of avian bornavirus (ABV) RNA in different tissues from cockatiels that had been intracerebrally or intravenously inoculated with ABV and from a noninoculated sentinel bird. The geometric mean cycle thresholds (Ct) are shown with their respective standard deviations. Ct >36.0 is considered negative. Low Ct, implying high amounts of ABV RNA, was detected in neuronal and gastrointestinal tissue.

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