Detection of Immunoreactivity to Psittaciform Bornavirus in the Serum of a Wild Cacatuid in Victoria, Australia.

An indirect immunofluorescence serologic assay, PCR assay, and histopathology were used to screen for psittaciform orthobornaviruses (PaBV) in wild Cacatuidae in Victoria, Australia. Anti-PaBV antibodies were detected, but PCR and histopathology did not detect PaBV. This study presents the first evidence of PaBV in wild birds in Australia.

Plasma protein, haematologic and blood chemistry changes in African grey parrots (Psittacus erithacus) experimentally infected with bornavirus.

Bornaviruses are considered to be the causative agent of proventricular dilatation disease (PDD) in psittacine birds. In order to detect haematological and blood chemistry changes during the development of PDD and a possible correlation with clinical signs and the virological status, six African grey parrots (Psittacus erithacus) were experimentally infected with parrot bornavirus 4 (PaBV-4) by subcutaneous route. All six parrots developed clinical signs of varying extent and successful infection was confirmed in all the birds by seroconversion or detection of RNA of the PaBV-4 infection strain. Based on population-based and intra-individual reference ranges established during 12 months prior to experimental infection, only minor haematological changes were detected in individual birds after infection. Changes in blood chemistry were restricted to aspartate aminotransferase, creatine kinase, total protein, glucose and uric acid. Plasma protein electrophoresis revealed marked changes starting 10 weeks post infection characterized by an increase in the γ-globulin fraction and a gradual decrease to normal values during weeks 22-34. Indications of an acute-phase reaction at the initial stages of infection were not detected. While three birds suffered from clinical signs of PDD, which included weight loss and neurological disorders and died before development of haematological and plasma protein changes, recovery of clinical disease was paralleled in the remaining birds by an increase in γ-globulins and bornavirus-specific antibody titres.

Viral vector vaccines expressing nucleoprotein and phosphoprotein genes of avian bornaviruses ameliorate homologous challenge infections in cockatiels and common canaries.

Avian bornaviruses are causative agents of proventricular dilatation disease (PDD), an often fatal disease of parrots and related species (order Psittaciformes) which is widely distributed in captive psittacine populations and may affect endangered species. Here, we established a vaccination strategy employing two different well described viral vectors, namely recombinant Newcastle disease virus (NDV) and modified vaccinia virus Ankara (MVA) that were engineered to express the phosphoprotein and nucleoprotein genes of two avian bornaviruses, parrot bornavirus 4 (PaBV-4) and canary bornavirus 2 (CnBV-2). When combined in a heterologous prime/boost vaccination regime, NDV and MVA vaccine viruses established self-limiting infections and induced a bornavirus-specific humoral immune response in cockatiels (Nymphicus hollandicus) and common canaries (Serinus canaria forma domestica). After challenge infection with a homologous bornavirus, shedding of bornavirus RNA and viral loads in tissue samples were significantly reduced in immunized birds, indicating that vaccination markedly delayed the course of infection. However, cockatiels still developed signs of PDD if the vaccine failed to prevent viral persistence. Our work demonstrates that avian bornavirus infections can be repressed by vaccine-induced immunity. It represents a first crucial step towards a protective vaccination strategy to combat PDD in psittacine birds.

Serological markers of Bornavirus infection found in horses in Iceland.

BACKGROUND: In a stable of eight horses in Northern Iceland, six horses presented with clinical signs, such as ataxia and reduced appetite, leading to euthanasia of one severely affected horse. Serological investigations revealed no evidence of active equine herpes virus type 1 infection, a common source of central nervous system disease in horses, nor equine arteritis virus and West Nile virus. Another neurotropic virus, Borna disease virus, was therefore included in the differential diagnosis list. FINDINGS: Serological investigations revealed antibodies against Borna disease virus in four of five horses with neurological signs in the affected stable. One horse without clinical signs was seronegative. Four clinically healthy horses in the stable that arrived and were sampled one year after the outbreak were found seronegative, whereas one of four investigated healthy horses in an unaffected stable was seropositive. CONCLUSIONS: This report contains the first evidence of antibodies to Borna disease virus in Iceland. Whether Borna disease virus was the cause of the neurological signs could however not be confirmed by pathology or molecular detection of the virus. As Iceland has very restricted legislation regarding animal imports, the questions of how this virus has entered the country and to what extent markers of Bornavirus infection can be found in humans and animals in Iceland remain to be answered.

Presence of avian bornavirus RNA and anti-avian bornavirus antibodies in apparently healthy macaws.

Recently a novel avian bornavirus has been described that has been suggested to be the possible etiological agent for proventricular dilatation disease or macaw wasting disease. This article describes two macaws that shed avian bornaviral RNA sequences and demonstrated anti-avian bornavirus antibodies as revealed by reverse transcriptase polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blot, yet are free of outward clinical signs of the disease.