Ich stelle mal wichtige neuere Erkenntnisse über den Zusammenhang von ABV und PDD als Zitate zusammen.
Da leider in Englisch, werde ich die wichtigsten Erkenntnisse im nächsten Beitrag dann zusammenfassen.
Link 1 : Bornavirus was first described in psittaciforms in 2008 by researchers at UCSF who were studying a group of five parrots suffering from Proventricular Dilatation Disease (PDD). Using microarray technology, the group isolated a negative-stranded RNA virus from three of the five birds. This virus was determined to be a member of the Bornaviridae family. The researchers named the avian strain 'Avian Bornavirus' (ABV).
Samples from over 500 cases of PDD diagnosed birds have been confirmed to have ABV antibodies as well as Borna virus RNA. However, there is also a large population of birds that have tested positive for ABV but have not developed any clinical signs of PDD.
ABV is also being studied as a possible causitive agent of conditions such as skin inflammation, feather plucking, self mutilation, major neurological problems, and chronic bacterial and fungal infections.
In May 2010, we recieved feather samples from 6 birds who are chronic feather pluckers. 5 of the 6 birds tested positive for ABV by rtPCR using feather samples. None of these birds were suffering from any weight problems as observed by the vetrinarian treating them.
It is still unknown if a percentage of birds may never develop any symptoms of disease but may continue to function as a reservoir for ABV and allow the virus to infect other birds.
ABI is looking forward to conducting experimental treatments using ABI's own parrot-specific gamma and alpha interferon, as well as combining these cytokins with specific anti-viral drugs.
Link 2 : PPD is caused by a nonpurulent inflammation of the autonomic nervous system of the upper gastrointestinal tract, the peripheral and central nervous tissue, and the cardiac conduction system (5,6). Gastrointestinal and neurologic signs can appear alone or in combination (4,7,8). The clinical signs are nonspecific, and PDD can be definitively diagnosed only by pathohistologic detection of lymphoplasmacytic infiltrates of ganglia in the upper gastrointestinal tract. However, a negative finding cannot exclude the presence of PDD
In 2008, 2 independent groups of research scientists described a new virus, avian bornavirus (ABV), which was amplified from samples from PDD-affected birds. Since then, 6 different ABV genotypes have been detected in psittacines birds.
Surveillance studies in aviaries showed that not all birds were affected after exposure to PDD-diseased and ABV-positive birds, and clinical signs and infection status varied considerably in birds that were affected. In addition, some ABV-positive birds showed no clinical signs
However, detailed information about the occurrence of clinical signs, seroconversion, histologic lesions, viral RNA, and infectious virus using a statistically adequate group and sample size was still lacking.
In our experiments, the discrepancies in infection status and in the development of clinical signs in infected but clinically healthy birds could be a result of several host factors (e.g., age, immune status), virulence, and adaption of the inoculated ABV suspension to the cell culture.
The cockatiels most likely had considerable variability in their genetic makeup, in contrast, for example, with inbred strains of laboratory mice. Such genetic variability could have a substantial effect on disease susceptibility.
ABV RNA and antibodies to ABV were detected in all inoculated birds, and titers of antibody against ABV steadily increased during the investigation period; however, these antibodies did not influence the outcome of clinical disease.
Thus, detection of antibodies to ABV does not indicate antiviral immunity; on the contrary, they indicate a resolved or ongoing ABV infection with possible risk for the development of PDD.
These findings indicate that bird se1 reacted differently than the experimentally infected birds, and it may have been more efficient than the experimental cohort in combatting the infection. This might be a result of infection by a different route, such as the oral or intranasal route. Additional investigations are needed to characterize the effects of different infection routes on the outcome of ABV infection and the development of PDD. It is already known from BDV infection of rats that the route of infection determines the severity of disease and that an early up-regulation of BDV-specific CD4 T cells can efficiently protect against infection by the virus
It remains to be determined whether immunopathologic mechanisms that are based on a T cell–mediated immune reaction, as known for BDV infection, play a role in ABV infection and the development of PDD.
Link 3 : Why do some birds die? Why do some birds survive as healthy carriers? The evidence that we generated recently suggests that this depends on how or when a bird becomes infected. If an adult bird becomes infected through contact with other infected birds, then it will likely develop PDD and die.
We have, however, also found ABV in the eggs of infected birds. This means that this virus may be “vertically transmitted.” This means it can be transferred from the mother to her offspring through the egg. Now one of the consequences of that mode of transmission is that the baby bird does not recognize the virus. The hatchling won’t make an immune response against the virus. For normal viruses, that would be bad news — we want an immune response to protect us from viruses. But, bornavirus is somewhat different than other viruses in that it does not kill cells directly. It infects cells, but doesn’t kill them. (That, by the way, is probably why it took so long to find this virus.)
So, if a bird becomes infected with ABV, and its immune system doesn’t attack those virus-infected cells, then the infection persists. We believe that this is the recipe for chronic long-term healthy shedders. If, however, the bird’s immune system recognizes the virus and the birds’ immune system starts to attack and destroy the virus-infected cells, then this, we believe, will cause the bird to develop PDD.
Is that how a possible vaccination can come about?
If our theory is correct, then vaccines may not be successful, but that doesn’t mean we shouldn’t try.
What are current treatments for PDD?
The current treatment, a favorite among avian vets, is to try to reduce the inflammation associated with infections with anti-inflammatory drugs. There’s a lot of anecdotal evidence that these [drugs] do help.
There’s also increasing evidence that drugs that suppress the immune disease will also enhance survival and improve the quality of life of the bird. This fits with the idea that it’s not the virus that causes the direct death, it’s the immune response to the virus,and, if you can suppress the immune response, you can cause clinical remission.
We’re also studying an anti-viral drug called Ribavirin, which we know will stop the virus growing in culture, but we have yet to show it’s effective in birds. That may be because the drug doesn’t reach the virus in birds — the problem may not be with the drug, it may be [with] how the birds handle the drug. We have a study underway to see how Ribavirin is handled by a bird.
- "Multimorbidität" (Mehrfacherkrankung) muss man halt immer irgendwie Kompromisse schließen... 
, aber ich habe mich gestern Abend sehr lange und ausführlich mit einem Experten, der mir versichert hat, auf dem neusten Stand zu sein, darüber unterhalten und ihn -neben vielem anderen- auch dazu befragt; denn Antikörper sind nunmal Antikörper, wodurch immer die entstanden sind...