When Danee has a chance to be back on line for ferret stuff she will
be able to tell you more about UGA work.  Meanwhile, you can look at
her past series of posts in archives such as those of the FML and FHL.
If the FML ones aren't up to that date, yet, then you should be
able to find them elsewhere (Maybe someone here knows where to see the
entire series.) or use the dates of the partial series in the FHL
Archives to work back to the digest numbers for the FML and then use the
GET FERRET nnnn feature to get those particular digests for yourself.
 
http://www.usu.edu/iar/Brochure/brochure.html
USU Institute for Antiviral Research  biographies include:
>Dr. Dale L. Barnard: ...Dr. Barnard's research interests are in the
>elucidation of the biochemical cytotoxicity and mechanisms of antiviral
>action of new antiviral agents.  A major thrust of his research is to
>pinpoint a viral enzyme which could be used as a target for developing
>selective and specific antiviral drugs.  He has been instrumental in
>studying methods by which mink aleutian virus disease can be treated.
 
BUT I think (relying on memory on this so that can be faulty) that he may
have done that work in what *may* now be a defunct national persistent
diseases lab (the budget cutbacks have hit some very good places with all
of the huge war debt and some labs have been destroyed and others were
mentioned in the ax's line up in the current budget) so don't know if
he now has funds which allow him to currently work on Aleutians.  Still,
he and the people in UGA should have the info sought, as should ADV
researchers elsewhere.  Also, I may be confusing him with someone else
so he might have current work going on into ADV.
 
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=114691&tools=bot
includes:
>Attempts to protect adult mink with capsid-based ADV vaccines have
>uniformly failed, even though vaccinated animals develop antiviral
>antibodies (1, 49, 52).  Indeed, upon challenge, vaccinated animals
>suffer a hyperacute disease with enhanced tissue lesions (1, 52)...
>Whereas virus neutralization by antibody may afford protection from
>infection, ADE facilitates the infection of macrophages that is
>central to the resulting immune disorder (15, 29, 35).  Antibodies to
>VP2:428-446 have been demonstrated in ADV-infected adult mink (28) and,
>if these antibodies function to mediate both ADE and neutralization
>in vivo, any protective effect might be counteracted or supervened.
>Thus, our results provide possible explanations for the failure of
>capsid-based ADV vaccines (1, 52).
 
There is more in this and further paragraphs on possible alternative
possible vaccine approaches beyond what currently exists, but the UGA
work is several years more recent, of course.
 
Notice that work is ongoing because there is not an effective vaccine,
and when that category of vaccines above was tried, although the mink in
the study did develop antibodies it is not shown that they provided much
if anything in the way of protection, and once they caught the disease
the result of was that the disease itself was actually worsened.
 
This British study is a few years older:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=112773&tools=bot
 
These may interest the persistent reader into virology:
http://jvi.asm.org/cgi/content/full/75/22/11116
 
and
http://jvi.asm.org/cgi/content/full/73/8/6882
which is a more recent British study includes
>Disease caused by ADV differs significantly from that caused by other
>parvoviruses in which infection leads to a protective host response.
>For ADV, the presence of the capsid elicits a host response that
>actually contributes to the disease process (50, 51).  Recent studies,
>in which the ADV capsid proteins were expressed in a series of
>nonoverlapping fragments, indicate that the unusual antibody response
>is targeted to specific epitopes (19).  and specific to your question:
>
>The ADV-G VP2 sequence is 38% identical to CPV at the amino acid level
>and more in the discussion section such as
>It is noteworthy that parvoviruses CPV, FPV, and B19, which can all be
>neutralized by a host-antibody response, lack the ADV mounds (Fig. 4
>and 6).  The unusual pathogenicity of ADV might arise if the mounds act
>as immunodominant decoys that somehow prevent a protective response
>from being generated during infection.
 
See also the paragraph beginning:
>Economic losses to the fur industry as a result of ADV infection of
>farmed mink are mainly a consequence of the unusual pathogenicity of
>ADV, in which infectivity is enhanced by capsid-antibody and capsid
>protein fragment-antibody complexes (1, 50, 51) formed during an
>infection.  This property has thwarted numerous attempts at particle-
>based vaccine development.  Current strategies for global development
>of vaccines against parvoviruses are focused on the use of virus-like
>particles or peptides...
 
There is more but I am out of time so just use these to get ideas of
places to search, keywords, phrases to search on, etc.
 
-- Sukie (not a vet)
Ferret Health List
http://www.smartgroups.com/groups/ferrethealth
FHL Archives
http://fhl.sonic-weasel.org
International Ferret Congress
http://www.ferretcongress.org
[Posted in FML issue 4946]