Peter Borst quoted the press, who has consistently "gotten
it wrong" in nearly every story they write about CCD:

> "The authors themselves recognize it's not a slam dunk, 
> it's correlative."

Sorry, there is no correlation.

There may not even been any actual IAPV virus at all.

The classification of samples into "CCD" and "Non-CCD"
groups was faulty.  Therefore any claimed correlation
is inherently bogus.  Read my analysis.  I explain it
in excruciating detail.

> "But it's certainly more than a smoking gun - more like 
> a smoking arsenal."

I agree that there is much smoke.
There is the smoke and mirrors of PCR, Sequencing, and "Metagenomics".
There is the smoking ruin of a paper that will be laughed at for
decades.
There may be the smoking ruins of multiple careers.
But there's no smoking gun.
Listen to the press conference - the backpedaling was deafening.

> "'It's very compelling,' said May Berenbaum, a University of Illinois 
> at Urbana-Champaign entomologist"

What is compelling is that no one has read the paper, and realized
that basic assumptions were made without any basis.

1) The assumption "irradiation killed the pathogen, therefore
   we can assume we are looking for a pathogen" is bogus.
   Bayer Cropscience, who would have every reason to dodge the
   question, states clearly that a mere day's sunlight breaks down
   their sprayable Imidacloprid pesticides.  The EPA tests for this
   as a part of their "environmental fate of pesticides" testing,
   so the pesticide companies DESIGN their products to break down
   in sunlight.  Not all neonicotinoid pesticides break down like
   this, but Bayer's do.

1a) So, let's think about sunlight versus gamma radiation sufficient
    to kill foulbrood spores.  Which might be stronger?  :)

2)  The assumption that any/all samples from a yard where CCD had
    been detected in SOME hives would be "CCD" samples was also
    bogus.  Despite the efforts of Dick Marron and the others
    who took samples, the paper clearly states that the folks
    doing the analysis divided samples into two categories -
    "CCD" and "Non-CCD", ignoring the more subtle classifications
    assigned by those who examined the hives and took the samples.

3)  The assumption that samples from a yard apparently free of
    CCD was not cross-checked later to verify that the hives
    remained free of symptoms.  So, there was no way to confirm
    that the "Non-CCD" samples were valid "healthy bee" samples.

There is a difference between "precision" and "accuracy".
The data is very precise, I'm sure.
But it is not at all accurate.
It is precisely useless as a result.

One can make no conclusions at all from samples that were 
apparently misunderstood as to their classification.

Up above, I suggested that there may not even been any actual 
IAPV virus detected at all.  This is a complex point, but the
process used may have detected genetic evidence of PRIOR 
IAPV exposure, rather than the evidence of an actual virus.
Prior exposure that may have been multiple bee generations ago.
(See my analysis for the details)

Understand that "metagenomics" is the equivalent of running
a bookshelf worth of books through a shredder, taking only
a few scraps of the shredded paper, and then looking at the 
scraps and trying to match the scraps to an author.  The 
problem here is that one can shred a Kurt Vonnegut book in
which he quotes Shakespeare, and end up thinking one had 
evidence of a book of Shakespeare.  Wrong.  
It was just a quote in a Vonnegut book.
There was no Shakespeare book on the shelf.

Speaking of Shakespeare, in the "race" to publish before 
those who actually found all the same stuff back in April
had a chance to do so, it appears that the team used the 
same reasoning as Macbeth:

"If it were done when 'tis done, 
then 'twere well If it were done quickly.  
If one could trammel up the consequence, 
and catch with his surcease success,
that would be the be-all and the end-all here..."

And we all know how things went for Macbeth.
Badly.

Somehow, I DO see a correlation in that.  :)

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