> I agree that there definitely could be a synergy, but KBV 
> may be a larger factor than IAPV. The problem is that 
> other things can cause CCD like symptoms, so it could be 
> KBV that is the larger factor, especially after Jim's analysis.

Actually, its worse than that.

It helps to read the "analysis" itself.
http://beeculture.com/content/CCD_Analysis.cfm


The admissions of the researchers themselves undercut/contradict 
the what is claimed in the paper.  Multiple parties (Jeff Pettis, 
Diana Cox-Foster, Edward Holmes...) have all stressed in the
press conference, and in follow-up interviews that they think
(and/or believe) they are dealing with "Multiple Factors" here.  
 
Despite saying what they think, they did no multivariate 
analysis.  Weird.  Would have been easy to do, even with an 
Excel spreadsheet macro, for Pete's sake. They used the mighty
SAS Institute statistical software, even easier to use.

Heck, anyone who can get a copy of the data can do the 
multivariate analysis on the entire bestiary of pathogens 
they detected, and compare the levels of infection between 
the samples, and publish a better analysis of the data.  
Its just math!

If everyone agrees that dealing with "Multiple Factors",
and they find 10 different pathogens and varroa, and even
bother to quantify the relative amounts of each found in
each sample (see Table S1 in the supplemental materials)
and then DON'T compare combinations of things to see if
multiple factors might show a higher correlation with 
the powerful statistical software they had at their
fingertips, what can we say?  I'm struggling here, as
I don't have anything nice to say about the lack of
such analysis.

Yet the paper still tries to call "IAPV" a "marker" for CCD,
and does everything but buy a full-page ad in the New York Times
to imply that this is the "cause of CCD", and to accuse Australia
of being the "source of the problem".  All this from mere
comparison of single-variables, one pathogen at a time, and
pathogens only, not even pesticide residue analysis thrown in.

But that's not all, it gets even worse.

Dr. Edward Holmes said in the press conference 
(37 mins into the audio):

"As for IAPV itself, again, the big unknown that comes out is 
'what is IAPV?'...  Is this a distinct virus in itself, is it 
a distinct lineage of an another virus called KBV? We really 
don't know that yet."

If they aren't sure they found IAPV or KBV, why did they make 
such a big deal about saying that IAPV was "strongly correlated 
with CCD", where KBV was not?  The key word is "distinct".  They 
are convinced that IAPV is different from KBV, even if it is 
nothing but a variation of KBV.  

But it gets still worse than even that.
Dr. Holmes went on to say:

"We know from other viruses, like West Nile. that very small 
genetic changes I mean, one amino acid change, can turn a 
benign virus into a very virulent one... it is quite possible 
that very small genetic changes... may make this virus behave 
differently in Israel, Australia, and the USA."

So, it just doesn't matter which virus is which, or which 
one is found where. If very small and sudden changes can 
turn a benign virus into a virulent one, and tiny changes 
could appear in local populations of viruses in different 
countries, the names of viruses are meaningless, and 
utterly useless.

We had better start numbering them, so that next year's 
IAPV is not confused with this year's version.  One could 
be deadly, and the other harmless.  Same thing with location,
as viruses can change in one place and not another. So, 
we had better start adding zip codes onto the end of 
the "names", to track where they were found.  

We need to also recall that pointing to "IAPV" as somehow
significant allowed them to publish at least one arguably 
NEW finding, something that no one else had yet mentioned.
Finding something arguably "new" is what gets a paper
published.  Finding something with international 
implications is what gets the paper noticed.

What was announced in April was "an unknown Iflavirus".
Note that the difference between an "Iflavirus" and
any of the "Dicistroviruses" is so insignificant that
"Dicistroviruses" are not even recognized as distinct
from "Iflaviruses" by the taxonomic authorities who 
name and classify viruses.

Now, lets cut everyone some slack here.  In April, the
team that openly announced their findings to the entire
so-called "Working Group" classified the virus they found
as an "Iflavirus".  This was the only name they COULD
use, and stay within the taxonomy that was "approved"
on the official taxonomic lists. 

The genetic sequences for "IAPV" did not become available
until after April, so, in April there was no way to match 
an unknown virus to IAPV.  

So everyone could be "right" about which virus is which,
depending on what they compared it to.  
But does it matter?

Edward Holmes described the difference between KBV and IAPV,
both now considered "Dicistroviruses" as "a moot point".

I agree, but not for any taxonomic reason.

Its a moot point because it is quite possible that what has
been found is the equivalent of finding maggots on the bodies
of victims of gangland slayings.  Yes, the maggots certainly
do "correlate" to death, as you won't find them on the bodies
of healthy living people, but the maggots are not the cause
of death.

The cause of death in the case of a gangland slaying is the 
gunshot wound to the back of the head.

 

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