While I'm at it, a few more thoughts come to mind.  I want to focus on the 
science, and leave the ugly politics out of my discussion--we all know that 
smart people can do dumb things, and there have been enough dumb things done 
to give Jim fodder for plenty of articles.  : )

First, re Bill Truesdell's references to mites being the main problem:
I've asked the researchers about the genesis of DWV, which we associate with 
varroa mite, and which varroa mite is  infected by, and vectors.
No one knows whether this was originally a bee virus, or mite virus. 
Researchers are hoping to test bees that have yet to be exposed to mites for 
any sign of DWV.  I'm also not sure if anyone knows whether the virus also 
kills the mite at high levels.  Ditto with IAPV, which appears to be 
universal in Israeli mites, and infects both mites and bees.

Clearly, the mite/virus association is a strong one--lending support to 
Bill's contention.  However, some colonies with apparently very low mite 
levels appeared to collapse from CCD (note all the qualifiers in that 
sentence?)

DWV has been shown to infect bumblebees.  As far as I know, no one has 
screened other insects as reservoirs for DWV or IAPV.

Jim's point should be well taken that we don't know whether CCD-collapsing 
colonies died from the viruses, or whether the viruses were opportunists 
that became active once the bees' immune systems were suppressed.  Dr Sela 
in Israel confirmed for me, however, that IAPV there really tears up the 
bees.  Further screening of colonies is necessary to determine if there are 
widespread latent infections of the virus, or viral genes incorporated into 
the bee genome in North America.  Ditto for Jim's point that viral immunity 
is conferred by incorporation of portions of the viral genome into the bees' 
DNA.  As Jim says, that may, ironically, lead us to seek out breeder stock 
from Australia or elsewhere where the bees have been exposed to IAPV!

Jim's point about a tiny change in the viral genome having potentially major 
effects on its virulence is also well taken.  Note that in the paper the 
authors claim to have identified 22 different "strains" (my word) of IAPV. 
I've asked about this, and an author stood behind their analysis, although 
other experts that I've spoken with question their ability to determine 
variations with such precision.  In any case, perhaps some forms are far 
more virulent, and will eventually "burn out."

And what's up with the nosema twins?  Large differences in relative species 
composition operation to operation.  And how did N. ceranae, which is 
supposed to be 10x more virulent than N apis, sneak into our bees over the 
last decade without us even noticing?

Another question:  a common factor with CCD was nutritional stress 2-3 
months prior to collapse.  Why so long a delay?  Look at the photos of the 
CCD colonies with all that sealed brood.  How the heck could a colony 
suffering from nutritional stress two months prior rear all that sealed 
brood?

Again, to me, the paper brings up far more questions than answers.  The 
value of the paper may be more in the elimination of some suspects, rather 
than the conviction of a perpetrator.

Randy Oliver

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