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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