> dsRNA technology uses only certain of those sequences that are unique to the targeted virus, not to any of the other bee RNA.  So there is little chance of messing up the cellular metabolism.

Aye, there's the rub. This is what was thought at first, but it now appears that the segments silence *not only* their targets but other sites that are *similar* but not identical. Try to wade through the following paragraph until you get to the phrase "suboptimal specificity". In plain English, suboptimal specificity means you are trying to hit a bullseye and are not having that good of luck. 

Early reports in the literature described siRNAs as
specific and non-immunogenic. Target genes were
silenced by complementary siRNAs but not by unrelated
siRNAs. Moreover, single mismatches at the cleavage
site of the siRNA abolished target silencing.

However, as more data became available, it emerged that
there are additional mechanisms of transcript targeting
by siRNAs. Previously unsuspected off-target activity of
siRNAs was revealed by unbiased, genome-scale expression
profiling. Initial studies with microarray expression
profiling seemed to support the idea that siRNAs could
specifically silence the intended target. However, it is
now recognized that certain properties of siRNAs and/or
the technologies used to deliver them lead to suboptimal
specificity.

Off-target activity of siRNAs can lead to unanticipated
phenotypes and complicate interpretation of the
therapeutic benefits of siRNAs. 

from: Recognizing and avoiding siRNA off target effects for target identification and therapeutic application, by Aimee L. Jackson and Peter S. Linsley. JANUARY 2010

Off target = misses the target. Like you are playing a dart game in a crowded room. Missing the target may lead to "off target effects" like a dart in someone's forehead. I am not saying it would, I'm simply pointing out that phrases like "suboptimal specificity" and "off target effects" actually mean something. They mean that the aim is not so good yet, and there is no telling what might get hit by a missed target.

Here's another weak point, in the following paragraph, they refer to a compensatory mechanism. Doesn't this raise more questions than answers? If the treatment fades after *the first few days*, isn't that sort of ineffective for treating a chronic problem? And just what is this compensatory mechanism? Might it not be the bees' immune system "taking out" the synthetic RNAs that you just introduced as a treatment, rendering them useless? 

Why the various parameters (specific silencing and effect on N.
ceranae viability and honeybee vitality) occasionally level off is
currently not clear to us. Beyond the obvious aspects pertaining
to the experimental setup and the level and stability of
inoculants, the robust effect in the first few days, as well as the
subsequent decline of the effect of the dsRNA, can result from
a compensatory mechanism in N. ceranae.

From: Effective Gene Silencing in a Microsporidian Parasite Associated with Honeybee (Apis mellifera) Colony Declines
, by Nitzan Paldi, et al. Sept. 2010

* * *

I am not saying there is a specific problem with this technique, I am saying there are some unanswered questions. I have attempted to get answers from the key players but with one exception, none of them have responded to my inquiries. Curious.

PLB

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