From:
Gregory, Pamela G., et al. "Conditional immune-gene suppression of honeybees parasitized by Varroa mites." Journal of Insect Science 5.1 (2005): 7.  This article is open access.

(Abstract)  The ectoparasitic mite, Varroa destructor, is the most destructive parasite of managed honeybee colonies worldwide. Since V. destructor transfers pathogens to honeybees, it may be adaptive for bees to respond to mite infestation by upregulating their immune responses. Mites, however, may overcome the host’s immune responses by suppressing them, which could facilitate the mite’s ability to feed on hemolymph. A humoral immune response of bees parasitized by V. destructor may be detected by studying the expression levels of antibacterial peptides, such as abaecin and defensin, known to be immune-responsive. Expression levels for these two antibacterial peptides changed non-linearly with respect to the number of mites parasitizing honeybee pupae. Bees exposed to low or moderate number of mites had fewer immune-related transcripts than pupae that were never parasitized or pupae with high mite loads. Although many of the pupae tested indicated the presence of bacteria, no correlation with mite numbers or immune-response levels existed. All bees tested negative for acute paralysis and Kashmir bee viruses known to be vectored by V. destructor.

....from the introduction:

Honeybees appear to mount a cellular immune response at wound sites caused by V. destructor (Kanbar and Engels 2003<http://jinsectscience.oxfordjournals.org/content/5/1/7.full#ref-13>). Bees also possess a humoral immune response leading to an upregulation of several antimicrobial peptides in response to both wound infections (Casteels-Josson et al. 1994<http://jinsectscience.oxfordjournals.org/content/5/1/7.full#ref-4>) and oral bacterial infections (Evans 2004<http://jinsectscience.oxfordjournals.org/content/5/1/7.full#ref-9>). To explore whether the presence of V. destructor affects the humoral immune response, transcript levels for two antimicrobial peptides, abaecin and defensin, that show activity against bacteria were examined. Both show activity against gram-positive and gram-negative bacteria (Casteels et al. 1990<http://jinsectscience.oxfordjournals.org/content/5/1/7.full#ref-5>, 1994<http://jinsectscience.oxfordjournals.org/content/5/1/7.full#ref-4>). It was found that bees exposed to low or moderate numbers of mites sharply reduce their immune-peptide transcripts when compared to both heavily parasitized and unparasitized bees.

These are immune responses to bacteria.  But how do bees respond to viruses, and is there any genetic basis for this mechanism?  Further hunting....

I found this:  Ting JP, Davis BK (2005) CATERPILLER: A novel gene family important in immunity, cell death, and diseases. Annu Rev Immunol 23:387–414.

From the introduction:  "To survive, each species develops a system of immune diversity that responds properly to these antigens. Immunoglobulin (Ig) and T cell receptor (TCR) are at the forefront of immune recognition and diversity in adaptive immunity of vertebrates. Of equal importance is the innate immune system. This arm of immunity is conserved in nearly all taxa and is clearly more ancient than the adaptive immune system.

....R proteins (IN PLANTS) are crucial for the immune defense against bacteria, virus, fungi, nematodes, insects, oomycetes, and even synthetic products such as insecticides. As a reflection of their importance, they are estimated to comprise >1% of the Arabidopsis and Oryza genomes, and to date more than 125 and 600 R genes have been found in these genomes, respectively."

It appears that the way these proteins work is not as straightforward as our antigen-antibody system.  The fact that this form of immunity is very ancient also suggests to me that it will not be a simple matter to tweak it via selection.  I say this because the longer a defense mechanism exists, the longer the pathogen has had time to develop a way to get around it.

The first paper I cited (Gregory et al) demonstrated that immunosuppression of the bee by the mite in concert with the introduction of the virus is what makes bees sick.  To add to this complexity, another paper I found (Di Prisco, Gennaro, et al. "Neonicotinoid clothianidin adversely affects insect immunity and promotes replication of a viral pathogen in honey bees."Proceedings of the National Academy of Sciences 110.46 (2013): 18466-18471) demonstrates that neonics suppress honeybee immune responses also.

I can imagine the "perfect storm" here...Varroa downregulates honeybee immunity, and if they are exposed to neonics, those also downregulate immunity via a different mechanism, and then those bees are exposed to viruses.  They get sick, some hives just linger while others collapse.

So I may have answered my own question about breeding virus resistance into bees.  It appears to be a polygenetic feature (probably compounded by epigenetic influences) and thus it will be difficult, if it can be done at all.

I'm back to thinking about mite behavior.

Christina

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