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Guessing the Future with Varroa: Part 1

Guessing the Future with Varroa

Part 1

Randy Oliver

First published in ABJ December 2018

      The Greek philosopher Heraclitus maintained that there is nothing permanent except change.  This certainly applies to biology and the business of beekeeping, both of which are always in some state of evolution.  However, beekeeping in the U.S. was unusual in that it changed little between the mid 1800’s and the arrival of a slew of new parasites starting in the late 1900’s.  Since then, it’s been hard to keep up with the changes.  As a biologist, it’s been fascinating to watch evolution before my eyes; as a beekeeper, it’s been, shall we say, “challenging.”


Caught up in the immediacy of our everyday lives, we humans often have a difficult time with grasping the long-term consequences of our actions.  This has certainly been the case since the invasion of varroa, which we’ve dealt with by one stopgap measure after another.  It’s frustrating to admit that after three decades, the mite continues to remain our most pressing problem.

It’s important to keep in mind that we’re in the middle of major evolutionary changes in the business of beekeeping, as well as the rapid biological coevolution of the honey bee, the varroa mite, and its symbiotic partner–Deformed Wing Virus (DWV).  There’s no way to predict the future, but I’d like to wrap up this series on The Varroa Problem by tying up some loose ends, and pointing out some likely directions of the ongoing evolution of the players.

The Evolution of varroa

The varroa mite may be only the size of a pinhead, but the tiny parasite possesses a genome twice the size of that of the honey bee [[1] [2]].  And it has demonstrated its ability to rapidly evolve and disperse traits that confer it increased fitness—remember how it took only about three years for most of the U.S. population of varroa to gain resistance to coumaphos?

Practical application: varroa has clearly demonstrated its ability to rapidly evolve, and our current beekeeping practices ensure that any successful mutants will get quickly distributed.

The fact is that varroa is well-adapted to parasitizing the drone pupae of its natural host Apis cerana, but is still under selective pressure to better adapt to its recent host shift—in which it primarily reproduces on the worker pupae [[3]].

Direction of evolutionary pressure: we can expect this parasite to continue to evolve its behavioral and physiological responses to cues from worker brood of Apis mellifera, adapt to the higher temperature and shorter postcapping period of that worker brood, as well as to develop further resistance to miticides.  We can likely expect varroa to become even more “virulent” than it is now.

And varroa has only begun to exploit its symbiotic coevolution with DWV—a marriage that has created a “Monster” that now acts more like a parasitoid than a parasite, killing its host colony towards the end of the season in order to benefit from greater dispersal to other hives.  Rather than it being to the mite’s advantage to be a relatively benign, vertically-transmitted parasite–as it is in its natural host–it may now be to the mite’s advantage for each female to complete a reproductive cycle or two, and then to try to hitch a ride to another hive [[4]].

Update and Clarification:  I need to make clear that I’m suggesting that we must consider what we define as the host or hosts of DWV, with regard to the honey bee. The virus can also infect other insect species, but evolution will select for strains of the virus best adapted to those species—thus I’m going to ignore those host species.  The hosts relevant to this discussion are honey bee larvae, bee pupa, bee adults, and the honey bee colony as a whole.  Some researchers claim that DWV also appears to reproduce in the body tissue of the varroa mite, but all but one of their studies were based upon the circumstantial evidence of detecting either positive strand DWV (indicating presence) or negative strand DWV (indicating reproduction) in whole-mite extracts, which typically include virus-laden honey bee fat body tissue.  On the other hand, a number of studies [] strongly suggest that DWV does not appear to replicate in actual varroa body tissue [[5]].  The only study that I’ve seen to date (February 2019) that appeared to find DWV actually replicating in mite tissue was by Campbell [[6]], and then only in mite brain tissue – unlike the virus’ replication in several tissue types as in its other hosts, so I am still unconvinced that varroa is anything but a vector of DWV.  This is an important consideration, since if varroa does not suffer from being infected by DWV, then there is no direct cost to it from vectoring it, and perhaps a major benefit.

This brings us back to the four remaining honey bee hosts of DWV – the larvae, pupae, adults, and the colony as a whole.  Recent research [[7]] indicates that DWV, whether acquired by feeding or injection, is relatively benign to bee larvae and pupae, and numerous studies indicate that adult bees carry a covert infection by the virus [[8]].  Thus, at the colony level, DWV virus appears to be a relatively benign parasite.

But when varroa enters the picture as a vector, things change.  Adult bees and brood start to die — although it’s not yet clear to me what is actually causing the brood to die.  But more important, the entire host colony then dies, but before then, drifting bees horizontally transmit DWV-vectoring mites to other host colonies in the vicinity.  If they didn’t do so, there would be a huge fitness cost to both the mite and the virus from killing the host colony.  Since the honey bee as a species (as well as we beekeepers) are more concerned about the death of entire colonies than of individual bees, we need to focus upon how the mite-virus parasitoid is evolving to cause the death of its host at the colony level.  The take-home message is that this would not be favored by natural selection unless humans kept artificially replacing the fallen host colonies.


Evolutionary note:  in A. cerana, it is the genes of mites that transmit vertically via swarms from healthy colonies that get into the next generation of host colonies.  Currently in A. mellifera, few mite bloodlines are transmitted vertically via purchased queens or packages—rather most genetic transmission is via bee drift from, or the robbing of, collapsing colonies.  Take home message: bee genetics may be largely controlled by the commercial producers, but mite genetics evolve in response to our beekeeping practices.

The take-home from this is that the current evolutionary strategy of varroa appears to be:

  1. Start in the spring with an assortment of near-clonal matrilines of the mite in each hive,
  2. For those inbred strains to race against each other to produce the most offspring during colony buildup in the spring and summer, and then,
  3. To then cross-mate within the hive with other successful strains [[9]] just before the mites, in conjunction with DWV, kill their host colony, and then,
  4. For the most numerically-successful mite/DWV strains to catch rides on exiting bees to other hives in the neighborhood.

By this strategy, the most successful mutations can quickly shift the genetic structure of the local mite/virus population, and we humans, with our motorized transport of the mite all over the continent, ensure that those strains get quickly and widely dispersed.

Direction of evolutionary pressure: We are currently on track to witness varroa continuing to coevolve with DWV to become an ever more effective colony-killing parasitoid. 

The evolution of DWV

DWV has long been around as an insect virus, but was rarely noticed as being a problem to honey bees until it hooked up with varroa [[10]] (Fig. 1).  The two species of parasite have now “figured out” how to work closely together in a mutualistic manner [[11] [12]], and can be viewed as a single threat [[13]].

Figure 1.  We normally observe the ugly signs of DWV only if a colony is highly infested with mites.  But that doesn’t mean that the virus isn’t there—most all bees in a hive nowadays carry DWV.  It’s the combination of varroa and DWV that is deadly.

As occurred with the invasion of Nosema ceranae replacing N. apis, a new strain of DWV (Type B) appears to be replacing the existing predominant Type A strain of the virus in this country [[14]], but it’s too early to tell what the effect will be.

Research needed: of great interest to me is that, although varroa and DWV are now closely linked, I’ve yet to see compelling evidence that the virus actually infects and reproduces in the mite’s body tissues (but there is strong suggestive evidence otherwise).  This question of whether varroa acts solely as a vector, or rather as an amplifying intermediate host, begs for further clarification.

DWV exists as a continually-mutating “cloud” of variants, with several strains often being found within a single hive or apiary.   A single strain may dominate for years in an area, or be replaced by another [[15]].  It’s not yet clear as to whether coinfection with more than one strain of the virus is more detrimental to the bee.   The thing to keep in mind that the virus has the capacity to evolve far more rapidly than either the mite or the bee, due to its very high mutation rate and quick generation time (hours rather than weeks or years).

I was recently speaking with Dick Rogers of Bayer about his observations that in some hives the workers may take more than 12 days to emerge after being capped over.  This brought to mind something that (now-doctor) Judy Wu pointed out some years ago [[16]]—that bees reared in miticide/pesticide-contaminated combs may exhibit a longer post capping period, thus possibly resulting in greater fecundity for varroa, since an extra day might allow the maturation of an additional daughter.

Direction of evolutionary pressure:  it’s not yet clear to what degree our miticide residues and other chemical contamination of the combs play a part in this, but it does point out a potential direction for DWV evolution—if DWV could manage to delay the development of worker pupae by a day or two, it would nearly double the reproductive success of the mite.  Scary, huh?

And that doesn’t even take into account how DWV (and some other viruses) apparently benefit from the suppression of the bee antiviral immune response by at least some insecticides [[17]].  Let me make clear though, that in my own operation, with zero exposure to neonics, DWV is still the main problem if I don’t keep varroa under check.

So long as beekeepers fail to control the level of mites in their hives (Fig. 2), we can expect DWV to be a major player in colony health and survivorship.


Figure 2.  I overlaid estimated alcohol wash counts (and some arrows) over the results of the USDA National Honey Bee Disease Survey results [[18]].  Note how poor a job that beekeepers in general are doing at keeping varroa levels below the orange economic harm line—above which DWV typically starts to become problematic.

Direction of evolutionary pressure: DWV has quickly adapted to take advantage of its mutualistic relationship with varroa.  The virus has now “learned” how to use varroa as a vector to spread itself to other hives.  So far, common beekeeping management practices have been playing into the virus’ hands.  I hesitate to guess the future, but wouldn’t bet against DWV becoming even more problematic.

The evolution of our beekeeping practices

Over the past three decades, in my own operation, I’ve gone from a hands-off approach of just letting the bees do their own thing, to now alcohol washing every single hive in the operation, and applying organic acids or thymol at least four times a year (but I’ve also gone from getting $12 for almond pollination to over $200). Prior to varroa hooking up with DWV so effectively, it was no problem to keep 72 hives in a yard.  Nowadays, that would be foolish unless one really stays on top of the mite.

The reason is the well-documented drifting of bees between hives (Fig. 3), and if those bees are carrying mites and DWV, that’s a problem.  Evolutionarily, late-season drift of mite-infested bees as colonies collapse from DWV widely disperses the most virulent strains.

Figure 3.  How many mite-carrying drifted bees are entering your hives?  At this hive entrance, the guards are checking out a drifted bee—which will likely be eventually accepted into the hive.  Even if not, there’s little to prevent a mite from jumping onto one of the guards during the scuffle.

A sneak peek: I’m currently running a large field experiment in which we’ve tagged over 5000 bees in varroa-infested hives, and tracked where those bees wind up.  I can already share that there is plenty of drift to hives over 500 feet away, and a fair amount of drift to an apiary a half mile distant.

Direction of evolutionary pressure: so long as beekeepers run non mite-resistant stock and have colonies crashing from DWV in late summer and fall, we will continue to reward the Monster for killing our hives, so long as we keep replacing those unfortunate colonies with yet another meal of the same sort of non-resistant bees.

Evolution of treatments

The writing was on the wall from the beginning—mites have an amazing ability to evolve resistance to synthetic miticides.  We’ve gone through several already, and much of our industry is now hanging by the thin thread of amitraz.  In country after country, beekeepers are being forced to learn how to use organic acids and thymol instead.  We can cross our fingers that some miracle in pheromones, botanicals, biocontrols, olfactory blockers, or RNAi is going to save us, but I know of nothing very promising in the pipeline.

Direction of evolutionary pressure: switching to integrated pest management of varroa, using “natural” treatments, will certainly buy us time, but there is no question that the ultimate solution to The Varroa Problem will be a wholesale shift to running bee stocks that are innately resistant to the mite.

Practical application:  my sons and I have run a successful small commercial operation since 2001 without using any synthetic miticides.  It can be done.  If your operation is completely dependent upon amitraz, I suggest that you start by practicing with a Plan B before you are forced to do so.  And start demanding that your queen producers get serious about selecting for mite resistance!

To be continued…


Thanks to Peter Borst for his assistance in literature search, to all the bee researchers I’ve spoken with on this subject, and to my wife Stephanie for her suggestions on my manuscript.


[1] Cornman, R. S. et al.  (2010) Genomic survey of the ectoparasitic mite Varroa destructor, a major pest of the honey bee Apis mellifera. BMC Genomics. 11: 602.

[2] The Honeybee Genome Sequencing Consortium (2006) Insights into social insects from the genome of the honeybee Apis mellifera. Nature. 443: 931-949.

[3] May I suggest reviewing my article Knowing Thine Enemy at https://scientificbeekeeping.com/the-varroa-problem-part-9/

[4] Nolan, MP IV (2016) Impacts of inter-colony distance, mite host choice, and colony polyandry on the host/parasite relationship between Apis mellifera and Varroa destructor. Dissertation, University of Georgia.


[5] Ongus, JR (2006) Varroa destructor virus 1: A new picorna-like virus in Varroa mites as well as honey bees. Thesis, van Wageningen Universiteit.

Todd JH, et al (2007) Incidence and molecular characterization of viruses found in dying New Zealand honey bee (Apis mellifera) colonies infested with Varroa destructor. Apidologie 38:354–367.

Fievet, J, et al (2006) Localization of deformed wing virus infection in queen and drone Apis mellifera L. Journal of Virology 3: 16.

Zhang, QS, et al (2007) Detection and localisation of picorna-like virus particles in tissues of Varroa destructor, an ectoparasite of the honey bee, Apis mellifera. J. Invertebr. Pathol. 96: 97–105.

Santillan-Galicia, MT, et al (2008)  Immunolocalization of deformed wing virus particles within the mite Varroa destructor.  Journal of General Virology 89: 1685–1689.

Ryabov, EV, et al (2014) A virulent strain of deformed wing virus (DWV) of honeybees (Apis mellifera) prevails after Varroa destructor mediated, or in vitro, transmission. PLoS Pathogens 10, e1004230; doi: 10.1371/journal.ppat.1004230.

Erban, T, et al (2015) In-depth proteomic analysis of Varroa destructor: Detection of DWV-complex, ABPV, VdMLV and honeybee proteins in the mite. Scientific Reports 5:13907.

Nordstrom, S. (2003). Distribution of deformed wing virus within honey bee (Apis mellifera) brood cells infested with the ectoparasitic mite Varroa destructor. Exp Appl Acarol 29, 293–302.

[6] Campbell, EM, et al (2016) Transcriptome analysis of the synganglion from the honey bee mite, Varroa destructor and RNAi knockdown of neural peptide targets. Insect Biochemistry and Molecular Biology doi: 10.1016/j.ibmb.2015.12.007.

[7] Tehel, A, et al (2019) The two prevalent genotypes of an emerging infectious disease, Deformed Wing Virus, cause equally low pupal mortality and equally high wing deformities in host honey bees.  Viruses 11: 114.

Remnant, EJ (2019) Direct transmission by injection affects competition among RNA viruses in honeybees.  Proceedings of the Royal Society B https://royalsocietypublishing.org/doi/10.1098/rspb.2018.2452

[8] Reviewed by de Miranda JR, Genersch E (2010) Deformed wing virus. J Invertebr Pathol 103:S48–S61

[9] Beaurepaire, AL, et al (2017) Seasonal cycle of inbreeding and recombination of the parasitic mite Varroa destructor in honeybee colonies and its implications for the selection of acaricide resistance. Infection, Genetics and Evolution 50: 49–54.

[10] Martin, SJ., et al  (2012)  Global honey bee viral landscape altered by a parasitic mite. Science 336:1304-6.

[11] Di Prisco, G, et al (2016) A mutualistic symbiosis between a parasitic mite and a pathogenic virus undermines honey bee immunity and health.  PNAS vol. 113(12): 3203–3208.

[12] Erban, T, et al (2015) In-depth proteomic analysis of Varroa destructor: Detection of DWV-complex, ABPV, VdMLV and honeybee proteins in the mite. Sci Rep. 5: 13907.

[13] For some reason, DWV doesn’t appear to be much of a problem in mite-infested colonies in Africa.

[14] Ryabov, EV, et al (2017) Recent spread of Varroa Destructor Virus-1, a honey bee pathogen, in the United States. Scientific Reports 7: 17447.

[15] Jamnikar-Ciglenecki, U, et al (2018) Genetic diversity of Deformed Wing Virus from Apis mellifera carnica (Hymenoptera: Apidae) and varroa mite (Mesostigmata: Varroidae). Journal of Economic Entomology https://doi.org/10.1093/jee/toy312

[16] Wu JY, et al (2011) Sub-lethal effects of pesticide residues in brood comb on worker honey bee (Apis mellifera) development and longevity. PLoS ONE 6(2): e14720.

[17] Di Prisco, G, et al (2013) Neonicotinoid clothianidin adversely affects insect immunity and promotes replication of a viral pathogen in honey bees.  Proc Natl Acad Sci 110(46): 18466–18471.

[18] https://www.aphis.usda.gov/plant_health/plant_pest_info/honey_bees/downloads/2014-2015-National-Survey-Report.pdf

Category: Varroa Management