This is the first, introductory part of a series of articles that address the issue of viruses and their complex relationship with varroa. It is a translation of an article written during Summer/fall 2021 in Greece, one of the most bee-dense countries in the world. The varroa/viruses situation was dramatically increased the recent years and therefore an updated overview is needed. The cold fact is that Bee Viruses cannot be managed empirically by the beekeeper. However, the literature provides plenty of useful knowledge.
Viruses and Virions
Viruses are simple biological structures that parasitize cells. It is impossible for them to multiply outside their host cell and they need to use its internal cellular functions. Viruses are specialized in infecting specific hosts, without precluding a gradual and evolutionary change of hosts.
The infectious form of the virus is called virion. The virion either carries an outer shell made from a portion of the host cell membrane, or otherwise it carries proteins that mimic the outer proteins of the host cells. It is important to emphasize that viruses are like biological machines. They are not life forms and do not have “behavior” or “intelligence”.
The viruses in the bee are mainly transmitted from one “bee” to another “bee”. In particular, the following can be transmitted:
- Among workers (crawling, friction),
- from a nurse bee to brood (not all viruses),
- from brood to bee (when, for example, hygienic cannibalism takes place),
- from a drone to a queen and from a queen to an offspring,
- The viruses are easily transmitted by a carrier parasite (varroa, trachea mite, etc.) through the wounds that the parasites feed themselves.
Viral diseases were rare before the spread of Varroa and Nosema Apis as bees could cope with them. There were viruses of minor beekeeping importance (sacbrood [1]), while the subject of bee virology had not been yet developed. The spread of Nosemosis brought to the fore a series of viruses [2], [3] and aroused scientific interest. Viruses such as the Black Queen Cell Virus, the Thread Virus, etc. appeared to manifest themselves as opportunistic infections. This is not surprising, considering the histological damage caused by the disease to the epithelial layers of the stomach (midgut).
In the absence of a vector, bee viruses quickly lose their infectivity. On surfaces (wax, food, etc.,) virions are rapidly destroyed, with the exception of the rather persistent chronic paralysis virus. Therefore, it is easy to conclude that the usual cleaning measures such as disinfection, honeycomb replacement, etc., have no practical effect against viruses. They have, on the contrary, an effect against sporogenic microorganisms (AFB bacteria, nosema, fungi, etc.).
Exposed tissues and damaged epithelial cells offer opportunities for viruses to penetrate the bloodstream while creating an ideal environment for viral infections. Other important viruses have probably spread from the tracheal mite (Chronic Bee Paralysis virus).
The global outbreak of varroa in the 1980s further increased the incidence of viruses and identified a different group of viruses than those which paired with nosema. These viral infections were not detected in the field, except at the final stage of mite parasitism. The textbooks of the time oversaw the viruses and focused on the fight against varroa. After all, in the ’80s and’ 90s scientists with knowledge of virology were few in the world and many viruses were attributed to other diseases. For example, even today the symptoms of the chronic paralysis virus are frequently attributed to Nosema. The dead brood due to hyperparasitism from varroa (due to sacbrood virus etc) was hastily attributed to American foulbrood or some atypical sepsis. This is usually undereported by European beekeepers for fear of measures by the authorities.
The fact that not much was known about viruses mystified the varroa problem, delaying the progress of studies. For example, in the mid-1990s, Steven Martin’s research team and colleagues studied varroa and sought to find out how many varroa it would take for a hive to collapse. The data did not lead to any conclusions. Other bees withstood great infestation, others collapsed with moderate infestation and each hive appear to have its own particularity. Then, few people specialized in bee virology brought up the first enlightening conclusion about the colony collapse by varroa:
“The collapse of untreated colonies is caused by viruses and not by the varroa population itself.”
The role of varroa in the transmission of viruses had been pointed out early [6], [7], [8] although the above hypothesis had not been made. One would argue that “it makes sense for a varroa infested hive to get viruses and then collapse”. It is not like that at all. In the presence of pathogenic strains of the virus, approximately 3,000-4,000 varroas per 20,000 bees are needed for a colony to collapse.
On the other hand, in the absence of viruses, huge varroa populations have to be build in order to cause the collapse of the colony (plain haemolymph/fat body parasitisation). There have to be as many mites as bees. This is evidenced by the examples of bee populations in areas of the world that have received large loads of varroa (Fernando de Noronha Island, South Africa). In the case of South Africa [9], functional bee colonies of A. Mellifera Scutellata were studied in 1999 with the average varroa population ranging from 12,000 to 17,000 varroa per 20,000 bees!
In 1990, the bees of Italian origin on the island of Fernando tolerated far more varroa infestation [10] than the ones our bees (Greece) tolerate. As it was found later [11], the absence of pathogenic strains of the deformed wing virus (and possibly other viruses) made them able to resist varroa, but only in their area. When the queens from the island of Fernando were experimentally transported to Germany in 1997, they demonstrated no resistance to varroa infestation.
Different types of viruses were detected in beehives with varroa problem and the next step was to distinguish which viruses play a role in the collapse. Studies by Martin (2001) and Sumpter and Martin (2004) ruled out the role of some paralytic viruses in collapse (SPV, ABPV, KBV) and showed by mathematical models that large populations of varroa of 10,000 per colony were required to cause collapse [12], [13]. These viruses are very aggressive and quickly kill the brood and /or bees. Their epizootic course within is stopped by the aggression itself. The models pointed to a much milder virus, the Deformed Wing Virus (DWV) as the main culprit. This discovery was preceded by suspicions from Scandinavian researchers [14] published in 1999, as well as other studies [15].
Indeed, the more scientists looked at the issue of viruses worldwide, the more the harmful role of the Deformed Wing Virus became apparent. The second conclusion that emerged as a hypothesis in the late 1990s and confirmed in the late 2000s is that the most frequent etiology for the rapid collapse of varroa bees is a single virus, the Deformed Wing Virus.
Furthermore, the deformed wing virus is the cause of the rapid multiplication of varroa, as we will see in the next article. One easily wonders, why did it take decades for a few scientists to come to these two basic conclusions and a few more years for these to be accepted by the scientific consensus?
First, the data were scarce because the geographical spread of the pathogenic Strain of the DWV was slow and also the molecular detection techniques were not sophisticated at that time. Second, there was skepticism about the role of the viruses. The new findings had to compete with the flawed presupposition that bees were collapsing due to the sucking of their hemolymph by varroa. Although the Deformed Wing Virus has been known and accurately described since at least 1991 by L. Bailey and B. Ball in a textbook [16], field observations often interpreted the deformed wings as “varroa-induced deformities” caused by “draining of growing bee’s fluids”.
To the contrary, varroa is a distinctive parasite in itself and would not risk damaging the chrysalis too much. It would lead the nurse bees to spot the infected cell and uncap it causing the end of the varroa breeding cycle. The brood is affected mainly by viruses and this is done at the right time when the colony can not manage the situation. This complex pathogenesis leads to classic empirical errors. An example of such an error is when varroa levels are estimated “by the plain eye”, just by checking the brood pattern. When a colony feeds well in autumn (eg. Erica, Ivy, pollen variety, etc.) the shotgun pattern tends to disappear and the brood is even, despite being infested with varroa. On the other hand, the brood shotgun pattern during pollen dearth is not necessarily associated with high levels of varroa.
In the past, treating viruses on a practical level consisted of keeping strong colonies and fighting varroa. Now the situation has changed and this approach is behind the circumstances. At least in Europe, varroa poses serious problems (with a few exceptions, such as in North Wales), and it has developed a symbiotic relationship with viruses. In the next post we will describe how the success of varroa breeding cycle depends on the levels of the deformed wing virus. Colonies eventually carry moderate to large viral loads almost all year round. Just because colonies are asymptomatic does not mean that they do not consume energy on mobilizing their immune system.
Bee Diet and viruses
The practical treatment of the varroa-virus complex will be described mainly in a next article, but since the nutritional issue was mentioned, it has to be clarified further. The prevailing view is that good nutrition (which translates into migrations in pollen abundant areas etc.) helps the bees to fight diseases, including viruses. This introduces a fallacy.
In spring, or when there are good autumn pollens, the bee is fed as it is supposed to be fed so the bees tend to be asymptomatic, or have the best possible health. Therefore, when bees feed well after a dearth, they appear “resilient to disease”, but it is just the bees returning to normality. Just because a poor diet makes bees vulnerable, does not mean that a particular diet can somehow used as a cure. After all, no matter how well the bee feeds, the varroa continues to bypass the colony’s natural defenses, while at the same time, the Deformed Wing Virus suppresses the pupae basic defenses (melanization, encapsulation [17]). So a conjuncture of a good diet in conditions of migratory beekeeping, will simply shift the underlying problems few weeks later.
The point to be emphasized is that when we deal with a disease, we either remove the harmful factors, or we remove the bees from the harmful factors. It is not advisable to waste time dealing with things sideways (through diet). This concerns both the good nutrition in its natural form (“wet” pollens, etc.) and the “artificial” (pollen substitutes, supplements, vitamins). Protein substitutes may be necessary in other climate zones (eg Australia, USA), but in most climates of Greece they are not necessary. For example, if deformed wing bees are found in a productive hive in the summer, the hive needs to be harvested and treated as soon as possible. We do not rely on the next migration which “will be in quality pollen and will benefit the bees”.
George Mitsikas (Amateur Beekeeper, Chemist)
Alexia Kalamida (Drug Technician)
First published January 2022
BIBLIOGRAPHY
[1] Bailey, L., & Fernando, EFW (1972). Effects of sacbrood virus on adult honey ‐ bees. Annals of Applied Biology , 72 (1), 27-35.
[2] Bailey, L., Ball, BV, & Perry, JN (1983). Association of viruses with two protozoal pathogens of the honey bee. Annals of Applied Biology, 103 (1), 13-20.
[3] The paper describes certain viruses among others associated with Nosema: Bailey, L., & Woods, RD (1977). Two more small RNA viruses from honey bees and further observations on sacbrood and acute bee-paralysis viruses. Journal of General Virology , 37 (1), 175-182.
[4] Martin, S., Hogarth, A., Van Breda, J., & Perrett, J. (1998). A scientific note on Varroa jacobsoni Oudemans and the collapse of Apis mellifera L. colonies in the United Kingdom. Apidology , 29 (4), 369-370.
[5] The deadlocks in early varroa studies are also described by S. Martin himself in the video https://youtu.be/5JP1f4UJ9v8?t=636
[6] Viral paralysis is described by YM Batuev (1979) and even blames varroa (the first reference to a causal relationship we identified), but the publication was not accessible.
[7] Ball, BV (1985). Acute paralysis virus isolates from honeybee colonies infested with Varroa jacobsoni. Journal of Apicultural Research, 24 (2), 115-119.
[8] Ball, BV and Allen, MF (1988). The prevalence of pathogens in honey bee (Apis
mellifera) colonies infested with the parasitic mite Varroa jacobsoni. Annals of Applied
Biology ‘, 113, 237-244.
[9] Allsopp, Mike. (2006). Analysis of Varroa destructor infestation of southern African honeybee populations
[10] Correa-Marques MH, De Jong D, Rosenkranz P, Gonçalves LS. Varroa-tolerant Italian honey bees introduced from Brazil were not more efficient in defending themselves against the mite Varroa destructor than Carniolan bees in Germany. Genet Mol Res. 2002 Jun 30; 1 (2): 153-8. PMID: 14963842.
[11] Brettell, LE, & Martin, SJ (2017). Oldest Varroa tolerant honey bee population provides insight into the origins of the global decline of honey bees. Scientific reports, 7 (1), 1-7.
[12] Martin, SJ (2001). The role of Varroa and viral pathogens in the collapse of honeybee colonies: a modeling approach. Journal of Applied Ecology , 38 (5), 1082-1093.
[13] Sumpter, DJ, & Martin, SJ (2004). The dynamics of virus epidemics in Varroa ‐ infested honey bee colonies. Journal of Animal Ecology , 73 (1), 51-63
[14] Nordström, S., Fries, I., Aarhus, A., Hansen, H., & Korpela, S. (1999). Virus infections in Nordic honey bee colonies with no, low or severe Varroa jacobsoni infestations. Apidology , 30 (6), 475-484.
[15] Bowen-Walker PL, Martin SJ, Gunn A. (1999) The transmission of deformed wing virus between honeybees (Apis mellifera L.) by the ectoparasitic mite Varroa jacobsoni, J. Invertebr. Pathol. 73, 101-106.
[16] Honey Bee Pathology – 2nd Edition (1991) Authors: Leslie Bailey, B. Ball.
[17] Di Prisco, G., Annoscia, D., Margiotta, M., Ferrara, R., Varricchio, P., Zanni, V., Caprio, E., Nazzi, F. and Pennacchio, F., 2016 A mutualistic symbiosis between a parasitic mite and a pathogenic virus undermines honey bee immunity and health. Proceedings of the National Academy of Sciences, 113 (12), pp.3203-3208 .
General Bibliography
“Virology and the Honey Bee” (2008) Edited by Michel Aubert, Brenda Ball, Ingemar Fries, Robin Moritz, Norberto Milani and Iris Bernardinelli.
BEE DISEASES- Unconventional methods of dealing with them – Michael D. Yfantidis. May 2011. Greek Editions “Beekeeping Inspection”
The Beekeeping Lab 
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