Prof Evans DWV talk at Canterbury BKA

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itma 

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There was a good attendance at the meeting yesterday - I recognised some that had come from as far afield as Orpington. The following is my 'takeaway' and I hope that others present won't feel restrained in correcting any misapprehensions.

I am posting this meeting report in this section (rather than under Association News), as I feel it deserves to have a wider audience, and generally inform the discussion of Varroa and DWV.



Prof Evans had come all the way from Warwick University where his speciality is virology, within the Department of Life Sciences.
An amateur beekeeper himself, he and his team have been working on Deformed Wing Virus and Varroa for the last three years, applying the technology and skills that they had developed over more than 20 years working principally on the, somewhat similar, human Polio virus.
The research uses 'black' bees transported from Colinsay, off the Scottish west coast, where they have never encountered varroa.
These were found to already have very low levels of DWV, and the actual viruses were of many diverse types. It seems that this virus has (until varroa) been able to coexist with its host without causing undue problems.
However, after exposure to varroa, the virus population could change dramatically, increasing in number by 10,000 times, and decreasing in diversity to a single utterly dominant strain.

To a certain extent, this merely confirmed the 2011 paper on the development of DWV following the arrival of varroa in Hawaii.
There the virus population was seen to change over a period of 3 years.

The difference with the Warwick research is that they have observed this process happening in individual bees, within just 6 days!
What seems to be happening is that when the normal virus cocktail is injected into the bee's haemolymph, virus recombination produces a new strain, which replicates very rapidly, to the high levels observed, and in turn affecting the genes responsible for development, which in turn produces the deformed bees that give the virus its name.
This recombination and wildfire replication does not happen when the bee larvae are simply fed the same virus cocktail.
However it does happen when the pre-existing virus cocktail is simply mechanically injected into the larvae (by a syringe rather than varroa).
Hence it appears that the role of varroa is passive in the virus development. It simply delivers the old viruses in a new way, with dreadful results. It does not appear that varroa incubates or selects or promotes any of the viruses - it just injects them.

The fact that the 'wildfire strain' (my term not the Prof's - blame The Andromeda Strain) appears to be a single virus type, and specifically a novel recombinant between the close relatives DWV and VDV-1 opens the way to the possibility of various novel genetic or genetically-informed therapies.

Beyond injecting the original virus cocktail, varroa has a role in picking up some of the wildfire strain and re-injecting it (so providing an unhealthy starter of the wildfire strain) with the result that the amount of that strain in the colony grows even faster.

It isn't (yet) a conclusion from the study, but Prof Evan's own feeling is that a reduced treatment-threshold varroa level may be called for -- if I correctly understood him through his reluctance to go beyond their completed research.

His starting point had been a reminder that elevated levels of DWV (but below the level causing stunted wings and abdomens) reduced worker foraging efficiency, reduced worker learning capability (an echo there of something else), and reduced worker lifetime which carried through (due to reduced winter-bee lifetime) into reduced colony winter survival.

It is the novel DWV/VDV-1 recombinant (a single virus type) that presents the real threat to our bees.
Varroa is its (remarkably passive) instrument, bringing about its creation, and spreading it.

DVW was detectable in something like 95% of colonies checked in DEFRA's "Random Apiary Survey".
Varroa-free colonies, placed in a field in the Midlands, were found to have acquired mites within a couple of weeks ... so the research colonies have to live in enclosed polytunnels ...
Something I found interesting (confirming my anecdotal observation that high-varroa-loaded bees tended to be aggressive) is that one member of the DWV virus 'family', one called "Kakugo Virus", specifically produces aggression in infected bees!
There were many other sidelights like this throughout an interesting, and remarkably in-depth talk.
I am left with a nagging concern about the result of Queens with the hybrid DWV and Queens bred for their offspring. Yes, the virus is transmitted vertically, mother to daughter.


The research continues.


/// All errors in the above are mine! -- itma
/// And my thanks to Prof Evans for making the long trek to speak at Canterbury.
 

pargyle 

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Fascinating ... and thanks for taking the trouble to post for the benefit of those of us too far away to attend ...

What did you mean by this:

"It isn't (yet) a conclusion from the study, but Prof Evan's own feeling is that a reduced treatment-threshold varroa level may be called for "
 

itma 

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It isn't (yet) a conclusion from the study, but Prof Evan's own feeling is that a reduced treatment-threshold varroa level may be called for -- if I correctly understood him through his reluctance to go beyond their completed research.
This was in response to questioning after the presentation.
Prof Evans said something along the lines of "That's the sort of question I get paid to answer!" when asked if his understanding of the mechanisms involved would indicate a lower tolerable varroa population (ie before the colony stress, etc, of treatment became worthwhile) and where that threshold ought to be.
He said that, interdepartmentally at Warwick, they were currently looking to see whether they had enough info to model things and make predictions. If I understood him correctly, he personally felt that "the fewer varroa the better", but that his researches had not yet borne directly upon this area of practical benefit.



One additional point from the presentation was that not all of the varroa-naive larvae produced high virus counts on exposure to live varroa. About 30% didn't. His groups current thinking was that this was not due to any genetic resilience on the part of those larvae (they had looked for it), but was most likely due to simple variability of the quantity of virus injected.
 

alanf 

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Now that's an interesting finding.
specifically a novel recombinant between the close relatives DWV and VDV-1
Did he mention any examples, other than this one, where a similar mechanism has been observed? I think the usual assumption is that virus recombination or mutation happens once to produce a new strain and that new strain of virus then spreads. I'm thinking of the H5N1 bird flu and H1N1 swine flu examples. Here, the precursor virus, prompted by physical factors, can recombine to form a recognisable strain, and what's more it can do it in repeatedly within days in isolated examples. Quite a discovery, and a big "what if" for epidemiology to think about.
 

mbc 

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but Prof Evan's own feeling is that a reduced treatment-threshold varroa level may be called for
My feeling is that this approach will largely be discarded within a few years, hopefully!
 

itma 

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Rather than relying on my report (first post, this thread), see the September 2014 edition of Beecraft for Prof Evans' own discussion of his group's research.
 

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