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  • Writer's pictureJohn Mackay

The Damning Debilitating Disaster of Deformed Wing Virus

UNDER THE MICROSCOPE I BROUGHT TO YOU BY dnature


By John Mackay

Many have heard myself and others like Dr Richard Hall (MPI) speak on Deformed Wing Virus (DWV) – or as I prefer to call it: Hive Killer 1. This was the virus that finally kicked our interest in bee pathogens into gear over a decade ago.

Deformed wing virus has four strains, only one is found in New Zealand.

Since then, much has been learned about this virus – in particular, the presence of different strains of the virus. Much the same way we’ve had Alpha, Delta and Omicron variants of the COVID-19 virus, DWV has two major strains (and two minor ones), imaginatively-named DWV-A, B, C and D. We have developed new variant-specific tests for A, B and C to show that only DWV-A is present in New Zealand and similar work by Richard and the team at MPI also shown this single strain present.

A new paper sought to confirm the differences between these strains in how they are vectored by varroa and their virulence differences: Transmission of deformed wing virus between Varroa destructor foundresses, mite offspring and infested honey bees (Piou et al., September 2022 open access). The paper, researched in France, looked at the virus strains in the mites, the bees they infected, and in the mite progeny.

However, the mites and bees used in this work were shown to have high levels of strain B of DWV – and this strain appeared to repress DWV-A when varroa was present and indeed, grow to higher viral levels – likely indicating the replicative ability of DWV-B in both varroa and the bees they infected. Our New Zealand strain (DWV-A) had levels in varroa that mirrored the bees they had infected. Like the nosema story from the September Apiarist’s Advocate describing the double whammy effects of both nosema species, then the paper describes a similar effect of varroa vectoring both DWV-A and B with a mortality rate over double that of a single viral strain.

Of particular note was the viral levels in the varroa offspring: closely related to their mother’s viral levels, thought to be due to shared feeding sites on pupa, rather than infected mites laying infected eggs (where virus couldn’t be detected). However, it looks like the mites are infectious as soon as they emerge from the cell, reinforcing the importance of timing varroa treatments appropriately.

So what? We don’t have DWV-B here in New Zealand it seems? And this work was done in a background of DWV-B in the mites. Maybe so, but it highlights the general timing of varroa infectivity to the colony (as soon as they emerge) as well as that virus-free bees are little protection when you have a dirty hypodermic needle called varroa sharing the DWV around.


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