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From:
Jack Grimshaw <[log in to unmask]>
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Informed Discussion of Beekeeping Issues and Bee Biology <[log in to unmask]>
Date:
Mon, 18 Jan 2016 08:53:40 -0500
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Ghislain,
Interesting paper,but the next paper listed on researchgate by the same authors caught my eye and suggests an even more interesting line of research.

"Superinfection exclusion and the long-term survival of honey bees in Varroa-infested colonies"

Abstract

Over the past 50 years, many millions of European honey bee (Apis mellifera) colonies have died as the ectoparasitic mite, Varroa destructor, has spread around the world. Subsequent studies have indicated that the mite's association with a group of RNA viral pathogens (Deformed Wing Virus, DWV) correlates with colony death. Here, we propose a phenomenon known as superinfection exclusion that provides an explanation of how certain A. mellifera populations have survived, despite Varroa infestation and high DWV loads. Next-generation sequencing has shown that a non-lethal DWV variant 'type B' has become established in these colonies and that the lethal 'type A' DWV variant fails to persist in the bee population. We propose that this novel stable host-pathogen relationship prevents the accumulation of lethal variants, suggesting that this interaction could be exploited for the development of an effective treatment that minimises colony losses in the future. 

This is a quote from results and discussion

" SIE has been well documented in viruses related to DWV, for example, Tscherne et al. (2007) used cell lines to show that infection by one genotype of hepatitis C virus prevented infection by others. SIE best explains the phenomenon of why, despite high DWV load and Varroa infestation, the isolated UK colonies do not collapse. We speculate that co-evolution of the honey bee-Varroa mite-DWV system has selected for a new stable equilibrium where both the Varroa and an avirulent type B variant of DWV protect the honey bee, and thus the colony, from the virulent type A (Figure 8). Further work to validate this and determine the mechanism of the viral exclusion is required. For example, to demonstrate whether type B can protect against type A or C at the cellular and individual honey bee-level using assays similar to those described by Ryabov et al. (2014). If true, this would be the first report of SIE acting on the Iflavirus pathogens of bees. Ironically, it may be the presence of the mite population that is protecting the colony as Varroa may be providing the opportunity for constant re-introduction of type B into the population via horizontal transmission. In addition, although recombinants were present in both honey bee and Varroa samples, it is unclear whether these originate in the honey bees, Varroa or both"

Superinfection exclusion and the long-term survival of honey bees in Varroa-infested colonies (PDF Download Available). Available from: 

https://www.researchgate.net/publication/283288701_Superinfection_exclusion_and_the_long-term_survival_of_honey_bees_in_Varroa-infested_colonies [accessed Jan 18, 2016].

The hives studied were from Ron Hoskins,a miticide-free beekeeper in the UK who has been breeding from mite-biters since 2004.


Jack



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