Recently accepted for publication
Ryabov 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
The globally distributed ectoparasite Varroa destructor is a vector for viral pathogens of the Western honeybee (Apis mellifera), in particular the Iflavirus Deformed Wing Virus (DWV). In the absence of Varroa low levels DWV occur, generally causing asymptomatic infections. Conversely, Varroa-infested colonies show markedly elevated virus levels, increased overwintering colony losses, with impairment of pupal development and symptomatic workers. To determine whether changes in the virus population were due Varroa amplifying and introducing virulent virus strains and/or suppressing the host immune responses we exposed Varroa-naïve larvae to oral and Varroa-transmitted DWV. We monitored virus levels and diversity in developing pupae and associated Varroa, the resulting RNAi response and transcriptome changes in the host. Exposed pupae were stratified by Varroa association (presence/absence) and virus levels (low/high) into three groups. Varroa-free pupae all exhibited low levels of a highly diverse DWV population, with those exposed per os (group NV) exhibiting changes in the population composition. Varroa-associated pupae exhibited either low levels of a diverse DWV population (group VL) or high levels of a near-clonal virulent variant of DWV (group VH). These groups and unexposed controls (C) could be also discriminated by principal component analysis of the transcriptome changes observed, which included several genes involved in development and the immune response. All Varroa tested contained a diverse replicating DWV population implying the virulent variant present in group VH, and predominating in RNA-seq analysis of temporally and geographically separate Varroa-infested colonies, was selected upon transmission from Varroa, a conclusion supported by direct injection of pupae in vitro with mixed virus populations. Identification of a virulent variant of DWV, the role of Varroa in its transmission and the resulting host transcriptome changes furthers our understanding of this important viral pathogen of honeybees.
I’m delighted to be talking – twice (!) – at the Yorkshire Beekeepers Association Spring Conference in York on Saturday the 12th. With Stephen Martin (bee recognition and the Asian hornet), Jay Evans (beenomics – is that a real word?), Ben Jones (nutrition) and Liz Collison (neonicotinoids) also on the programme it promises to be an enjoyable day.
Update – it was a very enjoyable meeting, well attended and with two parallel sessions to entertain the audience. The sessions finished with breakout groups to “ask the experts” (or wonder where the expert was as I couldn’t find the room) followed by a wrap-up meeting. I’d like to thank the YBKA, Roger Chappel and Michael Badger for their excellent hospitality.
I’m delighted to be speaking at the Bee Farmers Association (BFA) Spring Conference on Saturday 8th March. The BFA are the voice of professional beekeeping and their members are responsible for virtually all migratory beekeeping in the UK, together with contract pollination services and bulk honey production and sales.
Update: I spent an enjoyable afternoon with the BFA talking about Varroa and viruses. I’d like to thank John Howat and Murray McGregor for their hospitality and the audience for their wide-ranging and enthusiastic questions. It was a good opportunity to discuss the practical applications of research into honeybee viruses.
Page 3 CBKA newsletter
I’m pleased to be speaking at Canterbury Beekeepers on the 5th of March about The plight of the honeybee – identification of a virulent strain of Deformed Wing Virus and was amused they’d posted the announcement – complete with the cropped image I provided – on page 3 of their very professionally produced newsletter.
Probably the only acceptable topless page 3 image of me.
Update (7th March)… isn’t the interwebs a wonderful thing? Not only was there a discussion before the evening on the Beekeeping Forum about the talk and venue, but an account of the talk was subsequently posted online. The latter included debate of some of the points raised in the talk which got a little lost in translation. As a friend said to me “it’s like reading your own obituary“. It’s more than a little tempting to register and post something scurrilous …
I’d like to thank Canterbury Beekeepers for an enjoyable evening, an attentive and interesting audience and their excellent hospitality.
Rothamsted scientists have identified the specific mutation in the voltage-gated sodium channel (the target site for pyrethroids like tau-fluvalinate [Apistan] and flumethrin) that confers resistance in mites. Interestingly the mutation appears to be lost in the absence of pyrethroid application, suggesting it may be deleterious unless pyrethroids are present. This implies that areas historically associated with pyrethroid resistance – of which there are many – may be able to use these chemicals again to control the mite.
Identification of the mutation may enable genetic screening for resistance to be undertaken. In addition, now the mutation is identified it should be possible to determine how quickly it is acquired during Apistan treatment (which can of course also be tested for phenotypically), and how long it takes to be lost after treatment terminates. This may enable some sort of rational pyrethroid treatment regime to be developed, with alternating pyrethroid and non-pyrethroid applications.