> On Sep 5, 2015, at 8:34 AM, randy oliver <[log in to unmask]> wrote:
>
> Hence, high bee densities combined with ineffective treatment
> will not only increase the risk of colony damage
> but might also select for more virulent Varroa mites.
>
>
> Although I have the highest respect for Frey and Rosenkranz, I question
> their last hypothesis. The more severely varroa is controlled, the greater
> the selection pressure for virulence. It would be in an uncontrolled
> population that natural selection might select for avirulence.
Hmm. We could discuss this at length. I would begin by saying that the problem with mites is the virus, not so much the mites themselves. (Interestingly, the term “virulence” derives from the Latin virulentus, from virus “poison”). So the question becomes, what conditions promote or enhance the lethality of the viruses.
> Host-pathogen interactions can be broadly divided into asymptomatic or symptomatic infections [1]. In the former, the absence of symptomatic disease is typically due to restricted pathogen replication, which reduces the opportunities for horizontal transmission within its host population. Conversely, prolonged survival of the infected host increases the likelihood of vertical transmission of the pathogen [2]. The ‘lifestyle choice’ of asymptomatic or symptomatic infection is determined by multiple factors including the duration of host-pathogen co-evolution, host physiology and anti-pathogen responses, routes of transmission and environmental factors. Evolutionary changes in pathogen virulence may be triggered by changes in pathogen-host assemblages
Ryabov, Eugene V., et al. "A virulent strain of deformed wing virus (DWV) of honeybees (Apis mellifera) prevails after Varroa destructor-mediated, or in vitro, transmission." (2014): e1004230.
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