GG (or anyone), how did they know the virus was replicating*? I saw the distinction in a supplementary table but didn't see their justification for discriminating the two.
I hear that they captured bees (Apis and Bombus) at the same site using a net. How can they be sure that they are not cross-contaminating samples at the point of collection?
I don't see why they used variables like number of sunshine hours to fine tune their model ....
'including biologically relevant interactions while controlling for latitude, longitude and sunlight hours, and adding collection site and species identity as random factors. Our full model for DWV presence fitted the data significantly better than the null model without any of the test predictors and their interactions included (likelihood ratio test: X2519.03, d.f.55, P,0.002). '
... sounds like tinkering, no? And are we really to believe that fine-scale local variations in DWV/Varroa presence on honeybees influences levels of virus in bumble bees in the same local area? If so, how? Surely a mile or so down the road beekeeping practice will be different and DWV/Varroa levels different? And are Varroa supposed to do this apparently wholesale Apis-Bombus disease transfer?
*PS
What I mean is the distinction made in the paper between virus which is just present from virus which is replicating.
Bookmarks