Below is the abstract of a technical paper that examines aspects of GM studies that cast light on the processes by which bees gain resistance to viruses. That's followed by extracts from a second paper that seem to elaborate usefully.
Some people think this understanding could lead to new and useful techniques that beekeepers could use. Its also probable that Monsanto (who appear to have bought some of the leading research) will try to exploit to their own sweet ends.
In either case its probably worth having a working knowledge of what's going on.
I think one useful thing to try to figure out (we don't get it here) is how often it occurs that a fragment of virus is absorbed into a bee genome in a way that confers resistance to that virus. (It would also be good if somebody could explain _how_ it confers that resistance.)
In my view an important thing to remember, that is incorporated, but not elaborated in the text, is that when that happens it supplies a new mechanism that is then utilized in the normal adaptive/evolutionary processes.
With that second point in mind, we could usefully try to discover a response to the first - how often does it happen. I think an indication is supplied by the extracts, but that's as far as I've got.
Please feel free to pick these thoughts apart and correct me. I'm here to learn.
Maori E, Tanne E, Sela I: Reciprocal sequence exchange between non-retro viruses and hosts leading to the appearance of new host phenotypes.
[Abstract only available]
Divergence among individuals of the same species may be linked to positional retrotransposition into different loci in different individuals. Here we add to recent reports indicating that individual variance occurs due to the integration of non-retroviral (potyviral) RNAs into the host genome via RNA recombination followed by retrotransposition. We report that in bees (Apis mellifera), approximately 30% of all tested populations carry a segment of a dicistrovirus in their genome and have thus become virus-resistant. Reciprocally, segments of host sequences have been found within defective-interfering-like sequences of a dicistrovirus. Similarly, host sequences were found fused to potyviral sequences, previously described integrated into their host genome. A potential, continuous RNA exchange leading to divergence is discussed.
Isolation and characterization of Israeli acute paralysis virus, a dicistrovirus affecting honeybees in Israel: evidence for diversity due to intra- and inter-species recombination
Eyal Maori, Shai Lavi, Rita Mozes-Koch, Yulia Gantman, Yuval Peretz, Orit Edelbaum, Edna Tanne and Ilan Sela
[Full paper available]
Intra- and inter-species recombination of viral and viral-non-viral sequences
A DNA version of a segment of IAPV RNA has been found integrated into the bee genome, and reciprocally, a host sequence has been found embedded in an IAPV-related DI RNA (Maori et al., 2007). Figs 1⇑ and 5⇑ indicate the presence, within the virions, of RNAs carrying IAPV sequences which are smaller than full-length.
Although RNA recombination requires certain structural features, by and large, it is a random occurrence. Therefore, the amount and characteristics of encapsidated DI-like RNAs may change from one cycle of infection to the next, and viral populations may differ from each other in this respect. We showed different profiles in different viral preparations (Fig. 5⇑). Therefore, the reported quantitative values apply to that particular viral preparation, and may differ when other preparations are tested.
In many instances, bee viruses are found as non-apparent infections in their host. This may result from competition between the viral RNA and the abundant DI-like RNAs, but also from the abundance of double-stranded RNA structures carrying viral sequences. In the latter case, the balance between host factors silencing viral sequences and the virus-induced silencing suppressors may shift in favour of viral silencing. Another postulated consequence inferred from the various types of DI-like RNAs is the modification of proteins resulting from deletions, engendering deleted or frame-shifted proteins. Thus, RNA recombination may elicit protein divergence with obvious evolutionary impact. Furthermore, a reciprocal exchange between host DNA and viral RNA (or a DNA version of a recombinant viral RNA) has been demonstrated (Tanne & Sela, 2005; Maori et al., 2007). Therefore, RNA recombination may engender divergence in host genes, and the evolution of both virus and host may be interrelated and linked to the very same eliciting process. "