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Will Atkins wrote:On the question of 'ammodytes' genes for venom in SE populations of aspis, could it not perhaps be that 'ammodytes genes' are not the same as Vipera ammodytes? maybe these signature genes pre-date the extant species that we refer to as Vipera ammodytes? perhaps some ancestral species of Vipera even which branched into aspis and also ammodytes. Or maybe I'm being a bit too Dawkins-esque by considering the gene rather than the whole animal... !
Pure speculation, just thinking out loud..

Thinking in the right way and in the right direction, I would say. Thanks a lot.

thank you!

off topic, but interesting to read such a crazy thing.
http://vipersgarden.at/PDF_files/PDF-9739.pdf

Snake bites are common in many regions of the world. Snake envenomation is relatively uncommon in Egypt; such unfortunate events usually attract much publicity. Snake bite is almost only accidental, occurring in urban areas and desert. Few cases were reported to commit suicide by snake. Homicidal snake poisoning is so rare. It was known in ancient world by executing capital punishment by throwing the victim into a pit full of snakes. Another way was to ask the victim to put his hand inside a small basket harboring a deadly snake. Killing a victim by direct snake bite is so rare. There was one reported case where an old couple was killed by snake bite. Here is the first reported case of killing three children by snake bite. It appeared that the diagnosis of such cases is so difficult and depended mainly on the circumstantial evidences.

Back to the topic...

Regarding the “neurotoxic V. a. aspis” issue, I would recommend the following paper from 2007
as a particularly good, thorough, and revealing read:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2065900/

But when it comes to hybridization as some kind of a “universal, shortcut, ready-made solution”
for too many unclear and complicated issues, I’d prefer to remain silent.

I read this publication few days ago but did not cite it because there is also no clear explanation, especially for the V.a.z. ("Its genome contains an arsenal of PLA2 neurotoxins ready to be expressed under stimuli that still need to be identified"...). The scenario developed by Will could make sense for the SE population but hardly for the West one. What is interesting is that "Vaz venom neurotoxicity is due to a postsynaptic neurotoxin, PLA2-I, homologous to vipoxin", which explains why Viperfav treatment should work well for Vaz.

so you may read also this:
Author: Garrigues, T., C. Dauga, E. Ferquel, V. Choumet & A.-B. Failloux
Year of publication: 2005
Title: Molecular phylogeny of Vipera Laurenti, 1768 and the related genera Macrovipera (Reuss, 1927) and Daboia (Gray, 1842), with comments about neurotoxic Vipera aspis aspis populations
Journal: Molecular Phylogenetics and Evolution 35 (2005) 35–47
Abstract: We used mtDNA sequences (cytochrome b and NADH dehydrogenase subunit 2) to reconstruct molecular phylogenies of Vipera sensu lato, Vipera sensu stricto, and Vipera aspis. Three major clades were identified within the Vipera s.l. group: (1) the European vipers, (2) the oriental vipers, consisting of Montivipera (Vipera 2) plus Macrovipera lebetina, and (3) a group of Asian and North African vipers consisting of Daboia russelii, V. palaestinae, and Macrovipera mauritanica. We also distinguished three clades within the monophyletic European Vipera group: V. ammodytes, V. aspis, and V. latastei, and Pelias with monophyly of Vipera 1 uncertain. Within V. aspis, the specimens collected in France formed the sister group of an Italian clade. The “neurotoxic” French population of V. aspis, which has a specific venom profile, separated from other French V. aspis early in the history of this group.

PDF-0983 in db

A very good read, thanks Mario.

A recent retrospective analysis of 542 envenoming snakebites in southern Croatia (total population, ∼500,000) reported a mean annual incidence of bites of approximately 5 per 100,000. The most common signs and symptoms were coagulopathy, extensive swelling and edema, ecchymosis, and regional lymphadenitis, but clinical signs and symptoms of neurotoxicity such as ptosis, ophthalmoplegia, dysphagia, dysphonia, and neuromuscular weakness occurred in as many as 16% of the cases (2, 3)

(1) The venom of the Southeastern France population of V. a. aspis seems to be PREDOMINANTLY neurotoxic
(in contrast to that of the “normal” aspis elsewhere) - or so they say in the 2002 paper, or somewhere.

(2) The venom of V. a. ammodytes is predominantly haemotoxic, as illustrated by the statistics showing ONLY 16%
of the patients showing any symptoms of neurotoxic envenomation. They said “as many as” instead of my “only”,
but that is a usual way to stress a fact that was (at that time) rather new and surprising, rather than claiming that 0.16 is a big number as such. Actually, the team from the Split hospital in their 2006 paper used neither “as many
as” nor “only”, they just wrote down the statistics of their clinical observations. So, 16% = 0.16, that's it.
And that's what I had in mind when I said that the V. ammodytes venom is only MILDLY neurotoxic for humans.
(Also, if I got it right, this neurotoxic component of the V. ammodytes venom doesn't kill, and is treated as a rather
minor accompanying problem that soon goes away.)

So, why would the neurotoxic component of the venom of V. ammodytes be more pronounced/efficient in a hybrid like the "neurotoxic V. a. aspis" than in its "pure, original form"? (Of course I know life is complicated, I know genetics is complicated, but still, commonsensically...?)