Expected.
In the case of rabies and Lassa, animal hosts. In the case of Ebola, wherever the virus is when it’s not causing an outbreak in humans – which has to be some kind of animal host. RNA viruses cannot survive long out in the environment. (Unless they’re frozen, and neither Ebola nor Lassa occur in places where freezing temperatures occur.)
How then do you explain the following observations reported by Sanford & al regarding the epidemic of Dengue type-2 virus in several Pacific Islands from 1971 to 1974:
Dengue type-2 virus (DENV), a mosquito-borne, positive-sense, single-strand RNA virus, caused an epidemic in several Pacific Islands from 1971 to 1974. A recent paper [16] studied the epidemiological, clinical and biologic observations recorded during this time. The authors note that the time period, population dynamics and isolation of this epidemic gives a unique opportunity to study virus evolution minus many confounding factors. The initial outbreak of the disease, on Fiji and Tahiti, caused severe clinical symptoms, while the final outbreak on Tonga produced mild symptoms and near-silent transmission. Sequence and phyloge- netic analysis showed that the outbreaks were genetically related and all due to a single introduction. Also these analyses placed the Tongan viral isolates in a single clade, with some unique site substitutions compared to viral isolates early in the epidemic. It is these deleterious genetic changes that Steel et al. [16] believe was responsible for the reduced epidemic severity on Tonga in 1973/1974.
Severe acute respiratory syndrome (SARS) caused by an animal-derived
No, you really don’t. Your entirely imaginary scenario of viruses being repeatedly reintroduced from imaginary dormant reservoirs requires that the mutating virus repeatedly go extinct in the reservoirs we observe. That doesn’t happen for Lassa and rabies, for which we observe continuous, widespread transmission of ongoing lineages. It doesn’t even work for Ebola, where we don’t know the reservoir, since the various outbreaks can be placed on a phylogeny.
Really, this idea of dormancy in reservoirs is just insane.
Here’s the relevant sentence from the first paragraph of that section: “It is these deleterious genetic changes that Steel et al. [16] believe was responsible for the reduced epidemic severity on Tonga in 1973/1974.” Everything in that sentence is true except for the word ‘deleterious’, which is a fabrication by Sanford and co-authors. Nothing in the cited paper says anything about the changes being deleterious. Sanford et al have once again conflated virulence with fitness – even though the same paper mentions other outbreaks in which virulence increased.
The next paragraph includes this sentence, about the SARS outbreak in 2003: ‘This dramatic collapse cannot reasonably be attributed to human intervention.’ Unlike the previously quoted sentence, this one is wholly a fabrication. They’re just making up stuff here.
The opening of the paragraph after that: ‘Similarly, Ebola outbreaks have emerged explosively, initially being extremely virulent and extremely contagious, but very quickly they became self-contained
apart from human intervention.’ This is also blatantly false. I believe it was written before the 2014 Ebola outbreak make it plain just how ridiculous this claim was.
This is the same paper in which the authors invented values for the effects of mutations in viruses while citing a paper that gave completely different values. That makes four strikes in one paper, and I haven’t even read the whole thing. Stop reading this nonsense.
As our friend @glipsnort has pointed out, the mechanism of remaining frozen is not available to viruses like Ebola and Lassa in tropical climates.
Yet after millions of generations they are still going strong. How? They haven’t found any large bodies of ice in Gambia, that I am aware of. Are you?
So why do you keep pointing to the paper by Shoham, et al., as if that explained a mechanism for the persistence of viruses, when in fact it could not possibly apply outside of polar regions?
I am going to make a prediction, though: You are going to say you don’t have time to follow up on this, as you mentioned in this post 5 days ago. Nevertheless, sometime in the next few months, you will ignore the fact that you have been unable to answer empirical questions that undercut GE and once again post strong claims for the superiority of the GE hypothesis.
You in fact have already done so in this thread. You did not wait more than 5 days to claim the superiority of GE over consensus virology, even though you were unable to respond to strong empirical claims against GE in the post I linked.
But maybe starting today you will actually reckon with the tough questions instead of setting them aside and plowing ahead. I hope so. I would love for you to prove my prediction wrong.
Best,
Chris
It’s right there in the paper:
Dengue evolution has been characterized by vigorous purifying selection, occasional positive selection on certain amino acid sites and considerable genetic drift, particularly important in small populations. Genetic drift might be expected to predominate as a force of evolutionary change in the South Pacific simply because islands experience relatively more population bottlenecks, that is, drastic reductions of individuals leading to random fixation. Along with the bottleneck at each blood meal, which captures only a subset of virus variants, some Pacific islands experience substantial seasonal variation in rainfall and/or temperature. Mosquito populations on such islands that are dependent upon seasonal rainfall can fluctuate dramatically during the year (Iyengar 1960). On the southerly Pacific islands, seasonal temperature changes can affect vector gonotrophic cycle and/or the extrinsic incubation period. Nor are these seasonal bottlenecks alleviated by vector immigration from off-island since the islands are relatively isolated. In addition, susceptible host populations experience rapid fluctuations on islands where human populations are limited, clustered so as to be more vulnerable to high rates of transmission, and less often infused with new susceptibles due to isolation by geographic distance. Finally, viral lineage diversity should decrease in proportion to smaller population sizes and the degree of diminished frequency of importation imposed by the geographic isolation inherent in islands.
As for Sanford’s take “It is these deleterious genetic changes that Steel et al. [16] believe was responsible for the reduced epidemic severity on Tonga in 1973/1974.”, Steel uses “attenuated”, which is not synonymous with deleterious, which appears nowhere in the source paper.
And even if they had found that, the idea that a particular virus exists now today only because it has been periodically sleeping in ice for thousands of years, compared to some much more active counterpart, should be easy to test on a phylogenetic tree.
I don’t think he’s saying the mutation rate is so high that every single virus is completely scrambling it’s genome.
I believe he’s saying that among the many billions of viral particles produced by your body during a Corona virus infection, there is likely to be enough viral particles that among them we find one containing one of every possible single DNA substitution(as in one substitution pr viral particle), considering that it’s genome is relatively small and it’s high rate of mutation. Given that, there should also be plenty of mutants in a single infection to discover, for example, the RNA mutation from the codons GAU or GAC to GUU or GUC that cause the D614G amino acid substitution in the spike protein.
That doesn’t seem outside the realm of possibility to me.
No, there is not.
That paragraph blatantly misrepresents the evidence. Perhaps examining the evidence for yourself would be more informative than using secondary sources (hearsay).
Does anyone have any dispute with this paper? Basically, it seems the authors are saying RNA viruses drive themselves almost extinct, but not quite. We can tip them over the edge though…
An interesting comparison to GE.
That’s wrong. RNA viruses (except SARS-CoV- 2) have error frequency rates close to their respective error thresholds and that’s what the authors are saying.
Not really. In fact, the authors think RNA viruses are unlikely to go extinct naturally:
The epidemic of Dengue type-2 virus that Sanford talk about is characterized by strong bottleneck events. Since it is well known that strong bottleneck events cause fitness loss by the operation of Muller’s ratchet, it is then perfectly reasonable to assume that the genetic changes that have accumulated during this epidemic were deleterious and therefore affected fitness accordingly.
Nothing you’re saying is in conflict with what I said. I didn’t post it as a defense of GE.
Hi Gilbert,
Hope you are doing well today. I’m curious: Are you planning to respond to the issue of how it is that viruses like Ebola and Lassa on the African continent are able to thrive over millions and billions of generations without permanent ice formations to serve as “natural reservoirs”?
Thanks,
Chris
Maybe some RNA viruses can sneak into host DNA. Note that such a mechanism could raise serious questions about the safety of RNA vaccines.
These are your words:
RNA viruses aren’t driving themselves towards any form of nigh natural extinction and the authors of the paper agree, so its false to say they think otherwise.
We have a pretty good picture of the etiology of many zoonotic viruses, and their endemic behavior, and that is not it. However, even were the possibility of insertion and re-emergence to be entertained, far from providing a safe harbor, viral sequences embedded in host genomes are even more subject to unconstrained mutation. You do not need GE’s “slightly deleterious” or “gradual accumulation”. Bombs away.
@Giltil, the mechanism you point to requires recombination between RNA molecules in virus-infected cells. Recombination requires replication. RNA vaccines do not replicate, so I would gather that this risk is very, very minimal (if there is any at all).
This is just irrelevant. The Ebola virus outbreaks were spillover events from the natural reservoir of the virus to humans. For this to have happened, it means the virus must have been replicating in that reservoir and not sitting idle for thousands of years. Try again Gilbert.