Is that part evidence or rhetoric?
Again, evidence or rhetoric?
A simple, objective question: do RNA viruses really lack repair (correction) enzymes?
No it does not. It’s not even relevant to the question. Birds do not freeze dry infections. Virus’s are not bacteria or fungi. Sanford’s reply has nothing to do with the known and studied life cycle of the virus in its endemic reservoirs. This is complete dino coprolites.
That you find this convincing or plausible can only be attributable to confirmation seeking. Here is some actual research by actual viral researchers in regards to actual natural reservoirs, if you are actually interested.
we review the history of avian influenza viruses through the lens of their genetic makeup: from their relationship to human pandemic viruses, starting with the 1918 H1N1 strain, through to the highly pathogenic epidemics in birds and zoonoses up to 2018. We describe the genesis of novel influenza A virus strains by reassortment and evolution in wild and domestic bird populations, as well as the role of wild bird migration in their long-range spread.
Influenza Virus Evolution, Host Adaptation and Pandemic Formation
Here we review evolution of influenza A viruses in their reservoir hosts and discuss genetic changes associated with introduction of novel viruses into humans leading to pandemics and the establishment of seasonal viruses.
Virus‐specific factors associated with zoonotic and pandemic potential
New IAV strains emerge through the accumulation of mutations, natural reassortment, and adaptation to their new host.
Adaptive pathways of zoonotic influenza viruses: From exposure to establishment in humans
Human influenza viruses have their ultimate origin in avian reservoirs and may adapt, either directly or after passage through another mammalian species, to circulate independently in the human population. Three sets of barriers must be crossed by a zoonotic influenza virus before it can become a human virus: animal-to-human transmission barriers; virus–cell interaction barriers; and human-to-human transmission barriers. Adaptive changes allowing zoonotic influenza viruses to cross these barriers have been studied extensively, generating key knowledge for improved pandemic preparedness.
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I’m sure you know all these things, but it’s worth mentioning for the other readers . . .
DNA viruses can lie dormant within a cell nucleus (e.g. chickenpox causing shingles later in life) or insert itself into the host genome . RNA viruses can’t do either of these things.
As someone who works in that field, I can confirm that this is exactly why we go back to original stock cultures as much as possible. If you pick single colonies over many serial cultures you will inevitably fix mutations which is not what you want for reason of repeatability.
If we are talking about eukaryotic primary cell cultures then they do tend to stop dividing after many passages, but it isn’t due to mutations. It has more to do with the anti-cancer safeguards present in most cell lines. Immortalized cell lines have no problem dividing for many, many generations (e.g. HeLa cells).
Agreed.
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Just to reiterate, RNA viruses don’t lay dormant. They have to be continuously multiplying in a cell somewhere. There are enzymes in cells that chop up RNA so there is no way for an RNA virus to stick around for long. What Sanford claims is just false.
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Yep. Complete fabrication. @thoughtful, perhaps you should check the evidence instead of conflating it with silly, misleading rhetoric.
Another insanely wrong claim: did the most recent Ebola outbreak fizzle out because of entropy, or because of public health measures?
I can assure you that Sanford understands nothing about basic virology and how virologists isolate and propagate viruses. It’s just laughably wrong.
You could check the evidence instead of just believing Sanford’s rhetoric, correct?
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Well, I’m glad you guys are bringing evidence now so I can check it out.
That’s still not resolved, 33 years after I stopped doing herpesvirology (cytomegalovirus). As latency or dormancy is a negative (zero production of virus), it is very hard to empirically distinguish between zero viral production and extremely low-level persistent infection.
RNA viruses that stay within the RNA realm, yes. However, retroviruses have RNA genomes and routinely insert DNA proviruses into the host genome, but Sanford AFAIK ignores them.
And in both bacteriology and virology, those original cultures are almost always clonal (a single colony of bacteria or a single plaque for nearly all viruses). It’s really disturbing that Sanford pretends that there’s no cloning going on.
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Evidence of what? You really seem to have a difficult time with this idea that things don’t become true just because Sanford says it. Sanford conconcts some idea and you want us to disprove it. No, Sanford needs to provide evidence for his claims. And you shouldn’t just mindlessly accept them as true just because he says them.
What reference does Sanford give that RNA viruses survive outside of the body for extended periods of time, for example by making spores? Is there a footnote on that page with references that you cropped out of your picture? Does he given examples of such viruses? Do we have to guess why there are none of these things, and isn’t that curious in and of itself?
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Obviously you can, but will you? You haven’t checked out a speck of evidence AFAIK.
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Non-retroviral RNA viruses do pose a serious problem for Sanford’s claims. According to him they should have gone extinct already, but they haven’t. The 1918 H1N1 strain is still circulating in human population.
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Agreed. And many even generate large excesses of defective virions that have the effect of attenuating their virulence and increasing their fitness, pretty much the opposite of what Sanford claims.
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Note that we can actually measure the evolution of Ebola virus in the reservoir, based on the differences in the virus between human outbreaks. It evolves at the rate we would expect based on evolution within outbreaks.
Sanford works entirely in a fantasy world.
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I’ve had to beat this horse to death over the years. What you’ve said here is entirely false. The 1918 strain has been apparently extinct since 2009. What we have today are reassortments (related strains). H1N1pdm09, Swine Flu, being an example.
I am afraid Sanford’s use of the term “natural reservoir” is being grossly misinterpreted in this thread, and the vague and incomplete manner in which he explained himself in those pages may be somewhat to blame. Dr Carter makes it much more clear here:
https://creation.com/fitness [Box at the bottom, “Origin of Viruses”]
By “natural reservoir”, Sanford must be referring to the fact that pathogenic viruses can exist long term inside host animals in a non-pathogenic state, being regulated by the host’s system in a way that prevents them from reproducing out of control and racking up a high mutation count, such as they do in hosts for which they were not intended. This is an area of ongoing research. Viruses jump from one host, like a duck, to another (like a pig), to another (like a human). In ducks, the virus was stable and non-pathogenic. In humans, it starts to reproduce out of control, and becomes harmful. In this state, the virus starts racking up a mutational load.
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Hold on. How many vials did Noah bring onto the Ark? Lions and housecats are all one kind, but H1N1 is represented by a kind for every strain? Yeah, that is strained.
And what makes you think that the 1918 strain was not itself a reassortment? Animal reservoirs have multiple infections all the time, so genetic shift is going to happen.
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ROFL. You start by calling it a fact, but it’s not a fact. You call it an area of ongoing research, but who specifically is doing this research, and what have they found so far? What mechanism in particular is preventing the virus from mutating?
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You’re confused.
The origins of the original 1918 strain are shrouded in mystery. I think one theory is that it jumped from ducks originally. It may have been a reassortment of something else, for all I know. But the point is, viruses are usually not pathogenic, and in their non-pathogenic state, RNA viruses are apparently being regulated by the host and maintained. Only when they break free from the intended host do they begin to reproduce out of control (much like cancer).
That is not the way it works; but even if it were the case, then virulence would not be a proxy for fitness, which guts the whole point of the Sanford Carter paper.
But you are wrong anyways. There is plenty of variation in IAV in animal reservoirs. This has already been pointed out in prior posts.
And that process generally involves genetic shift and genetic drift, which are evolutionary processes which can be tracked over the course of an human epidemic as well as in reservoirs.
Interspecies transmission of influenza A viruses is the result of many factors. One of the key factors involved is a shift in the receptor-binding specificity of the virus, which is mostly determined by mutations in viral haemagglutinin (HA)…
The combination of distinct amino acids at positions 225 and 190 of HA is important for determining the receptor-binding specificity of the H1 subtype.To achieve interspecies transmission (known as a ‘host jump’), influenza A virus must change its tropism to preferentially target new host species, and both viral and host factors have been implicated in this event11,12. The high mutation rate of the virus enables it to evolve rapidly and thereby overcome host barriers. All eight gene segments evolve continuously, but this evolution is most pronounced for the HA and NA glycoproteins. Evolution is achieved by two main mechanisms: genetic reassortment between different subtypes (known as antigenic shift if it occurs in either the HA or NA segments) and point mutations owing to antibody-mediated immune pressure (known as antigenic drift), including substitutions, deletions and insertions within the antibody-binding sites. This results in the generation of modified influenza virus genomes, which facilitates virus evasion of the host immune response.
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Can you give us a real citation from the scientific literature for that? To my knowledge, the mutation rate per virus wouldn’t change from host to host, and the larger the viral population the less chance of a deleterious mutation becoming fixed.
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Influenza viruses usually are. But, hey, I’m just a virologist.
Please explain the mechanism of this alleged regulation.
To whose intent do you refer?
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Exactly how do you know which host is the intended host? Intended by whom? And if you think it’s intended by your deity, how did it come to infect unintended hosts?