To use an analogy, we are saying that pigs don’t fly. You think pointing to a bat is evidence that pigs fly because both are mammals.
We are saying that there is no evidence that influenza lays dormant anywhere. Pointing to Ebola does nothing to change that conclusion.
Nobody, especially not Sanford, said that “Dormant in a reservoir” means “not replicating except for during outbreaks”. What he said is that RNA viruses may replicate much more slowly in some of their reservoirs compared to what is observed during outbreaks. And it happens that the data from the recent Ebola outbreak has proven that is was right and that those here who have scoffed at this idea were wrong. I am wandering who is serious here.
Again let’s introduce some missing detail. What has been scoffed at is the idea that RNA viruses can just lie around in the body for extended periods of time without actually replicating and evolving. You haven’t shown any evidence against this. A five or tenfold reduction in the rate of genomic evolution due to some “latent” (not to be confused with inactive) infection seems to me to (at best) extend the time-to-extinction in a proportional amount, that is five-to-tenfold longer.
Of course let’s not shut off our brains completely here. If an RNA virus somehow survives as a latent infection somewhere in the body, it also has a much smaller population size, and thus the efficacy of selection at removing deleterious mutations must be strongly reduced in turn, effectively speeding up (compared to a larger population) the rate of fitness decline it should experience if GE is true.
Once again what we’re missing from GE proponents are actual quantifiable predictions. What is the actual rate at which the virus should be declining due to GE, and how do these factors (such as population size in the host population as a whole, compared to some tiny zone inside a host body) affect that rate?
You are splitting hairs. The fact of the matter is that Sanford has predicted that the evolutionary rate of RNA viruses may very substantially slow down in some of their reservoirs compared to what is observed during outbreaks and it happens that the data from the recent Ebola outbreak has proven that is was right and that those here who have scoffed at this idea were wrong.
How does “10 times slower” mean stasis? Even at such a comparatively slow rate (and only slow compared to other viruses), wouldn’t that GE have to occur within a few years, or decades at most? So why are Ebola viruses still alive?
The observations in ebola are not the same as Sanford’s claims about RNA viruses writ large.
Even with longer generation times, the per-replication mutation rate and the genome size don’t change, so the math in terms of sampling every possible single-base substitution doesn’t improve for GE. The populations should still be long extinct from GE.
That’s not what I asked for.
I’ll also point out a few problems.
" a very quiescent viral state, as might occur within a host where there is very little viral replication" does not describe what goes on with Ebola, influenza, etc. There are two things that viruses do that could approach that characterization: inactive retroviral insertions and genuinely dormant varicella zoster virus hanging out in dorsal root ganglia. Slower replication in a non-human host, or following recovery from an infection, are not that.
Sanford (and in this example Carter) perennially misuse “mutation rate”. The term has a very specific meaning: mutations/site/replication. What they are describing is a slower substitution rate in terms of substitutions/site/year due to less replication (i.e. longer generation times). This matters because Sanford uses “mutation rate” in both cases seemingly interchangeably, either not knowing the difference or employing a bait-and-switch when convenient. If one is going to claim to be overturning a consensus, one should at the very least employ the correct terms when doing so.
Look. There’s zero evidence for that.
It’s clear that you either don’t know what “latent” means in virology or you are trying to mislead.
Replicating more slowly is not latency, Gil.
This is false. We have known for a while that some viruses, including HIV, HCV, and HSV can achieve latency. What was scoffed at was that this latency was somehow an escape mechanism from GE. Its not, considering that these viruses have been circulating for thousands of years.
Nothing of that sort happened.
Note that HSV is a DNA virus and HIV a retrovirus. However, you’re partly right here. I should have been more precise in my formulation and say the following : Note that several opponents to GE on this site have scoffed at this idea of latent/quiescent viral infection for RNA viruses such as Influenza or Ebola, arguing that such latent/quiescent state had never been observed in these cases.
They scoffed at a straw man, for proponents of GE never said that a quiescent or latent viral state allows to completely escape GE but only something that slows down GE.
How do you know that Ebola has circulated for thousands of years?
It’s actually millions of years. Of course, since these viruses share a common ancestor in turn, it’s lineage must go back even further.
What’s your alternative hypothesis? Did God personally create the Ebola virus in the last century?
It doesn’t. According to GE, a 10 times slower evolutionary rate means slower fitness decline, not stasis.
HIV is an RNA virus, why did you conceal this? Don’t forget we also knew HCV and BDV are RNA viruses capable of causing latent persistent infection for many years.
Its good to see you own up to your false claim.
This is still false. No one here scoffed at the possibility of Ebola or Influenza achieving latent infections. What was scoffed at was the claim that somehow, latency could keep these viruses in evolutionary stasis for millennia. Get it right.
That was a slip on my part, not theirs. I actually meant slow down, not escape.
Actually its millions of years.
How do you propose that Ebola, or other non endogenous RNA or DNA viruses, survive the death of their host?
How have bacteriophages avoided GE?
The only way to make this consistent with GE is to decide that Ebola was created recently. Is that your contention?
Of course this is nonsense. HIV experiences a higher within-host evolutionary rate, enabling its adaptation to host environments. You are probably confusing evolutionary rate with mutation rate.
So what?
Can’t see your own error? You said:
The evolutionary rate of actively replicating HIV is a million times higher than that of humans, several orders of magnitude higher than that of DNA viruses, and the highest amongst all putative RNA viruses, yet GE has not extinguished it even though its been circulating within human populations for over a century, and its ancestor SIV for even longer periods. AFAIK, HIV benefits immensely from this high evolutionary rate and is showing no signs of decline. Other RNA viruses also benefit from their high evolutionary rates as well: the rapid development of highly transmissible SARS-CoV-2 variants within months, if not weeks, is a good example.
Can you now see your error? I don’t know if this is really a prediction of GE articulated by Sanford himself or its a prediction based on your misunderstanding of evolutionary rates. In any case, its wrong.
Compared to RNA viruses such as sars-cov2 or H1N1, HIV has some specific features that allows it to better resist GE, namely: