The new Ebola outbreak weakens an argument often put forward against genetic entropy of RNA viruses

Once again, this confounds individual case management with public health.

In terms of a given patient, the effectiveness and mechanism of action of mutagenic pharmacology still seems up for debate. But even assuming that such drugs are appropriate treatments for sick individuals, these are administered in cases where patients are diagnosed, ill, isolated, probably hospitalized, and not circulating in the general population. The objective is to lower the viral load in their own, individual bodies, hopefully so they recover. There is no goal of purposefully circulating further infections with some sort of hobbled virus.

Even were that to inadvertently happen, the epidemic would continue to spread unfettered from the fitter at large clads of the virus, which would crowd out any less transmittable variants. This is what happens in any event; there are always dead end variants which come and go.

Giving everybody a weakened, ineffective form of a virus, is a form of classic vaccination. The reason people have to be poked is because community spread will not happen by contagion. Far from cridible, that Sanford suggests circulating mutated viruses as a public health policy is an embarrassment and speaks to the shallowness of his understanding of epidemiology.

Did I write that? No.

Did he write that? No.

Anyway, looks like my point about infections being less transmissible is sort of moot, or maybe understated, since it may stop transmissibility in 24 hours.

The researchers infected ferrets with SARS-CoV-2 and initiated treatment with MK-4482/EIDD-2801 when the animals started to shed virus from the nose.

“When we co-housed those infected and then treated source animals with untreated contact ferrets in the same cage, none of the contacts became infected,” said study co-author Josef Wolf.

If these ferret-based data translate to humans, Covid-19 patients treated with the drug could become non-infectious within 24 hours after the beginning of treatment.

As far as I read IIRC, they’re also testing the drug at every level of diagnosis, both mild and severely ill.

What Brewer, Smith, and Sanford actually wrote:

Our numerical simulations strongly indicate that such
natural genetic attenuation can be enhanced during pandemics by: (a) employing
strategic use of antiviral pharmaceuticals that increase RNA mutagenesis;
(b) increasing genetic bottlenecking by reducing inoculum levels through
improved hygiene and other means; and (c) strategic use of broad-spectrum
vaccines that induce partial immunity and other means for reducing viral titers.

https://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0015

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Which has nothing at all to do with GE.

If a virus requires its own polymerase to replicate its own genome, inhibiting that polymerase will inhibit viral replication. True or false?

…was accurately paraphrased by you, so I don’t see why you think that quoting it helps.

Instead of just quoting it, if you understood that it has any validity, you’d be thoughtfully explaining instead of quoting.

It’s just a desperate attempt to rescue a concept that is falsified by evidence that the world is seeing on an almost daily basis.

@Giltil just read this. An oddity you may be interested in, or if others want to comment. Didn’t think it was worth starting a new thread, but anyone feel free if they want to.

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Seems very interesting indeed, thank you. I will read the original article and come back here for some comments if I feel they may have some merit.

Source paper:

Evolutionary stasis of a deep subsurface microbial lineage

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Doesn’t seem outside the realm of plausibility to me. The threefold combination of extremely low mutation rates, intermittent sporulation, and extremely slow doubling times(some times on the period of years to decades for a single cell division) of deep-crust bacteria would all contribute to very slow genetic divergence.

It’s a bit of a bummer that ScienceAlert decided to go with such a misleading headline, but it’s pretty par for the course with such sites. If you read the paper, you’ll see that the data show that these microbes are indeed evolving but doing so very slowly.

Yeah I got that from a sentence in the article too. Plausible but still surprising probably!

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They have merit as yet another case that disproves GE.

A quite surprising thing is that these bugs show no sign of adaptation despite having lived in different environments for long periods of times.

The dN/dS is calculated genome-wide at:

The genome-wide ratio of non-synonymous to synonymous substitutions (dN/dS) averaged between 0.21 and 0.68 in the studied populations (Fig. 2C).

dN/dS < 1 means purifying selection is operating across the genome as a whole(though as they say, it’s not unusually strong). We can’t really say that there are no signs of adaptation, as that could be restricted to a smaller subset of genes. I’m surprised the authors don’t appear to have even looked for it in specific genes as opposed to just a mean value across the genome as a whole.

Well, across protein-coding exons in the genome as a whole.