A "new study" has hit the headlines that apparently proves that SARS-CoV-2 was lab-grown I am QUITE SKEPTICAL for a number of reasons, would love your thoughts...pic.twitter.com/J9aJc1BeTq
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Anyway, would love some virologists perspectives on this because it does not seem likely despite being everywhere in the news @MackayIM @angie_rasmussen @trvrb
https://www.dailymail.co.uk/news/article-9629563/Chinese-scientists-created-COVID-19-lab-tried-cover-tracks-new-study-claims.html …pic.twitter.com/shMz0HKj0Q
From an evolutionary biology perspective this is an extremely simplistic view.
It‘s not simplistic ist is just plain wrong. Only if a Virus gets so deadly that it limits its spread there will be selection advantage for the less deadly variants.
You’re right, that’s definitely not true, see “the Spanish flu pandemic”. Also, how can you manufacture a virus in such a way that you can then predict its future behaviour once it’s loose? Also not a virologist unfortunately, but will be interesting to see other opinions.
I’ll second that “tell that to the Spanish flu”
This is pure bullshit: there's a *reason* virus variants that are less lethal generally have a replication advantage and it doesn't apply (strongly) to Covid-19 because Covid gets most of its infection spread done in the pre-symptomatic-and early symptomatic period.
We can expect this of highly fatal diseases that mostly spread when nearing host death - if the host is dying too fast to spread (e.g. Ebola), less fatal / less rapidly fatal variants may have selective advantage. COVID19 spreads well during asymptomatic & nonfatal infection. 1/2
So, natural selection: the huge delay between transmissible time - when many COVID-positive people are still physically well and out in the world - and eventual death from COVID, means minimal selective pressure AGAINST its morbidity but still pressure FOR transmissibility. 2/2
It basically happened with B.1.1.7. We are one year in knowing that virus, still arguing what the death rate of B1 is. So it is quite a whombat-shit statement.
This is, um, really dumb. Viruses are parasites. Parasites compete with each other for access to hosts. If hosts are plentiful, then rapid replication within hosts is the best strategy. If hosts aren't plentiful, then slow replication is better.
And, guess what. High replication rate=high virulence (because, of course, more host resources are being used up). Slow replication=low virulence. So, evolution of virulence depends on access to hosts, and competition from other parasites (viruses here).
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