your auntifa liza 🇵🇷 🦛 🦦

RE: https://zeroes.ca/@datum/116288248099142236

#COVID19 QUESTION:

at the beginning of the pandemic some scientists created a site graphing all its mutations and it blew mind by how many there were.

i think they stopped due to the speed of reports. am assuming its a consequence of how well epidemiology systems are integrated to the internet.

SO:

1. are we seeing more mutations vs other viruses due to faster reporting or because the virus itself is prone to mutate fast?

2. what makes #SARSCOV2 mutate so much? reinfections w/o immunity?

Mar 26 at 6:29pmWeb
Show threadjdm2 🇵🇷1d ago
@blogdiva the virus mutates fast. And it does so because we keep giving it opportunities to pick up stuff while infecting people out there. It’s depressing.
Show threadjfor1d ago

@Jdm2 @blogdiva

⬆️ This. Exactly this.

Show threadClifton Royston1d ago

@blogdiva

In 2020 when I read the virus outbreak was coronavirus I thought "Oh shit."

Coronaviruses, as a family, have been known for many years to have a particularly fast mutation rate.

There are many viruses which cause the "common cold"; some of those are coronaviruses and mutate fast, which is why there's never been a vaccine for the cold and might never be. This is one reason the original SARS virus outbreak was so worrisome and triggered a huge world-wide effort to shut it down.

Show threadHoward Chu @ Symas1d ago
@CliftonR @blogdiva it's interesting to think about. Fast mutation really means its genetic code is pretty unstable, getting transcription errors with high frequency as it reproduces. But also coupled with a fast reproduction rate so it continues to survive even with a lot of errors.
Show threaddatum (n=1)1d ago

@CliftonR @blogdiva

There are many viruses which cause the "common cold"; some of those are coronaviruses and mutate fast, which is why there's never been a vaccine for the cold and might never be

Cliffton really nailed it here.

(Meanwhile there are microbiological reasons for the shared high mutation rate, but I know I don't understand implications of https://www.nature.com/articles/s41467-025-61555-x )

But this base fact is MULTIPLIED by two more things:

1) as jdm2 said the sheer number of hosts

corollary 1.A) Rare per person is not rare at pandemic billions-of-infections scale. People with rare one-in-a-million immune dysfunction can suffer long term SARS-CoV-2 infection and serial passage https://www.medrxiv.org/content/10.1101/2021.09.14.21263564v2 . The mainstream hypothesis says that these conditions are the origin of variants containing large jumps of 20+ mutations at a time

2) the viral volume per host while contagious. (Note re-gaining contagiousness does rarely occur.). And to my understanding, it turns out that since SARS-CoV-2 is a vascular disease, and our bodies have blood vessels everywhere, there's a lot of viable host tissue; simultaneous to that it has a higher viral copy count than several other common viruses https://pmc.ncbi.nlm.nih.gov/articles/PMC7476607/figure/fig2/

#COVID19 #COVID #SARSCoV2 #CovidIsNotOver #virology

The mutational landscape of SARS-CoV-2 provides new insight into viral evolution and fitness - Nature Communications

Here, we report the mutation rate of SARS-CoV-2, the virus responsible for COVID-19. We find that the secondary structure of the RNA-encoded viral genome is crucial to modulating the mutation rate and evolves under strong selective constraints.

Nature
Show threaddatum (n=1)1d ago

@CliftonR @blogdiva also note from that first link that while SARS-CoV-2 DOES have a mutation correction mechanism, that mechanism's effectiveness is focused:

the mutation rate is significantly reduced in regions that form base-pairing interactions and that mutations that affect these secondary structures are especially harmful to viral fitness

https://www.nature.com/articles/s41467-025-61555-x

#SARSCoV2

The mutational landscape of SARS-CoV-2 provides new insight into viral evolution and fitness - Nature Communications

Here, we report the mutation rate of SARS-CoV-2, the virus responsible for COVID-19. We find that the secondary structure of the RNA-encoded viral genome is crucial to modulating the mutation rate and evolves under strong selective constraints.

Nature
Show threaddatum (n=1)22h ago

@blogdiva on eactly that point, trending on zeroes right now is a paper that found

The emergence of long branch subvariants like BA.3.2 without intermediates likely indicates that unmonitored persistent infections continue to drive large evolutionary shifts in this virus.

https://academic.oup.com/ve/article/12/1/veag011/8490867?login=false

Evolution and viral properties of the SARS-CoV-2 BA.3.2 subvariant

Abstract. The SARS-CoV-2 Omicron subvariant BA.3.2 descends from BA.3. It emerged two years after BA.3 ceased to circulate and differs by 39 spike mutation

OUP Academic
Show threadDaniel Lakeland1d ago

@blogdiva

I'm not an expert here, but I'd guess that most widespread infectious viral illnesses mutate like that, it's just that we looked very carefully at COVID with modern high tech sequencing techniques.