Long-term trends in Post-COVID severity: a machine learning analysis from the POP/COVIDOM cohort of the German NAPKON Cohort Network
https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(26)00069-6/abstract
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@longcovid
#LongCovid #PASC #PwLC #postcovid #postcovid19 #PostCovidSyndrome #LC #Covidlonghaulers #longhaulers #COVIDBrain #NeuroPASC
#Coronavirus
#COVID19 #COVID #COVID_19 #COVIDー19 #SARSCoV2 #auscovid19 #CovidIsNotOver
Severe acute COVID-19 and early long COVID signals in paediatric cohorts: an analysis of real-world data from two health departments, Germany
https://link.springer.com/article/10.1186/s12887-026-06724-7
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#LongCovid #PASC #PwLC #postcovid #postcovid19 #PostCovidSyndrome #LC #Covidlonghaulers #longhaulers #COVIDBrain #NeuroPASC
#Coronavirus
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@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
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.
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/
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.
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?
RE: https://zeroes.ca/@newsfeed/116296596573048884
Researchers
identified a distinct circulating CD14⁺ monocyte state associated with Long COVID [1]
and
showed dysregulated responses [1]
This subset of cells impacts:
back to the original paper, this section header is cause for concern:
LC has a distinct transcriptome after mild or moderate disease [1]
and they remind us that his is unlikely to be the only mechanism behind LC:
Although associations between LC-Mo and symptom severity were noted, correlations were modest, leaving causality undetermined [2]
[1] https://www.nature.com/articles/s41590-025-02387-1
[2] https://cytologicsbio.com/cd14-monocytes-cell-biology-and-research-applications/
#LongCOVID #SARSCoV2 #virology #COVID #COVID19 #COVIDIsNotOver #transcriptome #CD14 #health #publicHealth
RE: https://disabled.social/@tomkindlon/116293020588704115
T cell phenotypic alterations
Shame AJ Leonardi isn't on Fedi to be congratulated again.
From Switzerland 🇨🇭
Persistence of Post-Acute COVID-19 Sequelae (PASC) symptoms in healthcare workers four years after ancestral SARS-CoV-2 infection: a prospective multicentre cohort
https://link.springer.com/article/10.1007/s15010-026-02768-0
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Hashtags:
@longcovid
#LongCovid #PASC #PwLC #postcovid #postcovid19 #PostCovidSyndrome #LC #Covidlonghaulers #longhaulers #COVIDBrain #NeuroPASC
#Coronavirus
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Tuomas Mattila
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datum (n=1)
your auntifa liza 🇵🇷 🦛 🦦