2) This review explores the complex relationship between COVID-19 and carcinogenesis.
Key mechanisms include:
- Immune system disruption: COVID-19 triggers an excessive inflammatory response, leading to chronic inflammation - a known risk factor for cancer.
3) Inflammatory markers remain elevated even after recovery.
- Genetic and epigenetic changes: SARS-CoV-2 can alter the way genes are expressed in host cells, impacting the activity of oncogenes and tumor suppressor genes.
4) - Viral protein interactions: Certain viral proteins like ACE2, TMPRSS2, and FURIN may facilitate cancer progression through their roles in viral entry, activation, and signaling.
The review also highlights an increased risk of developing multiple cancers simultaneously or ..
5) ...over time in COVID-19 survivors, as well as more aggressive tumor behavior in some patients diagnosed after COVID-19.
Thanks for reading π
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During the acute phase of a COVID-19 INFECTION, individuals EXPERIENCE significant AGE ACCELERATION of up to 24.47 YEARS due to disrupted homeostasis π¨π¨π¨
... and some still failing to take necessary protective measures π€¦ββοΈπ€¦ββοΈπ€¦ββοΈ biorxiv.org/content/10.110β¦
2) The study developed a highly accurate transcriptomic clock to predict chronological age using 47 genes primarily involved in lymphoid immune function. This clock was validated across multiple healthy cohorts.
3) Remarkably, the transcriptomic age of COVID-19 patients showed dramatic acceleration of up to 24.47 years during acute infection. This age acceleration correlated with markers of inflammation, such as C-reactive protein and immune cell counts.
2) This study examined how COVID-19 vaccination affected the spread of the virus in the UK during 2021. The researchers used a mathematical model to analyze data on vaccination rates, circulating virus variants, and the reproduction number (R) across different local areas.
3) The key findings are:
- One dose of vaccine reduced virus transmission by 39%, and three doses by 49%, but two doses had little effect. This was likely due to the rise of the more contagious Delta variant during the two-dose rollout.
What a CHAOS!
Everyone seems to have their OWN DEFINITIONS for MILD and SEVERE. It's the perfect recipe for having inconsistent data and leaving us totally confused. medrxiv.org/content/10.110β¦
2) This study compared how different organizations classify people's risk of severe COVID-19 based on their medical conditions. The European classification labeled more people as high-risk ...
3) ...while national classifications in the Netherlands and Norway identified more people as moderate-risk.
The discrepancy was around 12-14% - meaning a significant portion of the population was assigned a different risk level depending on which classification was used.
2) Interesting study even if the sample size is small.
They found that people with long COVID had different levels of certain proteins in their blood compared to those who recovered from COVID-19 or never had it.
3) The long COVID group had higher levels of some proteins like IL-20, which can cause inflammation, and lower levels of others like TRAIL, which has anti-inflammatory effects.
What are the DIFFERENCES between INFLUENZA and SARS-CoV-2 in terms of MUTATION rates and
why are they VERY DIFFERENT VIRUSES ?
Influenza and SARS-CoV-2 differ in mutation rates due to their genetic mixing processes: reassortment and recombination.
2) REASSORTMENT occurs when two viruses infect the same cell and exchange RNA segments, generating new strains. This is typical for segmented viruses like influenza.
RECOMBINATION, which occurs in viruses with single, non-segmented genomes like SARS-CoV-2 ...
3) ...involves the simpler exchange of genetic material during replication. As a result, recombination with SARS-COV-2 allows for quicker generation of genetic diversity, while reassortment with Influenza requires a more complex mixing of entire genome segments.
VARIANT KP.3.1.1 and the MUTATION ORF1a:S4286C
(2nd part)
My dear friend @UseBy2022
As promised, I wanted to share some insights with you.
In recent months, the key variant has been KP.3.1.1 rather than KP.3, with two significant mutations: ORF1a:S4286C, S:S31- ...
2) ... instead of Q493E, as some have suggested.
It's interesting to note that while some people are quick to criticize, they often lack the ability for self-reflection.
Like you, I couldnβt shake the feeling that the most intriguing mutation was ORF1a:S4286C.
3) It seemed familiar to me, even though itβs not my area of expertise, and my mind, which is no longer as sharp as it once was, works more slowly.
By chance, I recalled a cryptic case that Marc mentioned in Ohio and a hypothesis ...