Emmanuel Profile picture
Sep 9 β€’ 5 tweets β€’ 2 min read β€’ Read on X
Our LIVES would be very DIFFERENT, if we could have CAMEL NOSES ! πŸ€—πŸ˜…

"Resistance to SARS-CoV-2 infection in camelid nasal organoids is associated with lack of ACE2 expression"
nature.com/articles/s4429…
Image
2) The study investigated whether camels and other camelids can be infected by SARS-CoV-2, the virus that causes COVID-19. The researchers used special 3D models of camelid nasal cells to test this. Image
3) They found that the camelid nasal cells were resistant to infection by different variants of SARS-CoV-2, including the Omicron variant. However, these cells could be easily infected by another coronavirus, MERS-CoV, which is known to infect camels. Image
4) The reason for this difference is that camelids lack the ACE2 protein, which SARS-CoV-2 uses to enter human cells. Instead, camelid cells express a different protein called DPP4, which allows MERS-CoV to infect them. Image
5) These results suggest that camels and other camelids are unlikely to act as reservoirs for SARS-CoV-2, unlike some other animal species. The study provides important insights into the factors that determine which animals can be infected by different coronaviruses.

Thanks πŸ™ Image

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More from @ejustin46

Sep 11
During the acute phase of a COVID-19 INFECTION, individuals EXPERIENCE significant AGE ACCELERATION of up to 24.47 YEARS due to disrupted homeostasis 😨😨😨

... and some still failing to take necessary protective measures πŸ€¦β€β™‚οΈπŸ€¦β€β™‚οΈπŸ€¦β€β™‚οΈ
biorxiv.org/content/10.110…
Image
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. Image
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. Image
Read 8 tweets
Sep 11
Let's CLARIFY the MISCONCEPTION that COVID-19 VACCINATION does not decrease the RISK of TRANSMISSION.

New study πŸ’―πŸ‘
medrxiv.org/content/10.110…
Image
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. Image
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. Image
Read 6 tweets
Sep 11
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/10.110…
Image
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 ... Image
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. Image
Read 5 tweets
Sep 11
DISTINCT INFLAMMATORY and NEUROLOGICAL PROTEIN PROFILES in the LONG COVID group compared to the recovered and uninfected groups.

medrxiv.org/content/10.110…
Image
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. Image
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. Image
Read 5 tweets
Sep 10
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.
Image
Image
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 ... Image
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. Image
Read 5 tweets
Sep 10
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 couldn’t shake the feeling that the most intriguing mutation was ORF1a:S4286C. Image
3) It seemed familiar to me, even though it’s 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 ... Image
Read 6 tweets

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