Emmanuel Profile picture
Jun 1, 2023 9 tweets 6 min read Read on X
😡 LONG COVID : 43% (NOT 10%) of those infected with SARS-CoV-2 develop LONG COVID SYMPTOMS on a period between 90 to 120 days ! 😡
(Meta-analysis 41 STUDIES)

WHY SUCH DIFFERENCES IN THE FIGURES? Image
2) There are 3 main reasons that can explain the differences in the figures provided.

A. THE BASELINE is NEVER the SAME !
Sometimes the study is carried out on those hospitalized, or asymptomatic, or children, or on questionnaires where only a small % of people answered ... Image
3) B. THE REFERENCE PERIOD IS NEVER THE SAME !
In some studies the period is 2 months, or 6 months, or 1 year and more, and sometimes they mixed several periods.
Yet precise criteria exist and were recently proposed by a group of 200 scientists.
pubmed.ncbi.nlm.nih.gov/34951953/ Image
4) C. THE SYMPTOMS STUDIED ARE NEVER THE SAME !
Depending on the studies, some are studying, one or more symptoms, or deciding on a minimum number of symptoms for LONG COVID.
We have everything, from neurological and cardiac symptoms, to studies combining up to 50 symptoms ! Image
5) In the jungle of studies (I have read 30 studies, line by line) there is, in my opinion only one, which is a meta-analysis of 41 studies, which offers reliable values, ​​with criteria for inclusion or exclusion that make sense. Image
7) Forest plot for worldwide post-coronavirus disease 2019 condition prevalence. Image
8) Forest plot for post-coronavirus disease 2019 condition prevalence by hospitalization status, region, follow-up time, and sex, as well as symptom-specific prevalence. Image
9) Thank you for helping us fight, those who want you to believe, that the LONG COVID does not exist.
FYI
@LauraMiers @elisaperego78 @WesElyMD @TRyanGregory @1goodtern @MeetJess @white_bite @HarrySpoelstra @xabitron1 @mrmickme Image

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More from @ejustin46

Aug 16
VIRUS TEAM-UP:
How SARS-CoV-2 Keeps Cells alive to Spread, Increase Disease Severity and Aid Influenza! 😰
advanced.onlinelibrary.wiley.com/doi/10.1002/ad…Image
2) This research shows that SARS-CoV-2, the virus that causes COVID-19, stops infected cells from dying. Normally, when cells die, it helps stop viruses from spreading. By keeping these cells alive longer, SARS-CoV-2 allows itself to multiply and also helps other viruses ... Image
3) ... like influenza A, grow more easily.
When someone has both SARS-CoV-2 and influenza A, the two viruses can make a person much sicker. The immune system gets overwhelmed, leading to more inflammation and damage to the lungs. Image
Read 4 tweets
Aug 8
ENTROPY UNLEASHED:
How Viral Protein Interactions Drive Coronavirus Adaptation in Bats and Humans

Entropy, in a general sense, refers to the level of disorder or randomness in a system.
biorxiv.org/content/10.110…Image
2) When we talk about protein interactions and viral behavior, entropy can be viewed as a measure of how complex and varied these interactions are.

In the context of the study about coronavirus interactions in bat and human cells, here's a simplified breakdown. Image
3) **Complex Interactions**: The study identifies how proteins from the coronavirus interact with host cells (both bats and humans). These interactions can be highly ordered (low entropy) or more chaotic (high entropy). Image
Read 8 tweets
Aug 5
COVID-19 and/or SARS-CoV-2
(opinion)

Patients care most about how COVID-19 affects their health and daily life, including for those with long COVID. Scientists focus on understanding the virus to find better treatments. Both views are important for dealing with the pandemic. Image
2) I'm bringing up this topic because, after talking so much about the disease, its long-term effects, treatments, and vaccines, many people have forgotten that we are dealing with the most dangerous virus humanity has ever faced.
3) What inspired me is this article about chaos theory and quantum mechanics and how it can help us to better understand SARS-CoV-2

A new study found a way to link them by showing that gravity may come from the disorder or "entropy" of matter and energy.
interestingengineering.com/science/quantu…
Read 10 tweets
Aug 1
INSIDE OUR INFECTED CELLS.
How SARS-COV-2 stealthy hijacks our cellular sanctuaries (organelles) ?
🤓 Visual explanations

Organelles provide the possibility for the virus to organize its RNA in PROTECTED structures, concentrate REPLICATION machinery ...
nature.com/articles/s4146…Image
2) ...compartmentalize the replication process, and hide from immune detection.

Figure 1g - The large perinuclear clusters of viral RNA demonstrate how the viral RNA is organized into PROTECTED structures. Image
2) Figure 3d- The nanoscale puncta of the viral RNA-dependent RNA polymerase (nsp12) within and around the viral RNA clusters show the concentration of REPLICATION machinery. Image
Read 5 tweets
Jul 30
SARS-CoV-2: The VIRUS That MASTERFULLY "ADAPTS" to SPREAD FURTHER !

If you were SARS-CoV-2, you could choose to spread in two ways: you could release a lot of tiny particles into the air to infect many people, or you could release just a few super infectious particles ... Image
2) ... that are really good at making someone sick.
This study published in Nature shows that some variants of the virus are especially strong, meaning they can infect with fewer particles, making it easier for them to spread quickly!
nature.com/articles/s4429…Image
3) Researchers found that different variants of SARS-CoV-2, like Alpha, Delta, and Omicron, have unique abilities to spread. For instance, the Delta variant was shown to be more infectious, meaning it could spread more easily and required fewer viral particles to cause illness... Image
Read 7 tweets
Jul 29
WHAT is OMICRON'S CLEVER TRICK ?
An explanation for kids 👫
... from a great study of @StuartTurville and colleagues

Omicron is different and spreads faster between people because Omicron attaches to a special protein in our bodies called ACE2 in a different way. Image
2) There are two types of ACE2 proteins - one that helps control blood pressure, and another that helps other proteins.

Previous COVID viruses could attach to both types of ACE2, with the help of another protein called TMPRSS2. Image
3) But Omicron can only attach to the ACE2 proteins that help other proteins, without needing the TMPRSS2 protein.

This allows Omicron to spread more easily in the nose and throat, but not cause as much damage deep in the lungs. Image
Read 4 tweets

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