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May 14, 2024 โ€ข 9 tweets โ€ข 3 min read โ€ข Read on X
๐˜ˆ ๐˜ท๐˜ฆ๐˜ณ๐˜บ ๐˜ช๐˜ฏ๐˜ต๐˜ฆ๐˜ณ๐˜ฆ๐˜ด๐˜ต๐˜ช๐˜ฏ๐˜จ ๐˜ด๐˜ต๐˜ถ๐˜ฅ๐˜บ :
"๐—ฃ๐—ฒ๐—ฟ๐˜€๐—ถ๐˜€๐˜๐—ฒ๐—ป๐˜ ๐—”๐—ฐ๐˜๐—ถ๐˜ƒ๐—ฎ๐˜๐—ถ๐—ผ๐—ป ๐—ผ๐—ณ ๐—–๐—ต๐—ฟ๐—ผ๐—ป๐—ถ๐—ฐ ๐—œ๐—ป๐—ณ๐—น๐—ฎ๐—บ๐—บ๐—ฎ๐˜๐—ผ๐—ฟ๐˜† ๐—ฃ๐—ฎ๐˜๐—ต๐˜„๐—ฎ๐˜†๐˜€ ๐—ถ๐—ป ๐—Ÿ๐—ผ๐—ป๐—ด ๐—–๐—ผ๐˜ƒ๐—ถ๐—ฑ"

biorxiv.org/content/10.110โ€ฆ
Image
2) The study evaluated 142 participants, including uninfected controls, acutely infected individuals, convalescent controls, and long COVID patients. Samples included PBMCs and plasma collected at various time points after infection. Image
3) Comprehensive immunological, virological, transcriptomic and proteomic analyses were performed to characterize the immune profiles in these groups.
4) Long COVID patients had persistent symptoms like fatigue, shortness of breath, brain fog, etc. similar to prior reports.
No differences were found in SARS-CoV-2 antibody titers between long COVID and convalescent controls, but higher spike-specific T cell responses ... Image
5) ...were observed in long COVID patients. No plasma SARS-CoV-2 was detected.
Transcriptomic analysis of PBMCs showed long COVID was characterized by upregulation of inflammatory markers, cytokines, complement and coagulation pathways compared to convalescent controls and ... Image
6) ... and uninfected controls.
Pathway analysis revealed persistent activation of IL-6, JAK-STAT, coagulation, complement, metabolism and T cell exhaustion pathways in long COVID. Image
7) Proteomic analysis of plasma showed similar differences, with increased immune cell signatures, cytokine signaling and complement/coagulation pathways in long COVID. Image
8) Early activation of IL-6 and complement pathways during acute infection correlated with subsequent development of long COVID.
Validation studies confirmed higher plasma IL-6R levels in long COVID patients compared to other groups Image
9) The study demonstrates long COVID is characterized by persistent chronic inflammation and immune dysregulation, suggesting novel therapeutic targets.

Thanks for reading ๐Ÿ™
FYI @VirusesImmunity @zalaly @DaniBeckman @DavidJoffe64
@LauraMiers @elisaperego78 Image

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More from @ejustin46

Aug 1
INSIDE OUR INFECTED CELLS.
How SARS-COV-2 stealthy hijacks our cellular sanctuaries (organelles) ?
๐Ÿค“ Visual explanations

Organelles provide the possibility for the virus to organize its RNA in PROTECTED structures, concentrate REPLICATION machinery ...
nature.com/articles/s4146โ€ฆImage
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/s4429โ€ฆImage
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 ๐Ÿ‘ซ
... 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
Jul 28
CORONAVIRUSES and the BRAIN:
Exploring Hidden Links to Neurological Diseases

Human coronaviruses (HCoVs) include seven types, with MERS-CoV, SARS-CoV-1, and SARS-CoV-2 being the most contagious and causing severe pandemics. Image
2) These viruses mainly affect the respiratory system, causing symptoms like cough, fever, and breathing difficulties.
Recent evidence suggests a link between HCoVs and brain disorders. Image
3) This study looks at how these viruses may be associated with neurodegenerative diseases such as Alzheimerโ€™s and Parkinsonโ€™s. It also examines the long-term effects of HCoV infections and on similarities between HCoV proteins and those related to brain diseases. Image
Read 4 tweets
Jul 28
The SARS-CoV-2 PUZZLE :
How Our Microbes Shape the Disease Picture ?

New technology called next-generation sequencing (NGS) shows that many germs can be present at the same time, affecting how diseases show up in people. Image
2) Instead of thinking one disease is caused by one germ, researchers now consider that multiple active germs can be involved, especially in illnesses like COVID-19.
The germs living in our bodies may play a role in how diseases develop. Image
3) This article looks at how these germs interact with viruses like Influenza and SARS-CoV-2. Changes in the types of germs present can affect the immune response and overall severity of the disease. Image
Read 6 tweets
Jul 28
NO ENVELOPE, NO LETTER ? ๐Ÿค”
Does removing the envelope gene make SARS-CoV-2 infection weaker ?

A modified virus without the Envelope (E) protein, known as ฮ”E, produces fewer viral particles despite having more Spike proteins on the cell surface.
biorxiv.org/content/10.110โ€ฆImage
2) This happens because the E protein plays a crucial role in the assembly and release of new virus particles.
When the E protein is absent, the virus struggles to efficiently package the Spike proteins into new viral particles. Image
3) Instead, more Spike proteins accumulate on the surface of the host cells. Although these Spike proteins facilitate cell-to-cell transmission and help the virus enter other cells, the lack of E disrupts the overall process of forming and releasing complete virus particles ... Image
Read 4 tweets

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