QUESTION to the VIRUS :
"You prefer to fuse with the cells, or to resist to interferons and to antibodies ?"
The virus : "I want both !"
2) This virus never ceases to surprise us. Before discussing a fascinating study on this interplay between fusogenicity and immune escape, a short clarification.
SYNCYTIA: Syncytia are structures formed by the fusion of multiple cells ...
3) ... into a single, multinucleated entity. This formation induce the fusion of infected cells with neighboring uninfected cells, leading to the formation of syncytia.
This allows the virus to spread more efficiently within the host and evade immune detection.
4) In this study,
they showed that "syncytia formation provides resistance to interferons and decreases antibody virus neutralization activity in cultured cells"
The researchers investigated also, "how the evolution of SARS-CoV-2 over timebiorxiv.org/content/10.110…
5) .. affected the fusogenicity of the S protein. They measured syncytia formation and assessed the number of syncytia, syncytial area, and fluorescent intensity as indicators of fusogenicity. The results showed variations in fusogenicity among different strains,
6) ...with an overall increase in fusogenicity as the virus evolved from the WA1 strain to the Delta variants. The original Omicron strain (BA.1) exhibited a decrease in fusogenicity compared to WA1, but there was a gradual increase in fusogenicity
7) with subsequent Omicron variants (BA.2, BA4/5, BQ.1 to XBB)."
The question is to know also, if there is a link between these gains or decreases in fusogenicity and therefore via the syncytia of more or less resistance to interferons and antibodies
8) ... and the mutations on the Spike allowing gain in immune escape.
Question which remains open.
Thanks for reading 🙏
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BATTLEGROUND WITHIN:
How CANCER CELLS and SARS-CoV-2 DISRUPT MITOCHONDRIAL FUNCTION to Undermine Immune Defense
(🧵mega-thread with articles, reviews and studies)
In a recent review, they show that Cancer cells can undermine the immune system ...
2) ... by transferring defective mitochondria to T cells, reducing their cancer-fighting abilities. This challenges the belief that mitochondria remain with their original cells.
Article : nature.com/articles/d4158…
Reference study : nature.com/articles/s4158…
3) While SARS-CoV-2 does not "poison" the immune system in the same manner as cancer cells with tainted mitochondria, it does interfere with mitochondrial function, which can compromise immune responses and contribute to disease severity.
Here are latest research in this area
OUTSMARTING IMMUNITY:
How SARS-CoV-2 EVADES T CELLS in a FIGHT for SURVIVAL
Two new and amazing studies in Nature. Thanks to @DavidJoffe64
2) SARS-CoV-2 is trying to escape to T cells because these immune fighters are crucial in controlling infections.
3) The first study highlighted that robust virus-specific T cells in the lungs of COVID-19 patients effectively reduce viral loads and improve respiratory health. nature.com/articles/s4159…
2) The COVID-19 virus can trigger a severe immune reaction called sepsis, which leads to organ failure and death. Systems biology research has found that the molecular changes in severe COVID-19 are very similar to those seen in sepsis from other causes.
3) This suggests the COVID-19 virus itself, rather than just secondary infections, is directly driving the sepsis-like immune dysfunction in some patients. Additionally, the long-term effects of both severe COVID-19 (called "long COVID") and sepsis (called "post-sepsis syndrome")
SARS-CoV-2 Spike Protein Drives Harmful Fusions in Blood Vessel Cells, Potentially Worsening COVID-19 Complications
The Role of Viral-Induced Syncytia in Endothelial Cells
Thanks to @atranscendedman nature.com/articles/s4159…
2) The SARS-CoV-2 virus can make lung cells fuse together, forming large cells called syncytia. Surprisingly, the virus's spike protein can also cause this in cells that line blood vessels (endothelial cells).
3) This is important because endothelial cell problems are linked to severe COVID-19 symptoms. The researchers found that a specific enzyme, myosin light chain kinase, is needed for these syncytia to form. Cells grown on stiffer surfaces were more likely to form syncytia.
2) The researchers developed a new way to quickly identify SARS-CoV-2 mutations that make the virus spread more easily. By analyzing over 7 million virus genome sequences, they found that most mutations have little impact, but a few significantly increase transmission.
3) Many of the mutations with the biggest transmission advantages are in the Spike protein, which helps the virus enter human cells. These include changes that enhance the virus's ability to bind to receptors or evade antibodies.