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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SARS-COV-2 and DISRUPTION of the gastrointestinal GI homeostasis
(in 3 figures)
2) Figure 1. SARS-CoV-2 infects intestinal epithelial cells. The RBD region of S protein enhances the ability of SARS-CoV-2 to bind to ACE2 on intestinal cells. TMPRSS2 and furin promote RBD binding to ACE2 in IECs, thereby enhancing viral infection and causing GI damage.
3) Figure 2. Composition of intestinal microbiota in healthy individuals and COVID-19 patients. The commensal symbionts are depleted, and opportunistic pathogens such as Coprobacillus, Clostridium ramosum and Clostridium hathewayi are markedly enriched in gut of COVID-19 patients
A significant portion of the global population reports a lack of clear memories
(credit @BrianRoemmele)
2) At the beginning, there may be a temporary and sudden loss of memory, related to a temporary disruption of blood flow to certain areas of the brain, the TGA (Transient global amnesia)
SARS-COV-2 hijacks cells, forces them to grow filopodia like-tentacles, then invade others ! (Part 2)
Without "over-hyped" 🤗 this mechanism of entry into cells, we would like to address in this 2nd part, the key role of lipids and in particular of cholesterol
2) We would first like to come back, to the last study of our previous thread which we had not explained.
SUMMARY :
SARS-CoV-2 induces the formation of actin-rich filopodia on infected cells.
3) These filopodia are thin, finger-like protrusions that extend from the cell surface. They provide a physical bridge between the infected cell and neighboring uninfected cells or target cells, such as respiratory epithelial cells.
2) We tried in this thread, to summarize the complex but very important theme of this study :
"SARS-CoV-2 induces delayed type-I/III interferon production, allowing it to escape the early innate immune response. The delay has been attributed to a deficiency ...
3) ... in the ability of cells to sense viral replication upon infection, which in turn hampers activation of the antiviral state in bystander cells."
If we come back to the infection, "the time required for the body to activate adaptive immunity against the SARS-CoV-2 virus ..
SARS-CoV-2 infection can cause PERSISTENT RESPIRATORY SEQUELAE.
"Prolonged COVID lung symptoms including fatigue, cough, and shortness of breath can persist for months. The residual lung abnormalities such as fibrosis were estimated in up to 11% of people nature.com/articles/s4200…
2) ...discharged after COVID-19-related hospitalization."
"We found that CoV2 and Flu infections mediate distinct pulmonary cellular and transcriptomic changes. CoV2, but not Flu infection fails to induce Krt5+ progenitor cell proliferation,
3) ... leading to more persistent and chronic pulmonary consolidation and scarring than other respiratory viral infections."
To measure the level of antibodies immunity, scientists determine the titers for neutralizing antibodies (nAb titers) which are specialized antibodies that bind the virus and prevent it from spreading.
2) VACCINATION (1)
The first vaccines against Wuhan strain were offering a very strong protection with a level of neutralization antibodies, nAb titers > 1000
3) BOOSTERS
With the recent boosters, the level of protection was lower but still at level around 500 nAbs titers which could consider as a good level of protection.