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)
We have seen a lot of posts on Singapore with graphs saying that vaccines do not protect against new variants.
IT'S WRONG !!!
We will explain why in this thread.
2) If we look at the statistics from the Ministry of Health in Singapore, we see that the majority of hospitalizations come from those over 60 years old.
3) The population over 60 in Singapore was 1.2 million in 2020 and increasing. It is a city with an elderly population, where I lived 2 years and that I know well.
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
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."