▶️ "Immune imprinting induced by wildtype (WT)-based vaccination would compromise the antibody response to Omicron-based boosters"biorxiv.org/content/10.110…
3) ▶️ Single Omicron-boosting is heavily limited by immune imprinting, especially when using variants antigenically distinct from WT, like XBB"
▶️ "Repeated Omicron infections could also alleviate WT-vaccination-induced immune imprinting and generate high neutralizing titers ...
4) ...against XBB.1.5 and XBB.1.16"
▶️ "Our findings suggest the WT component should be abandoned when updating COVID-19 vaccine antigen compositions to XBB lineages, and those who haven’t been exposed to Omicron yet should receive two updated vaccine boosters."
5) Fig. 2 | Humoral immune imprinting after repeated Omicron infections in humans.
6) Fig. 3 B cell immune imprinting after repeated Omicron infections.
7) Fig. 4 Epitope distribution and characterization of mAbs elicited by Omicron BTI and reinfection
8) Fig. 5 | Estimate the evolutionary trends of XBB.1.5 RBD from DMS profiles.
9) Fig. 6 Combination of escape mutations evades XBB.1.5-neutralizing antibodies from reinfection.
10) Extended Data Fig. 7 SPR sensorgrams for affinity of hACEZ and SARS-CoV-2 mutants RBD
11) Thanks for reading 🙏 and let see the reaction of the experts on this subject 😁
IS SARS-CoV-2 BECOMING "INVISIBLE"? The Hidden Truth Behind the Pandemic
As the world strives to move past the COVID-19 pandemic, a troubling narrative has emerged: the perception that SARS-CoV-2 is becoming "invisible."
2) Governments and communities are eager to return to normalcy, leading to a tendency to downplay the virus's severity. Reports of new infections and long COVID cases have been totally minimized, creating a false sense of security ...
3) ...that the virus is no longer a significant threat. However, this perception is not only a matter of public sentiment. The virus itself has evolved, most notably with the emergence of the Omicron variant. Recent research reveals that Omicron exhibits a remarkable ability ...
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 ...
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.
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…
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.
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).
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.
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.
Organelles provide the possibility for the virus to organize its RNA in PROTECTED structures, concentrate REPLICATION machinery ... nature.com/articles/s4146…
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.
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.