2) In this brief report, researchers looked at 20 individuals who previously had COVID-19 but were never vaccinated. Bone marrow samples and plasma were collected to analyze antibody-producing cells.
3) Two specific cell populations (subsets B and D) that secrete antibodies were analyzed using ELISPOT assays for SARS-CoV-2 spike protein and tetanus antigen.ย
Subset D is thought to represent long-lived plasma cells (LLPCs) responsible for durable antibody responses.
4) Fewer spike-specific cells were found in subset D compared to tetanus-specific cells.
No spike-specific cells were detected in subset D for individuals with previous severe COVID-19 infection, while tetanus-specific cells were found.
5) Plasma antibody levels against tetanus correlated with the percentage of tetanus-specific cells in subset D, but no correlations were found for spike antibodies.
A regression model explained variance in tetanus antibody levels based on subset B and D ...
6).. but not for spike antibodies, indicating a lack of LLPC contribution to spike antibodies. Model suggested competitive inhibition of LLPC expansion by short-lived B cells could explain the lack of spike-specific LLPCs, leading to more short-lived antibody protection for COVID
7) In summary, the study found deficient generation of spike-specific LLPCs in the bone marrow after COVID-19 infection, which may underlie the short-lived antibody responses compared to the long-lasting response induced by tetanus vaccination.
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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/10.110โฆ
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/s4146โฆ
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.