2) Ferroptosis, an iron-dependent form of regulated cell death, has been proposed as a potential driver of organ damage in COVID-19 and the post-COVID trajectory of aging and neurodegeneration.
3) COVID-19 infection promotes several events that can lead to ferroptosis, including neuroinflammation, iron dysregulation, oxidative stress, ACE2 receptor disruption, and clock gene alteration.
4) Melatonin has properties that allow it to address all of these ferroptosis-promoting factors. It is an antioxidant, anti-inflammatory, iron chelator, and modulator of the renin-angiotensin system and clock genes
5) Melatonin has shown effectiveness against viral infections, aging, and neurodegenerative diseases like Alzheimer's and Parkinson's in both experimental and clinical research.
This review proposes ferroptosis...
6) ... as a key mechanism behind post-COVID aging/neurodegeneration and presents melatonin as a potential treatment due to its unique ability to inhibit ferroptosis through multiple mechanisms. More research is needed to validate this hypothesis.
7) In summary, the paper puts forth the novel proposition that ferroptosis contributes to long-term issues seen after COVID-19, and identifies melatonin as a promising intervention given its multi-targeted effects against ferroptosis.
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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.