NO PROTECTION AGAINST SARS-COV-2 / DOPAMINE DROP / DOPAMINERGIC NEURONAL LOSS ?
This is only a hypothesis, but it is shocking, that the majority of the world's population has decided, to no longer protect themselves, against one of the most dangerous viruses.
2) Admittedly, when we study the history of pandemics, after a certain time, there has often been a relaxation of protective measures, linked to "pandemic fatigue".
3) But if pandemic fatigue alone wasn't enough to explain the phenomenal risk most people take by not protecting themselves ?
To try to understand, we must first go back to the construction of "habits" in our brain.
There are 3 stages.
4) Stage 1. As we repeat a behavior, a feedback loop between the sensorimotor cortex and the striatum becomes strongly engaged, which helps us stamp routines into a single unit, or chunk, of brain activity. The chunk partly relies on "dopamine input" from the midbrain.
5) Stage 2. New behavior explored: The prefrontal cortex communicates with the striatum, and the striatum communicates with the midbrain, where "dopamine" aids learning and assigns value to goals.
6) Stage 3. Habit imprinted and permitted.
Aided by "dopamine", the infralimbic cortex also seems to control when to allow us to engage in a habit; shutting down this region can suppress deeply ingrained routines.
7) In terms of habit formation, for example the habit of protecting or no longer protecting oneself, dopamine plays a decisive role.
This is not new and we know the major role of dopamine for motivation and conversely its role in depression. healthdirect.gov.au/dopamine#:~:te…
8) I will certainly be criticized for such an extreme hypothesis but several studies show that SARS-COV-2 attacks in the brain the mechanisms of regulation of dopamine. sciencedirect.com/science/articl…
9) "Yang et al. demonstrated that a Spike-enabled pseudo-entry virus is able to infect dopaminergic neurons"
Fig. SARS-CoV-2 antigens were detected in both dopaminergic and non-dopaminergic neurons of the substantia nigra nature.com/articles/s4153…
10) "Our findings expand the knowledge about the neurodegenerative process that the SARS-CoV-2 virus can induce, especially to dopaminergic neurons, underlying long-term neurological impairment in COVID-19 patients." biorxiv.org/content/10.110…
11) "Dopamine Transmission Imbalance in Neuroinflammation: Perspectives on Long-Term COVID-19" mdpi.com/1422-0067/24/6…
13) I repeat that this is only a hypothesis.
Has infection with the Dopaminergic Neuron SARS-COV-2 caused a drop in dopamine levels in many individuals, and caused a change in their risk compartment?
I will let the experts answer this question.
@MeetJess @LauraMiers @elisaperego78 @DavidJoffe64 @xabitron1 @HarrySpoelstra @1goodtern @0bj3ctivity @_ppmv @Alitis__ @FLAHAULT @Antonio_Caramia @mrmickme @C_A_Gustave @arijitchakrav DYSFUNCTION of DOPAMINERGIC system = RISK TAKING while SEEKING REWARD
We mentioned it at the start of this thread. Part of the population is taking risks in the face of the virus in search of an easy life. This study sheds new light on this subject. nature.com/articles/s4158…
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SARS-CoV-2 Spike Protein Drives Harmful Fusions in Blood Vessel Cells, Potentially Worsening COVID-19 Complications
The Role of Viral-Induced Syncytia in Endothelial Cells
Thanks to @atranscendedman nature.com/articles/s4159…
2) The SARS-CoV-2 virus can make lung cells fuse together, forming large cells called syncytia. Surprisingly, the virus's spike protein can also cause this in cells that line blood vessels (endothelial cells).
3) This is important because endothelial cell problems are linked to severe COVID-19 symptoms. The researchers found that a specific enzyme, myosin light chain kinase, is needed for these syncytia to form. Cells grown on stiffer surfaces were more likely to form syncytia.
LURKING DANGER:
H5N1 Influenza Clade 2.3.4.4b Exposes Vulnerability in Unprotected Populations and Raises Concerns About Pandemic Risk
"Detection of low pre-existing humoral immunity against influenza virus H5N1 clade 2.3.4.4b in unexposed individuals" biorxiv.org/content/10.110…
2) The study found that most people without prior H5N1 exposure have low levels of antibodies that can recognize and neutralize the emerging H5N1 clade 2.3.4.4b virus, though weaker than for seasonal flu.
3) By analyzing antibodies from these people, the researchers identified potent H5N1-neutralizing antibodies that cross-react with H1 flu strains. This suggests a pre-existing immune response that could help protect against the new H5N1 virus.
2) The study examined how SARS-CoV-2 infected cells respond to potential coinfection by a second virus over time. The key finding is that there is a critical window of vulnerability in the first hour after initial SARS-CoV-2 infection ...
3) ...when the risk of successful coinfection is highest.
However, this susceptibility to coinfection starts to diminish quickly. By 4 hours post-infection, the proportion of cells that can be coinfected decreases significantly.
2) The study found that COVID-19 can damage the testes, the male reproductive organs. A key finding was the high levels of a protein called vimentin in the testes of COVID-19 patients.
Vimentin is important because it may act as a "doorway" that allows the COVID-19 virus ...
3) ...to enter and infect the testes. The researchers suggest that the high vimentin levels make the testes more vulnerable to COVID-19 infection and damage.
The damage includes inflammation, immune cell infiltration, and reduced cell proliferation in the testes.
2) This study shows how the location and development of immune cells over time are critical for their function. In the intestine, CD8 T cells differentiate into distinct subsets based on their position along the intestinal lining.
3) Similarly, for fighting new variants of SARS-CoV-2, the spatial organization and temporal changes in CD8 T cell responses may be very important. CD8 T cells play a key role in recognizing and killing virus-infected cells, helping to clear the infection.