What if SARS-COV-2 MANIPULATED US, to SPREAD BETTER ?
2) There is always the risk with such hypotheses of being accused of anthropomorphism, i.e. lending human behaviors to a virus which cannot have any.
However, there have been several interesting studies on this subject and particularly in the field of behavioral neurovirology.
3) In fact, such behaviour-changing effects of viruses – so-called behavioural host manipulation – are not new, and have previously been reported for some viruses.
The theory is that pathogens do this to maximise their reproduction rate and in turn, their spread and survival.
4) The example of rabies virus :
"When a host is infected with the rabies virus it gets into the host’s central nervous system and triggers hyper aggression. The virus is also present in the rabid animal’s saliva ...
5) ... so being bitten transmits the infection to a new host and the old host is left to eventually die if untreated."
6) In a first study, they "hypothesized that the novel coronavirus, SARS-CoV2, which produces the COVID-19 disease may produce host manipulations that maximize its transmission between humans." ncbi.nlm.nih.gov/pmc/articles/P…
7) First hypothesis :
The virus may act on an area of the brain called the anterior cingulate cortex (ACC), which is involved in social behaviour and emotional regulation. By manipulating the ACC, instead of observing distancing rules, people would be drawn to "gather socially"
8) Second hypothesis :
"While there are effects on behaviour through virus-induced changes in the nervous system, Covid has the potential also to change the endocrine system that produces hormones that regulate many functions, from sleep to reproduction and social behaviour"
9) In another study, they show that SARS-COV-2 "bind to the host receptor neuropilin-1 in order to gain entry into the cell" but also can cause "interferon suppression and the resulting reduction in sickness behavior ...
10) ... enhanced transmission through neurally mediated cough induction, and reduction in sense of smell." link.springer.com/article/10.100…
11) We had already mentioned this hypothesis in particular because of the impact of the virus on dopamine.
12) Of course, these remain hypotheses but clearly the virus has more than one trick up its sleeve.
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"70% to 90% of our CELLS are completely RENEWED in less than 5 YEARS!
So If we’re mostly "New", why are so many still struggling with SARS-CoV-2?
We will tackle this question, which is more complex than it seems, in several posts.
2) First, let's say a few words about cell renewal.
70% to 90% of our cells are renewed over time. This turnover occurs in various cell types, including skin, blood, and immune cells, allowing the body to replace damaged or aged cells. sciencefocus.com/the-human-body…
3) For instance, red blood cells have a lifespan of about 120 days, while skin cells regenerate every few weeks.
Even with significant cell renewal, aging persists due to changes in our DNA. sciencefocus.com/the-human-body…
2) Co-infection occurs when a person is infected by more than one virus at the same time. This can lead to interesting and sometimes complex interactions between the viruses
3) In one study about SARS-CoV-2, researchers found that when different versions of this virus infect the same person, they can mix their genetic material through a process called recombination. This means that the new version of the virus can have traits from both parent viruses
For more than three years, we have been emphasizing that the envelope protein is an essential component and that we cannot limit our focus to just the spike protein. We are now uncovering its role in long COVID.
3) The Envelope (E) protein of SARS-CoV-2 plays a crucial role for several reasons:
▶️ Virus Assembly and Release: The E protein is essential for the virus's assembly and budding from infected cells, contributing to its stability and infectivity.
In 2022, COVID-19 was the second leading cause of death globally, with the repercussions of the virus far from over. The lasting impact of the pandemic continues to affect lives around the world.
Recent research may have identified a key factor contributing to long COVID: microscopic clots intertwined with immune system debris in the blood. These unusual structures were found to be nearly 20 times more prevalent ...
2) ...in long COVID patients compared to healthy individuals. The clots, associated with neutrophil extracellular traps (NETs), suggest a potential biological marker for persistent symptoms.
3) These microclots could impede blood flow in small vessels, leading to issues like brain fog, fatigue, and shortness of breath.
Unlocking the Secrets: A Comprehensive Megathread on Key Virus Subtypes of Human and Avian Influenza !"🧵
First, a quick overview of the different subtypes:
HUMAN INFLUENZA
H1N1 : The 2009 pandemic strain, which continues to circulate
...
2) H3N2: Strain spreading fast actually and causing significant morbidity
H6N1: Notable for potential human impact.
AVIAN INFLUENZA :
H5N1: High pathogenicity, zoonotic concerns.
H3N8: Emerging strain of interest.
H7N9: Associated with human infections, sporadic outbreaks.
3) H5N8: Emerging strain with health implications.
H5N6: Recent cases in birds and humans.
H7N7: Impact on poultry and occasional human cases.
H9N2: Common in birds, history of human infections.