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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2) This study looked at different ways to detect COVID-19 in a building. The researchers tested air, surfaces, and wastewater to see which methods could best detect the virus.
They placed air samplers in the lobby of a dorm where students with COVID-19 were isolating.
3) The air samples showed higher virus levels when students with COVID-19 were present.
The researchers also collected air samples from the building's rooftop exhaust, swabbed high-touch surfaces, and tested the building's wastewater.
2) The H5N1 bird flu virus has been spreading rapidly since 2020. An important change is that the neuraminidase (NA) protein on this virus now has a longer "stalk" region.
In the past, most H5N1 viruses had a shorter NA stalk.
3) But the current clade 2.3.4.4b H5N1 viruses mostly have the longer NA stalk.
The longer NA stalk may make these H5N1 viruses more able to spread between mammals, including potentially between humans.
What an UNFORTUNATE CHOICE of WORD it is to REFER to the term “VARIANT” in relation to SARS-CoV-2.
No one would think to call Prince William a "variant" or a mere variation of Queen Elizabeth; he shares the same family and lineage. That's all.
2) I wanted to use this analogy to highlight the significant differences in pathogenicity and transmission among the Alpha, Delta, and Omicron variants, as demonstrated by a recent study published in Nature. nature.com/articles/s4429…
3) By suggesting that the various lineages of SARS-CoV-2 consist of only minor mutations in the Spike protein—while overlooking the other proteins—and by using the term "soup of variants," which I consistently contest, we diminish the profound changes ...
2) Viruses like SARS-CoV-2 have proteins on their surface called spike proteins. These spike proteins help the virus attach to and enter human cells. The spike proteins are heavily coated with sugar molecules called glycans.
3) Researchers have developed a synthetic molecule called IDS060 that can bind to these glycans on the spike protein. This binding prevents the virus from attaching to human cells, blocking infection.
WHEN and WHERE was the H5N1 influenza A virus (genotype D1.1) DISCOVERED ?
A very interesting article from
@LouiseHMoncla @angie_rasmussen @MichaelWorobey @PeacockFlu and colleagues virological.org/t/timing-and-m…
2) The H5N1 influenza A virus (genotype D1.1) was discovered in dairy cattle in Churchill County, Nevada, on January 31, 2025. The detection followed a routine surveillance program, where bulk milk samples were collected from dairy processing plant silos on January 6 and 7, 2025.
3) These samples tested positive for the virus on January 10.
Investigations revealed that the virus likely jumped from birds to cattle sometime between late October 2024 and early January 2025 ...
What makes VIRUSES like Herpes, Epstein-Barr, Flu, H1N1, H5N1 and HIV so EFFECTIVE at INFECTING the BRAIN ?
Viruses can infect and damage the brain, leading to conditions like Alzheimer's, Parkinson's, schizophrenia, and depression link.springer.com/article/10.100…
2) Some Viruses are able to successfully infect the brain for a few key reasons:
▶️ Direct Brain Entry: Some viruses can directly enter the brain through the nose or other pathways, allowing them to directly infect brain cells.
3) ▶️ Evading Immunity: Certain viruses can hide from or suppress the immune system, enabling them to persist in the brain undetected.
▶️ Breaching the Blood-Brain Barrier: Viruses can damage the protective barrier between the brain and bloodstream ...