Covid-19 News

Quote from Shane D.

People in the low risk group (<55, healthy) do not fear sickness, or death from COVID because the stats show them they don't have to. So why push, or coerce them to get vaccinated?

Oh yeah? You should check that. Try:

https://19andme.covid19.mathematica.org/

Input a 50 year old male in DeKalb county with no health problems living with 3 other people. Results:

County prevalence

We found data from DeKalb County, GA for your zip code. As of April 25, 2021 , this county had 1,155 new reported cases in the last 14 days and 57,257 total reported cases of COVID-19. Many people who contract COVID-19 are not tested, and therefore not reported. We estimate that your county has an under-reporting factor of 4.3x .

Taking into account the under-reporting factor and average time from symptom onset to recovery, we estimate that:

There are 5,014 total sick people distributed throughout the county, including those who are not officially reported.

1 in every 151 people in your county is currently infected with COVID-19. . . .

Risk of contracting COVID-19

Among people in your county who have behaviors and levels of interaction with others that are similar to yours, the estimated probability of catching COVID-19 through community transmission in a week is 0.04% . For comparison, 0.41% of Americans catch the flu every week during flu season.

Good to know that you wash your hands per CDC guidance. In general, hand washing reduces people's risk of being exposed to COVID-19 by 55% . Good to know that you wear personal protective equipment per CDC guidelines . In general, wearing personal protective equipment reduces people's risk of being exposed to COVID-19 by 68% .

Risk of adverse outcomes from COVID-19

Among people who are the same age, sex, and health status as you and get sick from COVID-19, the risk of hospitalization is 11% , the risk of requiring an ICU is 3.5% , and the risk of not surviving is 0.79% .

That's only a 2% chance in year but . . . would you frequent a fast food joint where 1 in 50 people who ate regularly there got severe food poisoning? Would you take an Uber where 1 in 50 passengers got into serious accidents? I sure wouldn't. If you do get sick, you may well be more miserable for longer than you have been in your life. That was my experience with pneumonia. I wouldn't wish on my worst enemy. "The risk of hospitalization is 11%" means you will likely be at home, sleepless, hallucinating and suffering for weeks, but you may well end up in a hospital even worse off. Sleepless, suffering, with needles stuck into you. No contact with family members allowed. Terrible food. Ordinary ICU treatment, with no complications, can leave you debilitated for months.

It may not be terrifying, like getting severe cancer, but it is the most unpleasant thing you may ever experience. And for what? Why not ensure you will not get it, with a simple vaccine? Why risk giving it to other people, especially family members, who are in close quarters and most vulnerable? Apart from the pain and misery and danger, what about the money it costs you to be debilitated for weeks? Many thousands of dollars in medical expenses and lost work. You can avoid that with a zero cost vaccination that takes a half-hour. I cannot understand why any rational person would risk it. What benefit could there be to avoiding the vaccine? Are you afraid of a momentary pin-prick? Do you seriously think that after 530 million doses, there could be a significant problem?

This is very serious illness. It is often far worse than a typical cold or flu.

Quote from Shane D.

Were I younger, I would probably prefer to take the natural route (get exposed) and develop immunity that way.

Hey, well, if natural route is what you want, move to India. There is nothing more natural than crowding people two to a bed without enough oxygen to go around, and cremating bodies day and night. If you survive, you do get immunity, although the vaccine immunity is stronger.

The natural route is what I did when I was younger and in excellent health. There was no choice. The natural route for pneumonia is a week in the hospital followed by weeks of misery, coughing, and pleurisy, which feels like sandpaper in your chest every time you breath. Night and day. "Nothing to worry about!" -- the doctors say. "Go home. Take 4 ibuprofen every 4 hours." You would voluntarily subject yourself to that . . . because . . . why? Are you some sort of masochist?

The "natural route" for serious illness such as COVID and other pneumonia is what we had in 1918, and what they are going through in India now. It is to permanently destroy millions of lives and kill tens of millions of people.

No one is pushing or coercing anyone else to get vaccinated in the U.S. We are, however, insisting that after vaccines become available, if you don't want one, we don't want to be in the same store or movie theater or airplane with you. Go ahead and kill yourself, but do not endanger me. Breakthrough cases are rare and usually mild, but I don't want one.

Quote from Shane D.

In order to convince a younger me to get jabbed, someone would have to give me a better reason than "you might get sick, and die if you don't". Do we have that reason?

No better reason exists! There is never any other reason to get a vaccination. If there were no chance of getting sick or dying, why would anyone get a vaccination? We don't vaccinate people for harmless bacteria and viruses. Your body is full of them.

Even if it were very unlikely you might die -- or even if we could rule that out -- "you might get sick" is a far more compelling reason than you seem to realize. There are degrees of sickness. A bad cold for a few days is one thing. A bad case of COVID is far worse. It makes you sleepless, unable to breathe, hallucinating, vomiting, with no sense of taste or smell . . . It may stay with you for months or years, in long-haul effects, leaving you unable to walk up a flight of steps, or work. In short, it may ruin your life.

Quote from JedRothwell

The number of people in double blind tests for the Pfizer vax was 44,000. I think most double blind tests range from a few hundred in the first round, to a few thousand in the final round before approval.

This has pure mathematical/statistical reasons. To show a high efficiency with high certainty you need a large number of test persons. (It's also easier to clandestine exclude some bad cases - especially when half the tested live in a development country where supervision is limited...)

Normal drug testing has the following question: Does it work for 10%, 20% better than the old drug? That is why some companies do target untreated diseases. They can use a placebo instead of the old drug... RCT (0% action placebo) tests in most other cases are unethical!

Quote from JedRothwell

I gather they are all being watched closely, to see if any problems develop, and to measure how many antibodies they still have.

Can you show us the one year report?

The Ivermectin world map: https://ivmstatus.com/

Bangladesh authorises the Sputnik vaccine..

https://www.thedailystar.net/c…sputnik-v-vaccine-2084645

but suspends Astrazeneca..

maybe Bangladesh's ivermectin coverage will help stave off some of the Indian surge..

IVM is cheaper than the private $70 /shot Sputnik price in Kenya..

COVID-19 Silences the Immune Response in Infected Cells in the Gut

https://scitechdaily.com/covid…ted-cells-in-the-gut/amp/

Scientists transform human intestinal cells into ‘mini guts’ to follow the infection process.

In an effort to determine the potential for COVID-19 to begin in a person’s gut, and to better understand how human cells respond to SARS-CoV-2, the scientists used human intestinal cells to create organoids — 3D tissue cultures derived from human cells, which mimic the tissue or organ from which the cells originate. Their conclusions, published in the journal Molecular Systems Biology, indicate the potential for infection to be harbored in a host’s intestines and reveal intricacies in the immune response to SARS-CoV-2.

“Previous research had shown that SARS-CoV-2 can infect the gut,” says Theodore Alexandrov, who leads one of the two EMBL groups involved. “However, it remained unclear how intestinal cells mount their immune response to the infection.”

In fact, the researchers were able to determine the cell type most severely infected by the virus, how infected cells trigger an immune response, and — most interestingly — that SARS-CoV-2 silences the immune response in infected cells. These findings may shed light on the pathogenesis of SARS-CoV-2 infection in the gut, and indicate why the gut should be considered to fully understand how COVID-19 develops and spreads.

According to Sergio Triana, lead author and a doctoral candidate in EMBL’s Alexandrov team, the researchers observed how infected cells seem to start a cascade of events that produce a signaling molecule called interferon.

“Interestingly, although most cells in our mini guts had a strong immune response triggered by interferon, SARS-CoV-2-infected cells did not react in the same way and instead presented a strong pro-inflammatory response,” Sergio says. “This suggests that SARS-CoV-2 interferes with the host signaling to disrupt an immune response at the cellular level.”

Coronaviruses, including SARS-CoV-2, cause infection by latching on to specific protein receptors found on the surface of certain cell types. Among these receptors is the protein ACE2. Interestingly, the researchers showed that the infection is not explained solely by the presence of ACE2 on the surface of the cells, highlighting our still limited knowledge about COVID-19, even after a year of tremendous research efforts worldwide.

As the disease progressed in the organoids, the researchers used single-cell RNA sequencing, which involves several techniques to amplify and detect RNA. Among these single-cell technologies, Targeted Perturb-seq (TAP-seq) provided sensitive detection of SARS-CoV-2 in infected organoids. Lars Steinmetz’s research group at EMBL recently developed TAP-seq, which the researchers combined with powerful computational tools, enabling them to detect, quantify, and compare expression of thousands of genes in single cells within the organoids.

“This finding could offer insights into how SARS-CoV-2 protects itself from the immune system and offer alternative ways to treat it,” Lars says. “Further study can help us understand how the virus grows and the various ways it impacts the human immune system.”

SARS-CoV-2 spike protein alone may cause lung damage

https://medicalxpress.com/news…ov-spike-protein-lung.amp

Using a newly developed mouse model of acute lung injury, researchers found that exposure to the SARS-CoV-2 spike protein alone was enough to induce COVID-19-like symptoms including severe inflammation of the lungs.

SARS-CoV-2, the virus that causes COVID-19, is covered in tiny spike proteins. These proteins bind with receptors on our cells, starting a process that allows the virus to release its genetic material into a healthy cell.

"Our findings show that the SARS-CoV2 spike protein causes lung injury even without the presence of intact virus," said Pavel Solopov, Ph.D., DVM, research assistant professor at the Frank Reidy Research Center for Bioelectrics at Old Dominion University. "This previously unknown mechanism could cause symptoms before substantial viral replication occurs."

Solopov will present the new research at the American Society for Pharmacology and Experimental Therapeutics annual meeting during the virtual Experimental Biology (EB) 2021 meeting, to be held April 27-30.

Studying SARS-CoV-2 can be challenging because experiments involving the intact virus requires a Biosafety Level 3 laboratory. To overcome this hurdle, the researchers created a new model of acute lung injury that utilizes transgenic mice that express the human receptor for SARS-CoV-2 in their lungs.

"Our mouse model dramatically reduces the danger of doing this type of research by allowing COVID-19 lung injury to be studied without using the intact, live virus," said Solopov. "This will greatly increase and diversify the ability to do COVID-19 research. Our model will also likely be useful for studying other coronaviruses."

The researchers injected the genetically modified mice with a segment of the spike protein and analyzed their response 72 hours later. Another group of mice received only saline to serve as a control.

The researchers found that the genetically modified mice injected with the spike protein exhibited COVID-19-like symptoms that included severe inflammation, an influx of white blood cells into their lungs and evidence of a cytokine storm—an immune response in which the body starts to attack its own cells and tissues rather than just fighting off the virus. The mice that only received saline remained normal.

"These findings show that the genetically modified mouse together with just a segment of the spike protein can be used to study SARS-CoV-2 lung injury," said Solopov. "We can use this tool to develop a better understanding of how the spike protein causes lung symptoms—even without the intact virus—in order to develop new targets and therapeutics for COVID-19."

The researchers plan to continue this line of investigation by using the new mouse model to study the effectiveness of several drugs in reducing the severity of acute lung injury and COVID-19.

Antibody response induced by mRNA vaccination differs from natural SARS-CoV-2 infection

https://www.news-medical.net/a…SARS-CoV-2-infection.aspx

Researchers tested the antibodies elicited from mRNA vaccination and compared them to those from natural SARS-CoV-2 infection. They found the vaccine did not have antibodies to the virus nucleocapsid protein but had potent RBD antibodies.

Several vaccines have been approved for combatting the COVID-19 pandemic. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) messenger RNA (mRNA)-based vaccines, for example, those developed by Moderna and Pfizer, have shown exceptional efficacy. Evidence suggests strong protection within two weeks of vaccination.

Researchers from the University of California, Irvine, investigated the immune response produced by mRNA vaccines to better understand how they compare to antibodies generated by natural severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Their results are published on the bioRxiv* preprint server.

The authors used the data from ongoing seroprevalence studies in Orange County, California. The first survey was conducted in July 2020, and the second one was done in December 2020. Samples collected from surveys by the University of California Irvine Medical Center in May and December 2020 were also analyzed.

Samples from vaccinated individuals were collected in the months of January, February, and March 2021. They used the coronavirus antigen microarray to measure antibodies against 37 coronaviruses and influenza antigens.

Antibodies different in vaccination and natural infection

The seroprevalence in the Santa Ana zip codes was 18% in July 2020 and 26% in December 2020. At the hospital, the seroprevalence was 13% in December 2020. After vaccination started at the hospital, there was 98.7% seroprevalence by the end of March 2021, suggesting the mRNA vaccine is able to elicit a strong antibody response.

There was a difference between the antibodies elicited by natural infection compared to that from the vaccine. Since the vaccine does not have the nucleocapsid protein, there are no antibodies against this in the vaccine-induced antibodies. However, antibodies against nucleocapsid were seen in natural infection, suggesting this could be a biomarker for natural infection.

Further testing revealed that vaccines elicit more antibodies against the spike protein receptor-binding domain (RBD) compared to the antibodies seen in natural infection. All individuals had antibodies to seasonal flu, and cold and the levels were the same for all irrespective of whether they had COVID-19.

Natural infection produces antibodies to the nucleocapsid and all fragments of the spike protein. The highest antibody levels were against the nucleocapsid, full-length spike protein, and the S2 subunit. Antibody levels against RBD were weak and could be a mechanism for new virus variants to evolve

Vaccinated individuals showed high antibody levels against the full-length spike protein, S2 subunit, and much higher levels to the RBD and S1 subunit. These individuals also had cross-reactive antibodies between the spike protein and RBD, absent in natural infection.

The mRNA vaccine likely adopts a protein conformation that presents cross-reactive epitopes. This could be useful against emerging virus variants and suggests the antibodies produced could still be effective against them.

mRNA vaccines elicit a strong antibody response

Natural infection produces a uniform level of antibodies against the nucleocapsid and spike protein. Vaccinated individuals fall into two groups, those with antibodies against the nucleocapsid protein and those without. Those with nucleocapsid antibodies may have been infected naturally before.

Some individuals showed good antibody levels after the first dose, but most required a booster dose for robust antibody levels, which were seen about 35 days after the first dose. The data also suggests people who have been infected naturally before have a more robust antibody response to the vaccine.

The study results are similar to the antibody levels seen in clinical trials of the mRNA vaccines, showing rapid production of antibodies. High levels of antibodies against the RBD seen in vaccinated individuals suggest good protection. The RBD is the portion of the spike protein that binds to the angiotensin-converting enzyme 2 (ACE2) receptor on host cells.

Antibodies from natural infection do not have high levels against the RBD. This could be because the RBD epitope may be hidden to prevent host immune recognition. The less robust and variable antibody response to natural infection suggests immunity acquired by natural infection may not be as strong as that from vaccination. “We should not assume that previously infected individuals are immune or that they cannot transmit the virus,” write the authors.

Thus, vaccination induces a more robust antibody response, and even people who have been previously infected may benefit from the vaccine.

Bob dylan sang everybody must get stoned. It might cure Covid!!! Way ahead of the times!!!!!!!

Cannabidiol Inhibits SARS-CoV-2 Replication and Promotes the Host Innate Immune Response

https://www.biorxiv.org/conten…/2021.03.10.432967v1.full

ABSTRACT

The rapid spread of COVID-19 underscores the need for new treatments. Here we report that cannabidiol (CBD), a compound produced by the cannabis plant, inhibits SARS-CoV-2 infection. CBD and its metabolite, 7-OH-CBD, but not congeneric cannabinoids, potently block SARS-CoV-2 replication in lung epithelial cells. CBD acts after cellular infection, inhibiting viral gene expression and reversing many effects of SARS-CoV-2 on host gene transcription. CBD induces interferon expression and up-regulates its antiviral signaling pathway. A cohort of human patients previously taking CBD had significantly lower SARS-CoV-2 infection incidence of up to an order of magnitude relative to matched pairs or the general population. This study highlights CBD, and its active metabolite, 7-OH-CBD, as potential preventative agents and therapeutic treatments for SARS-CoV-2 at early stages of infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for coronavirus disease 2019 (COVID-19), a pandemic that has overtaken the world during the past year. SARS-CoV-2, related to severe acute respiratory syndrome-related coronavirus (SARS-CoV), is the seventh species of coronavirus known to infect people. These coronaviruses, which include SARS-CoV, 229E, NL63, OC43, HKU1, and MERS-CoV cause a range of symptoms from the common cold to more severe pathologies (1). Despite recent vaccine availability, SARS-CoV-2 is still spreading rapidly (2), highlighting the need for alternative treatments, especially for populations with limited access to vaccines. To date, few therapies have been identified that block SARS-CoV-2 replication and viral production.

SARS-CoV-2 is a positive-sense single-stranded RNA (+ssRNA) enveloped virus composed of a lipid bilayer and four structural proteins that drive viral particle formation. The spike (S), membrane (M), and envelope (E) are integral proteins of the virus membrane and serve to drive virion budding, while also recruiting the nucleocapsid (N) protein and the viral genomic RNA into nascent virions. Like SARS-CoV, SARS-CoV-2 primarily enters human cells by the binding of the viral S protein to the angiotensin converting enzyme 2 (ACE2) receptor (3–5), after which the S protein undergoes proteolysis by transmembrane protease, serine 2 (TMPRSS2) or other proteases into two non-covalently bound peptides (S1, S2) that facilitate viral entry into the host cell. The N-terminal S1 binds the ACE2 receptor, and the C-terminal S2 mediates viral-cell membrane fusion following proteolytic cleavage by TMRSS2 or other proteases. Depending upon the cell type, viral entry can also occur after ACE2 binding, independent of proteolytic cleavage (6–8). Following cell entry, the SARS-CoV-2 genome is translated into two large polypeptides that are cleaved by two viral proteases, MPro and PLPro (9, 10), to produce 15 proteins, in addition to the synthesis of subgenomic RNAs that encode another 10 accessory proteins plus the 4 structural proteins. These proteins enable viral replication, assembly, and budding. In an effort to suppress infection by the SARS-CoV-2 beta-coronavirus as well as other evolving pathogenic viruses, we tested the antiviral potential of a number of small molecules that target host stress response pathways.

One potential regulator of the host stress and antiviral inflammatory responses is cannabidiol (CBD), a member of the cannabinoid class of natural products (11). CBD is produced by Cannabis sativa (Cannabaceae; marijuana/hemp). Hemp refers to cannabis plants or materials derived thereof that contain 0.3% or less of the psychotropic tetrahydrocannabinol (THC) and typically have relatively high CBD content. By contrast, marijuana refers to C. sativa materials with more than 0.3% THC by dry weight. THC acts through binding to the cannabinoid receptor, and CBD potentiates this interaction (12). Despite numerous studies and many typically unsubstantiated claims related to CBD-containing products, the biology of CBD itself is unclear and specific targets are mostly unknown (11). However, an oral solution of CBD is an FDA-approved drug, largely for the treatment of epilepsy (13). Thus, CBD has drug status, is viable as a therapeutic, and cannot be marketed as a dietary supplement in the United States (11). Although limited, some studies have reported that certain cannabinoids have antiviral effects against hepatitis C virus (HCV) and other viruses (14).

results suggest that CBD can block SARS-CoV-2 infection at early stages of infection, and CBD administration is associated with a lower risk of SARS-CoV-2 infection in humans. Furthermore, the active compound in patients is likely to be 7-OH-CBD, the same metabolite implicated in CBD treatment of epilepsy. The substantial reduction in SARS-CoV-2 infection risk of approximately an order of magnitude in patients who took FDA-approved CBD highlights the potential efficacy of this drug in combating SARS-CoV-2 infection. Finally, the ability of CBD to inhibit replication of MHV raises the possibility that CBD may have efficacy against new pathogenic viruses arising in the future.

One mechanism contributing to the antiviral activity of CBD is the induction of the interferon pathway both directly and indirectly following activation of the host immune response to the viral pathogen. In fact, interferons have been tested clinically as potential treatments for COVID-19 (21). Importantly, CBD also suppresses cytokine activation in response to viral infection, reducing the likelihood of immune cell recruitment and subsequent cytokine storms within the lungs and other affected tissues. These results complement previous findings suggesting that CBD suppresses cytokine production in recruited immune cells such as macrophages (22). Thus, CBD has to the potential not only to act as an antiviral agent at early stages of infection but also to protect the host against an overactive immune system at later stages.

CBD has a number of advantages as a potential preventative agent against SARS-CoV-2. CBD is widely available without restricted access if the content of THC is <0.3%. There are multiple means of ingestion, including potential for inhalation and nasal delivery. CBD blocks viral replication after entry into cells and, thus, is likely to be effective against viral variants with mutant spike proteins. Unlike drugs such as remdesivir or antiviral antibodies, CBD administration does not require injection in hospital settings. Finally, CBD is associated with only minor side effects (15).

However, several issues require close examination before CBD can be considered or even explored as a therapeutic for COVID-19 (11). Although many CBD formulations are available on the market, they vary vastly in quality, the amount of CBD, and their pharmacokinetic properties after oral administration, which are mostly unknown. CBD is quite hydrophobic and forms large micellar structures that are trapped and broken down in the liver, thereby limiting the amount of drug available to other tissues after oral administration. The inactive carriers have a significant impact on clinically obtainable concentrations. As CBD is widely sold as a preparation in an edible oil, we analyzed flavored commercial hemp oils and found a CBD content of only 0.30% in a representative sample (fig. S12). The purity of CBD and, in particular, the composition of the materials labelled as CBD are also important, especially in light of our findings suggesting that other cannabinoids such as THC might act to counter CBD antiviral efficacy. This essentially eliminates the feasibility of marijuana serving as an effective source of antiviral CBD, in addition to issues related to its legal status. Finally, other means of CBD administration such as vaping and smoking raise concerns about potential lung damage.

Future studies to explore the optimal means of CBD delivery to patients along with clinical trials will be needed to fully test the promise of CBD as a therapeutic to block SARS-CoV-2 infection. As the clearance rates for CBD in plasma are substantially lower in humans than mice, we would suggest moving to clinical trials rather than doing preclinical studies in animal models (15). We advocate carefully designed placebo-controlled clinical trials with known concentrations and highly-characterized formulations in order to define CBD’s role in preventing and treating early SARS-CoV-2 infection. The necessary human in vivo concentration and optimal route and formulation remain to be defined. We strongly caution against the urge to take CBD in presently available formulations as a preventative or treatment therapy at this time, especially without the knowledge of a rigorous randomized clinical trial with this natural product (23).

Quote from Fm1

CBD and its metabolite, 7-OH-CBD, but not congeneric cannabinoids, potently block SARS-CoV-2 replication in lung epithelial cells. CBD acts after cellular infection, inhibiting viral gene expression and reversing many effects of SARS-CoV-2 on host gene transcription.

Big pharma, since a long time, fights against the use of cannabis based drugs. The same they do now with ivermectin....

There are many other multi potent drugs that would severely cut down the income of big pharma. There are also simple methods to cut down the amount chemo needed by at least a factor of 10. Not even to talk about stool transplantation to heal Alzheimer.. and many other diseases...

Quote from Shane D.

I understand what you are saying, but speaking for myself, I am vaccinated and have no problem with being in the company of those who are not.

That depends on where you are. In a park or grocery store I would have no problem at all. Unless the grocery store was jammed with people, as some of our farmer's markets are on weekends. In an airplane or a movie theater, I would have a problem with unvaccinated people, especially if they did not wear masks.

The latest CDC recommendations may be a little too conservative, but they do show the vaccinated person in the green "safe" space in all situations.

https://www.cdc.gov/coronaviru…singSaferActivities11.pdf

Quote from Fm1

The mRNA vaccine likely adopts a protein conformation that presents cross-reactive epitopes. This could be useful against emerging virus variants and suggests the antibodies produced could still be effective against them.

mRNA vaccines elicit a strong antibody response

That's good news. It seems to me, this report is saying that in some ways the vaccine antibodies are better than the ones from natural acquired immunity. I find that surprising, but perhaps the experts do not. I have read that doctors recommend you get the vaccine even if you previously got the disease. If there are any advantages to the vaccine antibodies, you get the best of both that way. That is the conclusion:

"Thus, vaccination induces a more robust antibody response, and even people who have been previously infected may benefit from the vaccine."

They also say that the vaccine helps relieve some of the long haul effects in some patients. That is excellent news!

Quote from Fm1

SARS-CoV-2 spike protein alone may cause lung damage

https://medicalxpress.com/news…ov-spike-protein-lung.amp

That could be bad news, because the mRNA vaccines produce only the spike protein. The assumption has been that the spike alone causes no harm.

It the spikes cause problems, it does not seem to happen often in humans. Hundreds of millions of people have been vaccinated. The problems described in this paper have not been reported as far as I know. Maybe it only happens with transgenic mice, the poor things. They are put upon from conception, with people messing with their genomes.

Quote from JedRothwell

That could be bad news, because the mRNA vaccines produce only the spike protein. The assumption has been that the spike alone causes no harm.

It the spikes cause problems, it does not seem to happen often in humans. Hundreds of millions of people have been vaccinated. The problems described in this paper have not been reported as far as I know. Maybe it only happens with transgenic mice, the poor things. They are put upon from conception, with people messing with their genomes.

It happens in humans.

There are many studies published on this.

This is heading to the biggest war crime in human history. The people who did this will be brought to justice, in time.

This is cute!

"If the COVID-19 Vaccines Interviewed for a Job"

Quote from Navid

It happens in humans.

There are many studies published on this.

No, it doesn't. What internet sewer did you dredge that from? The Journal of Imaginary Results?

Quote from Navid

This is heading to the biggest war crime in human history.

Paranoia strikes deep when you spend all your time in the Internet sewers. You should come up for air.

Quote from JedRothwell

No, it doesn't. What internet sewer did you dredge that from? The Journal of Imaginary Results?

Paranoia strikes deep when you spend all your time in the Internet sewers. You should come up for air.

Psychological projection. The ring is the spike protein, and who is Gollum?

Quote from JedRothwell

That could be bad news, because the mRNA vaccines produce only the spike protein. The assumption has been that the spike alone causes no harm.

It the spikes cause problems, it does not seem to happen often in humans. Hundreds of millions of people have been vaccinated. The problems described in this paper have not been reported as far as I know. Maybe it only happens with transgenic mice, the poor things. They are put upon from conception, with people messing with their genomes.

I made this point last august, targeting the s protein could lead to a vaccine resistant virus. Wyttenbach has said the same thing. Mrna vaccines have never been used simply because the s protein is not stable. Mrna treatments are showing great promise in cancer treatments targeting the N protein

Quote from JedRothwell

No, it doesn't. What internet sewer did you dredge that from? The Journal of Imaginary Results?

Paranoia strikes deep when you spend all your time in the Internet sewers. You should come up for air.

The sewer that is the NIH,

SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680014/

Currently, the world is suffering from the pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. So far, 60 million people have been infected with SARS-CoV-2, and 1.4 million people have died because of COVID-19 worldwide, causing serious health, economical, and sociological problems. However, the mechanism of the effect of SARS-CoV-2 on human host cells has not been defined. The present study reports that the SARS-CoV-2 spike protein alone without the rest of the viral components is sufficient to elicit cell signaling in lung vascular cells. The treatment of human pulmonary artery smooth muscle cells or human pulmonary artery endothelial cells with recombinant SARS-CoV-2 spike protein S1 subunit (Val16 – Gln690) at 10 ng/ml (0.13 nM) caused an activation of MEK phosphorylation. The activation kinetics was transient with a peak at 10 min. The recombinant protein that contains only the ACE2 receptor-binding domain of the SARS-CoV-2 spike

protein S1 subunit (Arg319 – Phe541), on the other hand, did not cause this activation. Consistent with the activation of cell growth signaling in lung vascular cells by the SARS-CoV-2 spike protein, pulmonary vascular walls were found to be thickened in COVID-19 patients. Thus, SARS-CoV-2 spike protein-mediated cell growth signaling may participate in adverse cardiovascular/pulmonary outcomes, and this mechanism may provide new therapeutic targets to combat COVID-19.