Worse Than the Disease? Reviewing Some Possible Unintended Consequences of the mRNA Vaccines Against COVID-19

Authors: Stephanie Seneff1and Greg Nigh21Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge MA, 02139, USA, E-mail: seneff@csail.mit.edu 2Naturopathic Oncology, Immersion Health, Portland, OR 97214, USA

ABSTRACT

Operation Warp Speed brought to market in the United States two mRNA vaccines, produced by Pfizer and Moderna. Interim data suggested high efficacy for both of these vaccines, which helped legitimize Emergency Use Authorization (EUA) by the FDA. However, the exceptionally rapid movement of these vaccines through controlled trials and into mass deployment raises multiple safety concerns. In this review we first describe the technology underlying these vaccines in detail. We then review both components of and the intended biological response to these vaccines, including production of the spike protein itself, and their potential relationship to a wide range of both acute and long-term induced pathologies, such as blood disorders, neurodegenerative diseases and autoimmune diseases. Among these potential induced pathologies, we discuss the relevance of prion-protein-related amino acid sequences within the spike protein. We also present a brief review of studies supporting the potential for spike protein “shedding”, transmission of the protein from a vaccinated to an unvaccinated person, resulting in symptoms induced in the latter. We finish by addressing a common point of debate, namely, whether or not these vaccines could modify the DNA of those receiving the vaccination. While there are no studies demonstrating definitively that this is happening, we provide a plausible scenario, supported by previously established pathways for transformation and transport of genetic material, whereby injected mRNA could ultimately be incorporated into germ cell DNA for transgenerational transmission. We conclude with our recommendations regarding surveillance that will help to clarify the long-term effects of these experimental drugs and allow us to better assess the true risk/benefit ratio of these novel technologies.

For More Information: https://ijvtpr.com/index.php/IJVTPR/article/view/23/51

Hidden History When Vaccines go wrong…This chicken vaccine makes its virus more dangerous

Authors: By —Nsikan Akpan

The deadliest strains of viruses often take care of themselves — they flare up and then die out. This is because they are so good at destroying cells and causing illness that they ultimately kill their host before they have time to spread.

But a chicken virus that represents one of the deadliest germs in history breaks from this conventional wisdom, thanks to an inadvertent effect from a vaccine. Chickens vaccinated against Marek’s disease rarely get sick. But the vaccine does not prevent them from spreading Marek’s to unvaccinated birds.

“With the hottest strains, every unvaccinated bird dies within 10 days. There is no human virus that is that hot. Ebola, for example, doesn’t kill everything in 10 days.”

In fact, rather than stop fowl from spreading the virus, the vaccine allows the disease to spread faster and longer than it normally would, a new study finds. The scientists now believe that this vaccine has helped this chicken virus become uniquely virulent.

For More Information: https://www.pbs.org/newshour/science/tthis-chicken-vaccine-makes-virus-dangerous

Imperfect Vaccination Can Enhance the Transmission of Highly Virulent Pathogens

Authors: Andrew F. Read ,Susan J. Baigent,Claire Powers,Lydia B. Kgosana,Luke Blackwell,Lorraine P. Smith,David A. Kennedy,Stephen W. Walkden-Brown,Venugopal K. Nair

Abstract

Could some vaccines drive the evolution of more virulent pathogens? Conventional wisdom is that natural selection will remove highly lethal pathogens if host death greatly reduces transmission. Vaccines that keep hosts alive but still allow transmission could thus allow very virulent strains to circulate in a population. Here we show experimentally that immunization of chickens against Marek’s disease virus enhances the fitness of more virulent strains, making it possible for hyperpathogenic strains to transmit. Immunity elicited by direct vaccination or by maternal vaccination prolongs host survival but does not prevent infection, viral replication or transmission, thus extending the infectious periods of strains otherwise too lethal to persist. Our data show that anti-disease vaccines that do not prevent transmission can create conditions that promote the emergence of pathogen strains that cause more severe disease in unvaccinated hosts.

There is a theoretical expectation that some types of vaccines could prompt the evolution of more virulent (“hotter”) pathogens. This idea follows from the notion that natural selection removes pathogen strains that are so “hot” that they kill their hosts and, therefore, themselves. Vaccines that let the hosts survive but do not prevent the spread of the pathogen relax this selection, allowing the evolution of hotter pathogens to occur. This type of vaccine is often called a leaky vaccine. When vaccines prevent transmission, as is the case for nearly all vaccines used in humans, this type of evolution towards increased virulence is blocked. But when vaccines leak, allowing at least some pathogen transmission, they could create the ecological conditions that would allow hot strains to emerge and persist. This theory proved highly controversial when it was first proposed over a decade ago, but here we report experiments with Marek’s disease virus in poultry that show that modern commercial leaky vaccines can have precisely this effect: they allow the onward transmission of strains otherwise too lethal to persist. Thus, the use of leaky vaccines can facilitate the evolution of pathogen strains that put unvaccinated hosts at greater risk of severe disease. The future challenge is to identify whether there are other types of vaccines used in animals and humans that might also generate these evolutionary risks.

For More Information: https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1002198

How Likely Are Vaccinated People To Get Meaningfully Sick From Delta?

Authors: DYLAN HOUSMAN

The reality that breakthrough cases exist and being vaccinated doesn’t guarantee protection from COVID-19 has raised a new question in the minds of many Americans: just how likely is it that someone will get seriously ill from the delta variant of COVID-19 if they are vaccinated?

Some clinical data suggests that vaccine efficacy may be slightly lower against the delta variant than previous iterations of the virus, but the overall numbers are still promising. A July study by Public Health England found that the Pfizer vaccine is still 88% effective at preventing symptomatic disease from the delta variant, only about 6% lower than against the alpha variant. A Canadian study found the Moderna jab to be 72% effective against Delta after just one dose, but more data is needed to determine how much more protection the second dose provides. The Moderna shots have shown to be around 93% effective after six months without accounting for the Delta variant.

The Centers for Disease Control and Prevention (CDC) reported 6,915 hospitalizations related to COVID-19 in vaccinated people as of Aug. 2, but the answer to how risky COVID-19 is for the vaccinated isn’t as simple as a single stat. Anecdotal accounts and a deep dive into the data indicates that a wide variety of experiences are possible when vaccinated and infected.

The CDC doesn’t track or publicly release nationwide breakthrough case data. For that reason, it’s impossible to know exactly how frequent breakthrough cases are, how many of them are asymptomatic or how many result in just mild symptoms. It’s also less likely that asymptomatic or mildly sick individuals will think to get tested for COVID-19, especially if they are vaccinated.

For More Information: https://dailycaller.com/2021/08/10/delta-variant-how-sick-vaccinated-covid-coronavirus/

Covid-19 Pandemic-Scared-Vaccinated

Authors: Authored by Emily Miller via Emily Posts

The Scared Vaccinated and the Grateful Vaccinated

Fauci, CNN and Aniston are spokesmen for the Scared Vaccinated. Their opposites are the Grateful Vaccinated, who have little to worry about COVID. Nine out of 10 of the vaccinated will not catch the virus. That one “breakthrough” case will be much less severe or no symptoms. None of them will die of COVID.

As it stands now, 71 percent of adults have gotten one shot and 61 percent are fully vaccinated. When you add in the under 18 kids, the average is still 51% of the country is fully vaccinated. Most likely, that number will only increase with children vaccinations because the adults have had time to make a final decision. 

The Grateful Vaccinated have gone back to their normal lives — sightseeing, parties, traveling, unmasking. They wonder why other vaccinated people are so angry as things have improved so much.

What splits the vaccinated is fear. The Scared Vaccinated are scared of what they can’t control, which at this point in the pandemic, is simply other people’s health decisions. They are driven by emotions, not facts.

When we are traumatized — which I believe much of the country is from the March 2020 lockdowns — our frontal lobe turns off and our bodies take over for survival. This is why the Scared Vaccinated are so reactive. They are constantly in a state of fight or flight. They see someone without a mask and feel like they could die. They hear someone say he or she is not vaccinated, and they feel like they are being personally attacked. 

It is impossible to reason with someone whose body is pumping cortisol and adrenaline. This is why the facts of vaccine effectiveness and the pandemic don’t work when trying to debate with the Scared Vaccinated. 

For More Information: https://www.zerohedge.com/covid-19/pandemic-scared-vaccinated

What Does COVID Do to Your Blood?

Authors: Panagis Galiatsatos, M.D., M.H.S., Robert Brodsky, M.D.

COVID-19 is a very complex illness. The coronavirus that causes COVID-19 attacks the body in many different ways, ranging from mild to life threatening. Different organs and tissues of the body can be affected, including the blood.

Robert Brodsky, a blood specialist who directs the Division of Hematology, and Panagis Galiatsatos, a specialist in lung diseases and critical care medicine, talk about blood problems linked to SARS-CoV-2 — the coronavirus that causes COVID-19 — and what you should know.

Coronavirus Blood Clots

Blood clots can cause problems ranging from mild to life threatening. If a clot blocks blood flow in a vein or artery, the tissue normally nourished by that blood vessel can be deprived of oxygen, and cells in that area can die.

Some people infected with SARS-CoV-2 develop abnormal blood clotting. “In some people with COVID-19, we’re seeing a massive inflammatory response, the cytokine storm that raises clotting factors in the blood,” says Galiatsatos, who treats patients with COVID-19.

“We are seeing more blood clots in the lungs (pulmonary embolism), legs (deep vein thrombosis) and elsewhere,” he says.

Brodsky notes that other serious illnesses, especially ones that cause inflammation, are associated with blood clots. Research is still exploring if the blood clots seen in severe cases of COVID-19 are unique in some way. 

The Impact of Coronavirus Blood Clots Throughout the Body

In addition to the lungs, blood clots, including those associated with COVID-19, can also harm:

The nervous system. Blood clots in the arteries leading to the brain can cause a stroke. Some previously young, healthy people who have developed COVID-19 have suffered strokes, possibly due to abnormal blood clotting.

The kidneys. Clogging of blood vessels in the kidney with blood clots can lead to kidney failure. It can also complicate dialysis if the clots clog the filter of the machine designed to remove impurities in the blood.

Peripheral blood vessels and “COVID toe.” Small blood clots can become lodged in tiny blood vessels. When this happens close to the skin, it can result in a rash. Some people who test positive for COVID-19 develop tiny blood clots that cause reddish or purple areas on the toes, which can itch or be painful. Sometimes called COVID toe, the rash resembles frostbite.

For More Information: https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/what-does-covid-do-to-your-blood

How To Increase Platelet Count In COVID Patients? What Is Thrombocytopenia?

Authors: Ananya Varma

Platelets are said to play an important role in inflammatory signalling. Here is why it is important to keep a check of Platelet count in COVID patients. 

Given that COVID-19 is a relatively novel disease, newer research continues to emerge into its characteristics with scientists now linking rapidly decreasing platelets to be a symptom of the infectious virus. Genetically linked to the 2002 SARS-CoV-1 virus, research has now drawn a link between Thrombocytopenia (a condition with low platelets) to the severity of a COVID-19 infection. Here is why it is important to keep a check of Platelet count in COVID patients. 

Platelet Count in COVID patients

As per a recent study, Platelets are said to play an important role in inflammatory signaling as well as in the infectious response of Coronavirus. An analysis of 7,613 COVID-19 patients revealed that patients with severe COVID had a lower platelet count than those with the non-severe disease. Moreover, mild Thrombocytopenia was also detected in those who had severe cases of COVID-19, that is those patients with a lower platelet count. 

Thrombocytopenia & COVID

A normal platelet count in human body ranges from 150,000 to 450,000 platelets per microliter of blood. Having less than 150,000 platelets is known as Thrombocytopenia. Older research has shown that of the patients affected by the 2003 SARS epidemic, 20–55% had Thrombocytopenia and these patients experienced greater morbidity/mortality. In a similar way, Thrombocytopenia has also been detected in 5–41.7% of COVID-19 patients and mild Thrombocytopenia has been detected in 58–95% of severe cases of COVID-19. Notably, severely affected patients had a platelet count only 23 ×109/L to 31 ×109/L lower than those with the non-severe disease.

For More Information: https://www.republicworld.com/india-news/general-news/how-to-increase-platelet-count-in-covid-patients-what-is-thrombocytopenia.html

Thrombocytopenia following Pfizer and Moderna SARS‐CoV‐2 vaccination

Authors: Eun‐Ju Lee, 1 Douglas B. Cines, 2 Terry Gernsheimer, 3 Craig Kessler, 4 Marc Michel, 5 Michael D. Tarantino, 6 John W. Semple, 7 Donald M. Arnold, 8 Bertrand Godeau, 5 Michele P. Lambert, 9 , 10 and James B. Bussel 11

Cases of apparent secondary immune thrombocytopenia (ITP) after SARS‐CoV‐2 vaccination with both the Pfizer and Moderna versions have been reported and reached public attention. Public alarm was heightened following the death of the first identified patient from an intracranial hemorrhage, which was reported on the Internet, then in USA Today 1 and then in The New York Times. 2 Described below, we have collected a series of cases of very low platelet counts occurring within 2 weeks of vaccination in order to enhance our understanding of the possible relationship, if any, between SARS‐CoV‐2 vaccination and development of ITP with implications for surveillance and management.

Twenty case reports of patients with thrombocytopenia following vaccination, 17 without pre‐existing thrombocytopenia and 14 with reported bleeding symptoms prior to hospitalization were identified upon review of data available from the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), agencies of the U.S. Department of Health and Human Services (HHS) Vaccine Adverse Events Reporting System (VAERS), published reports, 3 and via direct communication with patients and treating providers. These cases were investigated as suspicious for new onset, post‐vaccination secondary ITP; we could not exclude exacerbation of clinically undetected ITP. Search terms relating to “decreased platelet count”, “immune thrombocytopenia”, “hemorrhage”, “petechiae”, and “contusion” were utilized to identify cases reported in VAERS.

The reports describing 19 of 20 patients included age (range 22–73 years old; median 41 years) and gender (11 females and 8 males). Nine received the Pfizer vaccine and 11 received the Moderna vaccine. All 20 patients were hospitalized and most patients presented with petechiae, bruising or mucosal bleeding (gingival, vaginal, epistaxis) with onset of symptoms between 1–23 days (median 5 days) post vaccination. Platelet counts at presentation were available for all 20 cases with the majority being at or below 10 × 109/L (range 1–36 × 109/L; median 2 × 109/L).

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8014568/

Platelets Promote Thromboinflammation in SARS-CoV-2 Pneumonia

Authors: Francesco TausGianluca SalvagnoStefania CanèCristiano FavaFulvia MazzaferriElena CarraraVarvara PetrovaRoza Maria BarouniFrancesco DimaAndrea DalbeniSimone Romano,

Abstract

Objective:

Pulmonary thrombosis is observed in severe acute respiratory syndrome coronavirus 2 pneumonia. Aim was to investigate whether subpopulations of platelets were programmed to procoagulant and inflammatory activities in coronavirus disease 2019 (COVID-19) patients with pneumonia, without comorbidities predisposing to thromboembolism.

For More Information: https://www.ahajournals.org/doi/10.1161/ATVBAHA.120.315175

Platelet Gene Expression and Function in COVID-19 Patients

Authors: Bhanu Kanth Manne (University of Utah, United States) Frederik Denorme (Molecular Medicine Program, University of Utah, United States), Elizabeth Middleton (University of Utah, United States), Irina Portier (University of Utah, United States) Jesse Rowley (University of Utah, United, States) Chris Stubben (University of Utah, United States) Aaron Petrey (University of Utah, United States) Neal Tolley (University of Utah, United States) Li Guo (University of Utah, United States) Mark Cody (University of Utah, United States) Andrew Weyrich (University of Utah, United States) Christian Yost (Department of Pediatrics, University of Utah, United States) Matthew Rondina (University of Utah Health Sciences Center, United States) Robert Campbell (University of Utah, United States).

Abstract:

There is an urgent need to understand the pathogenesis of coronavirus disease 2019 (COVID-19). In particular, thrombotic complications in
patients with COVID-19 are common and contribute to organ failure and mortality. Patients with severe COVID-19 present with hemostatic
abnormalities that mimic disseminated intravascular coagulopathy associated with sepsis with the major difference being increased risk of
thrombosis rather than bleeding. However, whether SARS-CoV-2 infection alters platelet function to contribute to the pathophysiology of COVID19 remains unknown. In this study, we report altered platelet gene expression and functional responses in patients infected with SARS-CoV-2.
RNA sequencing demonstrated distinct changes in the gene expression profile of circulating platelets of COVID-19 patients. Pathway analysis
revealed differential gene expression changes in pathways associated with protein ubiquitination, antigen presentation and mitochondrial
dysfunction. The receptor for SARS-CoV-2 binding, ACE2, was not detected by mRNA or protein in platelets. Surprisingly, mRNA from the SARSCoV-2 N1 gene was detected in platelets from 2/25 COVID-19 patients, suggesting platelets may take-up SARS-COV-2 mRNA independent of
ACE2. Resting platelets from COVID-19 patients had increased P-selectin expression basally and upon activation. Circulating platelet-neutrophil, –
monocyte, and -T-cell aggregates were all significantly elevated in COVID-19 patients compared to healthy donors. Furthermore, platelets from
COVID-19 patients aggregated faster and showed increased spreading on both fibrinogen and collagen. The increase in platelet activation and
aggregation could partially be attributed to increased MAPK pathway activation and thromboxane generation. These findings demonstrate that
SARS-CoV-2 infection is associated with platelet hyperreactivity which may contribute to COVID-19 pathophysiology.

For More Information: https://medicine.utah.edu/internalmedicine/generalmedicine/files/campbell-covid-platelet-blood-2020.pdf