Hidroxid of grafen

ȘOC TOTAL – compușii din vaccin se transformă în Lame ce taie țesutul celular ducând la hemoragii insuportabile

Ceea ce credeam că e grav, de fapt e foarte grav! Specialist, un Prof Univ Doctor din Germania – fost responsabil pe Europa pt crearea Cărbunelui Activ afirmă că în vaccinelele anti-Covid se află HIDROXID DE GRAFEN.

Deci nu e doar Oxid, ci e și Hidroxid.

Acesta transformă Grafenul din sânge în niște Lame care taie țesutul epitelial și de aceea mor oamenii – de la hemoragie moleculară, ulterior apărând trombozele!

„Dacă ești chimist de rang înalt și injectezi așa ceva în venele oamenilor, atunci știi că ești un ucigaș!”.

Despre acest cercetător foarte valoros se bănuiește că ar fi fost pierdut voit, la bărcuţa ca urmare a dezvăluirilor sale !

Excess deaths in the UK are being caused by circulatory issues

STEVE KIRSCH
JAN 16, 2024
494
196
Executive summary
UK researchers have discovered that the enormous rise in excess deaths in the UK is being caused by circulatory issues.

We also know from other research that the COVID vaccines greatly increase your risk of dying from circulatory issues.

All you have to do is put 2 and 2 together if you want to know what is causing the vast majority of the excess deaths.

However, the health officials simply do not want to know. As the UK researchers wrote, “In January, Esther McVey asked for an urgent investigation into excess deaths – none has been forthcoming.”

The same is true in the US. They don’t want to investigate. Autopsies done with the proper stains would be dispositive, but the CDC doesn’t want to do this. They are afraid of what they might find.

https://kirschsubstack.com/p/excess-deaths-in-the-uk-are-being

Important Update: Dr Yeadon Writes Supporting Letter for New Criminal Complaint by Former PO Mark Sexton Against MHRA, Pfizer and UK Government.

On March the 14th Former police officer Mark Sexton has recorded an IMPORTANT UPDATE regarding the law and informed consent quoting stated cases and adding his own opinion as to what this means with regards to the Covid injections. (see below)

Former police officer, Mark Sexton has been issued with a new crime number by Acton police station, London on Friday the 8th of March 2024 following his allegations against Sir Graham Brady MP, Dame June Raine, The MHRA, Pfizer and the U.K Government. The allegations include misconduct in public office, misfeasance in public office, gross negligent manslaughter, corporate manslaughter and fraud by false representation. Dr. Michael Yeadon who is the most senior, former “big pharma” and biotech research executive, has written a letter to support Mark Sexton’s complaint which he has asked to be shared widely.

While understandably, many people will feel that this effort is futile as “nothing is ever done”, and those responsible for the crimes against humanity will never be brought to justice, but, what is the alternative? Would we honestly prefer that the few who are continually thrusting evidence of crimes and excess deaths by jab in the faces of the police or Parliament would just not bother? Do we sit back and simply acknowledge that these crimes have been and still are being committed, and wait just for them to cease? Well we can all see that that is not going to happen.

The Excess Deaths Cannot Be Ignored
Mark Sexton writes “Ladies and Gents, please accept this for what it is, be respectful and understand how hard I’ve worked to get this done AGAIN. We all know about the system, but we are 27 months further down the line since the first crime report. They can’t whitewash this one because too many people know what’s going on and the excess deaths cannot be hidden or ignored any longer.“

Mark has continued to work hard throughout those months since September 2021 when he submitted 1100 pages of evidence to Hammersmith Criminal Investigation Department, where two detectives accepted and signed the paperwork. He also invited BBC and Sky to report the ‘biggest story in the last 100 years’.

On December the 21st, Mark Sexton, together with lawyers Philip Hyland, Lois Bayliss and Dr Sam White reported June Raine of the MHRA and GMC chief Charlie Massey to the police for Misconduct in public office and gross negligent manslaughter were they were issued the Crime number 6029679/21.


A significant amount of evidence was submitted. 400 victim, witness, whistleblower statements, Doctor’s, nurses, carers/teachers were given to the Metropolitan police plus names and details of 40 world experts prepared to give evidence of criminality.

Mark said “NOT ONE…that’s right NONE were ever contacted or spoken to by any Met Detectives.” and the criminal complaint was subsequently shut down by the Metropolitan police.Source

However, that did not stop Mark Sexton from continually trying to put a stop to the crimes being committed and bring the perpetrators to justice. See below.

Actions taken and contact with all public bodies from October 2020 up-to February 2024.

They All Knew of the Dangers of the Jab.
Thousands of Letters were sent to PM Rishi Sunak all MP’s and King Charles, the letters clearly state we’ve had enough, the King must honour his Oath and remove the corrupt and criminal government. Both letters can be viewed in this link. They all know. http://donotconsent.co.uk

MHRA, Pfizer and UK officials accused of misconduct, fraud and gross negligent manslaughter in new criminal investigation03/22/2024 // Lance D Johnson //

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MHRA, Pfizer and UK officials accused of misconduct, fraud and gross negligent manslaughter in new criminal investigation
03/22/2024 // Lance D Johnson // 6.4K Views
Tags: badhealth, badmedicine, Big Pharma, biological weapons, Censored Science, coercion, crimes against humanity, criminal investigation, Dame June Munro Raine, Dr. Yeadon, experimentation, health freedom, Mark Sexton, mass harm, medical malfeasance, Medical Tyranny, medical violence, MHRA, negligent homicide, PCR fraud, pharma fraud, science deception, Sir Graham Stuart Brady, unlawful mandates


On March 8, 2024, a new criminal investigation was launched against Pfizer, MHRA and UK officials. The investigating officer, Mark Sexton of the Acton Police Station in London, has charged UK officials with misconduct in public office, misfeasance in public office, fraud by false representation, corporate manslaughter and gross negligent manslaughter. Officer Sexton is backed by a team of lawyers, including Philip Hyland, Lois Bayliss and Dr. Sam White.
UK officials who mandated covid-19 “vaccines” charged for gross negligent manslaughter
Under crime number 6029679/21, the investigation specifically seeks to hold accountable a member of the British Parliament, Sir Graham Stuart Brady, and a British doctor, Dame June Munro Raine, who serves as the Chief Executive Officer of the UK’s Medicine and Healthcare products Regulatory Agency (MHRA). This investigation is part of a much larger investigation that Officer Sexton submitted back in 2021. Three years ago, Officer Sexton submitted 1100 pages of evidence to Hammersmith Criminal Investigation Department, which was signed off by two detectives.

Mark Sexton writes that the investigation is twenty-seven months in progress since the original crime report was released. He says, „They can’t whitewash this one because too many people know what’s going on and the excess deaths cannot be hidden or ignored any longer.”

Excess deaths in the UK are driven by cardiovascular events that are tied to the covid-19 vaccine. The Metropolitan Police of Greater London, which is tasked with protecting members of the royal family, members of the government, and other public health officials, is trying to shut the case down.

Human knowledge is under attack! Governments and powerful corporations are using censorship to wipe out humanity’s knowledge base about nutrition, herbs, self-reliance, natural immunity, food production, preparedness and much more. We are preserving human knowledge using AI technology while building the infrastructure of human freedom. Learn about our free, non-commercial AI / LLM project here. Support our efforts to build the infrastructure of human freedom by shopping at HealthRangerStore.com, featuring lab-tested, certified organic, non-GMO foods and nutritional solutions.

However, over 400 expert witnesses, whistleblowers and victims stand to testify against the criminal actions taken by pharmaceutical companies and government officials over the past four years. At least 40 world experts are prepared to give evidence of criminality. One of the expert witnesses is former biotech research executive, Dr. Michael Yeadon. Yeadon’s letter to Ben Bates of the UK metropolitan police is being shared widely. Yeadon is a former Vice President for Pfizer. For several years, Yeadon led Pfizer’s global research in the field of Allergic & Respiratory Disease Therapeutics, and knows how these interventions are made and what they are for.

Former Pfizer VP lays out the evidence for crimes against humanity
Yeadon lays out verifiable evidence that the covid-19 „vaccines” weren’t vaccines at all, but were intentionally formulated to cause mass harm and then unlawfully mandated on populations. He refutes the existence of an alleged “global pandemic” and documents the harms caused by government lockdowns and other restrictions that coerced populations to take part in a deadly experiment.

The illusion of a pandemic was created by the misuse and abuse of a clinical diagnostic test called PCR. Governments funded PCR fraud and erected a web of deceitful financial incentives, encouraging hospital systems and laboratories to use high cycle thresholds on new PCR tests. This created a wave of artificial positives for an alleged disease that there was no symptom-specific diagnostics for. The illnesses that were presented in 2020 were not treated properly; therefore, the lack of early antiviral treatment, misdiagnoses, prescription error, ventilator-associated pneumonia and various forms of medical malfeasance and malpractice was behind the deaths observed in hospitals in 2020 and beyond.

Yeadon writes, „The heart of this entire deception is the incorrect belief that PCR is nearly flawless and so a positive result means that a person ‘had covid.’ There is no such disease. Not one symptom is unique to the claimed new disease.”

„Anybody dying within a few weeks of a positive test was declared ‘a covid death,'” Yeadon said. Once this medical fraud was established as the basis of a ‘pandemic,’ mass formation psychosis ensued, leading to government officials taking actions that violated the rights and autonomy of the individual. Then, Yeadon said, „Government & media lies were initially all it took to maintain the illusion.”

„Crucially,” he added, „The epidemiological evidence shows that there was no additional illness or deaths compared with the same period in any other year. Numerous scientific papers and authors will present their evidence on this point, including university professors qualified in epidemiology.”

Yeadon’s second charge concerns the mRNA biological weapon experiments that were marketed as „safe and effective vaccines.” The pandemic propaganda was used to coerce people into taking up this biological weapon. Statistics on excess deaths began, not during the alleged pandemic, but only after the rollout of covid-19 „vaccines.”

Yeadon charges that the injections „have been carefully designed to intentionally cause toxicity in those injected with them.” When the mRNA forces the body’s cells to express it, it is immediately attacked by the immune system, leading to potential autoimmune issues. Moreover, the lipid nano particle formulation allows the spike proteins to concentrate in the ovaries, harming fertility. This is just the beginning of intentional mass harms inflicted on the next generations.

The full letter can be accessed here.

Sources include:

Expose-News.com

Kirschsubstack.com

Twitter.com

NaturalNews.com

NaturalNews.com

About spike protein

19 (COVID-19)
is a major threat to worldwide population health and
economies1,2. One week after onset of the COVID-19
infection, the clinical condition of the disease can
become severe, progressing with hypoxemia and
dyspnea, and rapidly develop to acute respiratory
distress syndrome (ARDS) in 17% of patients, and 65%
of these patients worsened and died due to multi-organ
dysfunction3,4,5. Similar clinical characteristics have
also been observed in patients infected with other highly
pathogenic respiratory viruses such as the severe acute
respiratory syndrome (SARS) virus (SARS-CoV)6
, the
middle east respiratory syndrome (MERS) virus
(MERS-CoV)7
, and the avian H1N5 and H7N9
influenza viruses8,9. In some cases the viral load was
low or undetectable at the time of severe illness10
,
suggesting that there were other causes of death than the
virus alone. It has been reported that over-reacting
immune responses as well as the accompanying
cytokine storms played a critical role in the deaths of the
infected11,12,13, yet what initiated the cytokine storms
remains a mystery. We have made the unexpected
discovery in a mouse model that injection of
anti-influenza sera into pregnant mice induced lung
inflammation in mouse pups born to the dames14. Thus,
we suspected that certain antibodies induced by a highly
pathogenic virus may be pathogenic themselves,
through the targeting of host cells or tissues. To prove
this hypothesis, we investigated the pathogenic effects
of anti-coronavirus antibodies, including
anti-COVID-19 viral antibodies, in this study.
Results
Anti-COVID-19 antibodies bound to damaged lung
epithelium cells
Pathogenic antibodies induced by spike proteins of COVID-19 and SARS-CoV
viruses
Huiru Wang1*, Qiuchi Chen2
, Yue Hu3
, Xiancong Wu2
, Lin Dai2
, Yuekai Zhang3
, Fang Li2
, Jinfeng Lu3
, Yuxing
Chen2
, and Xiaoling Liu2*
1. Huirui Biopharma, Co., Ltd. Hangzhou, China
2. HuaAn McAb Biotechnology, Co., Ltd. Hangzhou, China
3. Biolynx Technology (Hangzhou), Co., Ltd. Hangzhou, China
Abstract
This study, using a virus-free mouse model, explores the pathogenic roles of certain antibodies specific to the
spike proteins of highly pathogenic coronaviruses such as the COVID-19 and the SARS-CoV viruses. Our data
showed that these pathogenic antibodies, through a mechanism of Antibody Dependent Auto-Attack (ADAA),
target and bind to host vulnerable cells or tissues such as damaged lung epithelium cells, initiate a self-attack
immune response, and lead to serious conditions including ARDS, cytokine release, and death. Moreover, the
pathogenic antibodies also induced inflammation and hemorrhage of the kidneys, brain, and heart. Furthermore,
the pathogenic antibodies can bind to unmatured fetal tissues and cause abortions, postpartum labors, still
births, and neonatal deaths of pregnant mice. Novel clinical interventions, through disrupting the host-binding
of these pathogenic antibodies, can be developed to fight the COVID-19 pandemic. In addition, the new concept
of ADAA explored by this study may be applicable to other infectious diseases, such as the highly pathogenic
influenza infections. It should be noted that the majority of anti-spike antibodies are non-pathogenic, as only 2
of 7 monoclonal antibodies tested sh

flow cytometry
analysis for determination of
the sialic acid levels on the
surface of human lung
epithelium A549 cells that are
either healthy (untreated) or
damaged (sialidase treated)
with missing sialic acid on the
cell surface (A); and binding
of antibodies specific to the
spike (S) or nucleocapsid (N)
proteins of COVID-19 virus
and SARS virus, to the healthy
(intact) or damaged A549
cells (D-E). B-C: binding of
human monoclonal anti-spike
antibodies B38, REGN10987,
and CR3022-b6 (control
MAb), to healthy (B) or
damaged (C) A549 cells.
B C
MAb-REGN10987 MAb-B38 Control MAb
FL1: WGA-FITC
Blank Untreated
Sialidase
A
A n ti-S A R S S A n ti-S A R S N
0
2 0
4 0
6 0
P o s itiv e c e lls (% )
In ta c t
D a m a g e d
E
4813%
Anti-SARS S Anti-SARS N
Positive cells (%)
A n ti-S A R S -C o v 2 S A n ti-S A R S -C o v 2 N
0
2 0
4 0
6 0
P o s itiv e c e lls (% )
In ta c t
D a m a g e d
D
3497%
Anti-COVID-9 S1 Anti-COVID-9 N
Intact
Damaged
Positive cells (%)
Intact
Damaged
The coronavirus of SARS-CoV-2 is responsible for the
COVID-19 infection. Antibodies specific to the
SARS-CoV-2 (COVID-19) virus and the SARS-CoV
virus were tested for their binding to the human lung
epithelium cell line A549. Seven of the antibodies tested
were monoclonal antibodies specific to the
SARS-CoV-2 spike protein. These antibodies have been
previously reported by others and were isolated from
the B cells of COVID-19-infected patients15,16,17,18,19,20
.
These seven monoclonal antibodies were reproduced
according to the gene sequences encoding the
antibodies, from the NCBI crystal structure site (Table
1). The other anti-coronavirus antibodies tested include
polyclonal rabbit anti-SARS-CoV-2 spike one
(anti-COVID-19 S1), rabbit anti-SARS-CoV spike
glycoprotein (anti-SARS S), and monoclonal mouse
anti-SARS-CoV nucleocapsid (N) proteins (anti-SARS
N). These antibodies were commercially available
(Bioss Antibodies) and were produced by immunization
of animals with related recombinant proteins of the
SARS-CoV-2 and SARS-CoV viruses. The polyclonal
anti-SARS-CoV-2 nucleocapsid (N) protein
(anti-COVID-19 N) antibodies were obtained by
immunization of rabbits with the recombinant
nucleocapsid (N) protein of SARS-CoV-2 virus
(HuaAn McAb Biotechnology).

inding of those antibodies to healthy (intact) or
damaged lung epithelium cells were tested with A549
cells. In order to induce damaged cells, A549 cells were
treated with neuraminidase (sialidase) according to
manufacturer’s instructions (Roche) 21. The fluorescent
labeled wheat germ agglutinin (WGA), which
specifically binds to N-Acetylneuraminic acid (Vector),
and a flow cytometry analysis were used to determine
the levels of sialic acid on the surface of A549 cells. The
damaged cells with missing sialic acid on the cell
surface were used to imitate the in vivo conditions of
infected lung epithelium cells (sick cells). As shown in
Figure 1A, the level of sialic acid on the surface of A549
cells treated with sialidase was lower than those of
untreated cells (Figure 1A).
The seven human monoclonal antibodies specific to the
COVID-19 spike protein (Table 1) were tested for their
binding to A549 cells. As shown in Figure 1C, two out
of seven (28.6%) such antibodies, REGN1098717 and
B3815
, strongly bound to the damaged A549 cells with
missing sialic acid. REGN10987 also weakly bound to
healthy A549 cells while B38 did not bind to the healthy
A549 cells (Figure 1B). The control antibody of
CR3022-b620 did not bind to the healthy A549 cells nor
the damaged cells (Figure 1B and 1C). The other four
human monoclonal antibodies bound neither
significantly to healthy A549 cells nor to damaged cells.
Further, the antibodies specific to the spike glycoprotein
of SARS-CoV virus (anti-SARS S) strongly bound to
the damaged A549 cells missing sialic acid, but not to
the healthy A549 cells with sialic acid (Figure 1E). In
addition, the polyclonal antibody specific to the
nucleocapsid (N) protein of COVID-19 virus
(anti-COVID-19 N) and the antibody specific to the
nucleocapsid protein of SARS-CoV virus (anti-SARS N)
bound neither significantly to the healthy A549 cells nor
to the damaged cells (Figure 1D and 1E). Similar results
were also observed with kidney embryonic cells of
HEK-293 (data not shown).
Taken together, the results of the in vitro assay indicated
that certain antibodies specific to the spike proteins of
the COVID-19 and SARS-CoV viruses have the
potential to mislead the immune system to attack the
host by binding to sick cells such as human lung
epithelium cells in vivo. We termed this mechanism of
action of the antibodies as “Antibody Dependent
Auto-Attack (ADAA)”. The antibody of REGN10987
may have a higher ADAA potential by activating
immune responses in vivo since it binds not only to sick
cells but also to healthy cells, albeit at a lower rate.
Figure 2. A timed-pregnant mouse
model. A: the procedure of injection of
anti-coronavirus antibodies into
pregnant mice. B: representative
images of mouse pups born to the
dames with antibody injection. C: the
rates of sickness and death of newborn
mouse pups caused by
anti-coronavirus antibodies, and the
therapeutic effect of the antibody
mixtures of anti-S1 plus anti-N, or
REGN10987 plus CR3022-b6 and
CC12.3 (2-MAbs).

i-COVID-19 spike antibodies alone induced
systemic inflammation and injury in vivo
For further confirmation, a timed-pregnant mouse
model without viral infection was used since the surface
glycoprotein of fetal organs is not completely developed
or unmatured. The purified and endotoxin-free IgG of
the anti-COVID-19 S1, anti-COVID-19 N, anti-SARS
S, anti-SARS N, human monoclonal antibody of
REGN10987 and B38 (Table 1) were used in the mouse
model. The purified and endotoxin-free IgG of healthy
sera from rabbit, mouse, and human, as well as the
monoclonal antibody of CR3022-b6 were used as
controls. Two dosages of each antibody IgG were
injected intraperitoneally (IP) into timed-pregnant mice
twice every three days at pregnancy (embryonic) days
E15 and E18, respectively, as described in the methods
(Figure 2A).
The frequencies of sickness and death of the fetus and
newborn mouse pups are summarized in Table 2 and
Figure 2C. Injection of REGN10987 into pregnant mice
induced significant fetal death and neonatal death of the
mouse pups delivered to those dames (Table 2). The
fetal death was confirmed by autopsy (Figure 2B). The
results with this animal model indicated that
REGN10987 has the highest potential for inducing
sickness and death (61.9%), followed by B38 (45.8%)
and the polyclonal anti-COVID-19 S1 (45.5%). The
polyclonal anti-SARS S also caused significant sickness
and death in the newborn mouse pups (37.6%). In
addition, hyperemia at the end of left up and down limbs
and a small hemangioma at the side of left eye of one
pup was observed. The pup was born to a dame injected
with the polyclonal anti-COVID-19 S1 antibody.
Neither the healthy control antibodies nor the
anti-COVID-19 N nor the anti-SARS N caused
significant sickness or death of the newborn mouse pups
(Table 2).
It was surprising that when the pathogenic polyclonal
anti-COVID-19 S1 antibody was mixed with an equal
amount of the non-pathogenic anti-COVID-19 N (50 g
+ 50 g), the sickness and death rate induced by the
antibody mixture was significantly lower than that
induced by the anti-COVID-19 S1 alone (Table 2).
Moreover, the sickness and death rate induced by the
highly pathogenic REGN10987 antibody also decreased
significantly when a mixture of the antibody and other
two non-pathogenic antibodies, CR3022-b6 and CC12.3, were injected (Table 2). The mixture consisted
of 40 g of REGN10987, 20 g of CR3022-b6, and 20
g of CC12.3. The data suggested that co-existing of
non-pathogenic antibodies can reduce the pathogenicity
of pathogenic antibodies.
Histology changes. The tissue sections of lungs, brains,
hearts, kidneys, intestines, and livers from the newborn
mouse pups were stained with hematoxylin-eosin (HE)
for histology evaluation. The human IgG or rabbit IgG
bound on the tissues in vivo was detected by an
immunofluorescent staining with fluorescent labeled
anti-human IgG, or anti-rabbit IgG as secondary
antibodies.
Lung inflammation and injury. Acute lung
inflammation was observed with the HE stained tissue
sections from the mouse pups born to the dames injected
with anti-COVID-19 S1, anti-SARS S, REGN10987,
and B38 (Figure 3). The lung lesion included pulmonary
congestion, alveolar epithelial hyperplasia and
thickening, hemorrhage, alveolar atresia, alveolar
dilatation, and alveolar fusion (Figure 3 and Figure S1).
Infiltration of inflammatory cells at the local lesion
areas were also observed. There were insignificant or
minor histological changes with the lungs from the pups
born to the dames injected with the antibodies of
anti-COVID-19 N, anti-SARS N, CR3022-b6, and the
control IgGs of human, rabbit, and mouse (Figure 3).
Other organ inflammation and injury. Inflammatory
reactions and hemorrhage were also observed with the
tissues of kidneys, brains, and hearts from the mouse
pups, as mentioned above. The histology of the kidneys
from the mouse pups delivered to the dames with the
injection of anti-COVID-19 S1, anti-SARS S, B38, and
REGN10987 showed acute tubular injury. Renal tubular
epithelial cells showed granular or vacuolar
degeneration, dilated or obstructed lumen, renal
interstitial edema with a small amount of inflammatory
cells infiltration, and some of the epithelial cells fell off
(Figures 3 and S2). The kidney injury caused by
REGN10987 was the most significant (Figure 3).
Furthermore, small amounts of cerebral hemorrhage or
inflammatory cell infiltration was observed in the brains
of mouse pups delivered to a dame injected with
antibodies of anti-COVID-19 S1, anti-SARS S, B38,
and REGN10987 (Figure 3 and S2). Additionally,
myocardial hemorrhage was observed in the hearts of

he mouse pups delivered to the dames injected with
anti-COVID-19 S1, anti-SARS S, and B38 (Figure 3
and S2). Lastly, myocardial swelling and inflammatory
cell infiltration were observed in a mouse pup delivered
to a dame injected with antibodies of B38 (Figure 3).
There were insignificant or minor histological changes
with the tissues from the pups born to the dames
injected with the antibodies of anti-COVID-19 N,
anti-SARS N, CR3022-b6, and the control IgGs of
human, rabbit, and mouse.
Taken together, the in vivo results of the virus-free
animal model proved that certain antibodies specific to
the spike proteins of the coronaviruses such as
COVID-19 and SARS-CoV viruses can induce, through
the mechanism of Antibody Dependent Auto-Attack
(ADAA), significant fetal and neonatal deaths and the
systemic inflammation or injury of lung and other
organs in vivo. The results are consistent with the
clinical observations of COVID-19 patients with severe
illnesses5
. Therefore, certain antibodies of
anti-COVID-19 S1, anti-SARS-CoV S, B38, and
REGN10987 are pathogenic and induce ADAA. The
pathogenic antibodies and ADAA are probably
responsible for the serious conditions of a severe
COVID-19 infection. On the other hand, the antibodies
of anti-COVID-19 N, anti-SARS-CoV N, and
CR3022-b6 are non-pathogenic since they did not
induce significant adverse reactions in vivo.
Inflammatory cytokines
As further evidence of the pathogenicity of the anti￾spike antibodies, the cytokine levels of monocyte
chemotactic protein 1 (MCP-1), tumor necrosis
factor-  (TNF-), interleukin-4 (IL-4), IL-6, and IL-10
in the sera of mouse pups were tested by a multiplex
Luminex assay kit (Millipore) according to
manufacturer’s instructions. The results of MCP-1 are
summarized in Figure 4.
Both the pathogenic anti-COVID-19 S1 and
REGN10987 induced significantly higher levels of
MCP-1 (Figure 4). Consistent with the surprising results
of the histological changes, the treatment using the
antibody mixture comprised of the pathogenic
anti-COVID-19 S1 and the non-pathogenic
anti-COVID-19 N, significantly reduced the cytokine
levels of MCP-1 (P < 0.001) compared to that induced
by the anti-COVID-19 S1 alone (Figure 4). In addition,
the treatment with the antibody mixture comprised of
the pathogenic REGN10987 and two non-pathogenic
antibodies of CR3022-b6 and CC12.3 also significantly
reduced the level of MCP-1 (P < 0.001) compared to
that induced by REGN10987 alone (Figure 4). The
levels of other cytokines were not significantly
elevated, probably due to the undeveloped immunity of
the newborn mouse pups. The results were consistent
with the results of the sickness and death rates (Table 2)
and the histology changes (Figure 3). The data
demonstrated that 1) pathogenic antibodies alone can
induce high levels of inflammatory cytokines and have
the potential to induce a cytokine storm or cytokine
release syndrome (CRS); and 2) co-existence of
non-pathogenic antibodies can reduce the inflammatory
cytokine release induced by pathogenic antibodies and
prevent the possible cytokine storm or CRS caused by
the pathogenic antibodies.
In vivo antibody binding to multiple organs of mouse
pups
As more evidence of the pathogenic ADAA of the
anti-COVID-19 spike antibodies, in vivo antibody
binding to tissues of mouse pups was detected using an
immunofluorescent staining as described in methods.

The human and rabbit anti-COVID-19 spike antibodies
were significantly detectable at the inflammatory and
lesion areas of the tissues of lungs, kidneys, brains,
hearts, livers, and intestines from the mouse pups with
severe sickness (Figure 5). Those mouse pups were
delivered to the dames injected with the pathogenic
antibodies of anti-COVID-19 S1, anti-SARS-CoV S,
REGN10987, and B38 (Figure 5). Neither human IgG
nor rabbit IgG was significantly detected on the tissues
of the pups treated with the non-pathogenic antibodies
of anti-COVID-19 N, anti-SARS N, and CR3022-b6
(Figure 5). The results indicated that certain
anti-COVID-19 spike antibodies went through the
placenta, bound to the fetal tissues, activated the
self-attack immune responses, and led to the systematic
inflammation and injuries of multiple organs such as the
lungs, kidneys, heart, and brain. The results are
consistent with those of histological changes (Figure3)
and provided the in vivo evidence for the pathogenic
ADAA of some anti-spike antibodies of COVID-19
virus and SARS-CoV virus.
Binding of pathogenic antibodies to fetal and diseased
tissues
In order to further evaluate the pathogenicity of the
pathogenic anti-COVID-19 spike antibodies in humans,
the REGN10987 with the highest pathogenic potential
was tested for antibody binding to various human fetal
tissues, or mutiple human diseased tissues from tissue
array slides (US Biomax). The results are shown in
Figure 6. Antibody REGN10987 bound to mutiple
human fetal tissues of the lungs, heart, kidneys, brain,
pancreas, liver, thymus, and testicles, but not of the
esophagus (Figure 6A). In addition, the REGN10987
also bound to the fetal tissues of retina and coroid,
sclera, and eye ball (data not shown). The data indicate
that the unmatured fetal tissues are vulnerable to a
Kidney
Vehicle
Lung Heart Brain Liver Intestine
Anti-SARS S Anti-Cov19 S1 Rabbit-IgG
A
B38 REGN10987
Lung Kidney Heart Brain Liver Intestine
CR3022-b6

EGN10987.
Binding of pathogenic antibodies to human healthy
tissues
As more evidence of the pathogenicity of the
pathogenic anti-COVID-19 S1 antibodies, REGN10987
and mutiple healthy human tissues from a tissue array
slide (US Biomax, FDA999w) were used to further
evaluate the pathogenicity of REGN10987. The tissue
array slide was comprised of 32 types of normal human
organs encompassing most of human tissues,
representing FDA guidelines for antibody
cross-reactivity testing. The results showed that
REGN10987 bound significantly to human healthy
tissues of lung, kidney, pancreas, stomach, intestine,
adrenal gland, peripheral nerve, thyroid gland, spleen,
adenohypophysis, testicle, prostate, bone marrow,
uterine cervix of cancer adjancent normal tissue (Figure
7). In addition, REGN10987 also bound to the tissues of
parathyroid gland, pericardial mesothelium, and
adjacent normal sclera of eye (data not shown). The data
indicate that certain anti-COVID-19 S1 antibodies, such
as REGN10987, are highly pathogenic because it has
the high potential to bind to healthy human tissues,
activating self-attacking immune responses (ADAA)
and inducing serious adverse reactions in vivo. Based on
the results, clinical detection of pathogenic antibodies
during the COVID-19 infection may be helpful in
predicting the consequences of a patient with a serious
infection.
Taken together, the in vitro and in vivo data of the
current study revealed that certain pathogenic
antibodies specific to the COVID-19 spike protein can
be the cause of a serious COVID-19 infection, and can
cause serious complications during COVID-19
infections through ADAA. Further, the pathogenic
antibodies can bind to unmatured fetal cells or tissues
and cause abortions, postpartum labors, still births, and
neonatal deaths of pregnant females.
It should be noted that the majority (70% or more) of the
anti-COVID-19 spike antibodies inducible by the
COVID-19 virus are non-pathogenic since the
pathogenic antibodies consist of less than 30% of the
total number of antibodies, according to the data of
monoclonal antibodies in this study.
Discussion
The current study revealed the pathogenic roles and the
new mechanism of action (ADAA) of certain antibodies
specific to the spike proteins of coronaviruses such as
the COVID-19 virus and the SARS-CoV virus (Figure
8). We had discovered that in a mouse model,
pre-injection of anti-influenza immune sera induced e severe infections than the mice infected with an
influenza virus alone14
. Wang and co-workers reported
that anti-SARS-CoV spike antisera promoted SARS
infection through antibody-dependent enhancement
(ADE) in vitro22
. Liu and co-workers reported that
anti-SARS-CoV spike immune sera induced by a
SARS-CoV vaccine caused acute lung injury by
promoting MCP1 and IL-8 production and monocyte or
macrophage recruitment and accumulation in
SARS-CoV infected macaque models23
. The previously
reported mechanism of action (MOA) of these
anti-spike antibodies is ADE-based, in that the
antibodies enhance viral infectivity24
. The current study,
revealed for the first time, the self-cell targeting MOA
of pathogenic antibodies, in which the antibodies bind
to host vulnerable cells or tissues and mislead immune
responses to attack host-self (ADAA). Our study also
explored a new mechanism of pathogenisis (MOP) of
highly pathogenic viral infections. The MOP is caused
by the pathogenic antibodies inducible by highly
pathogenic viruses such as the COVID-19 virus and
SARS-CoV virus. Moreover, the pathogenic antibodies
may be related to the cause of infection-related
autoimmune diseases, including those in COVID-19
long haulers, through ADAA.
Dualistic roles of anti-viral antibodies
Based on the traditional concept, the antibodies induced
by an infectious pathogen are protective to a host
because they can neutralize the pathogen and prevent or
treat the infectious disease. Nevertheless, the roles of
such antibodies can be dualistic. Not wishing to be
bound to theory, we noticed that some antibodies can
cross react to host cells or tissues and trigger immune
reactions to attack the self-cells and self-tissues
(ADAA). The data of the current study showed such
pathogenic actions of anti-spike antibodies of the
COVID-19 and SARS viruses.
Sialic acids are predominant components of the mucous
membrane at the outer surface of cell membranes and
mainly act as biological masks or receptors25. Cells or
tissues with sialic acid are recognized as “self”
25. After
the loss of sialic acids the cellular structures become
“non-self”25, which can activate immune responses.
Sialic acids are also an important attachment molecule
of receptors for some viruses, such as coronaviruses and
influenza viruses25,21. During an infection of such
viruses, the sialic acid on the infected cells such as lung
epithelium cells could be removed or destroyed by the
receptor destroying enzyme (RDE) of a coronavirus
such as the COVID-19 virus, or the sialidase of
influenza viruses. The damaged cells with missing sialic
acid on the cell surface become vulnerable to the
pathogenic antibodies induced by the virus (Figure 8).
For example, the current study showed that antibodies
specific to the SARS-CoV-2 spike and the SARS-CoV
spike glycoprotein could significantly bind to the
damaged lung epithelium A549 cells (Figure 1) and
kidney embryonic HEK-293 cells with missing sialic
acid on the cell surface. The antibody binding could
activate and mislead the immune response to attack self
and induce the injury of multiple organs in vivo. For
example, injection of the antibodies specific to the
COVID-19 S1 or the SARS-CoV S proteins to pregnant
mice induced fetal and neonatal deaths and the injury of
multiple organs of mouse pups born to the dames, as
shown in Figures 1-4 and Table 2. In contrast, the
non-pathogenic antibodies of anti-COVID-19 N and
anti-SARS N did not induce significant injury in vivo.
Neither the anti-COVID-19 N nor the anti-SARS N
antibodies significantly bound to the healthy A549 cells
nor to the damaged A549 cells (Figure 1E). The fetal
model was selected because many fetal tissues,
including the surface glycoproteins, are unmatured and
vulnerable to the pathogenic antibodies.
Seven naturally occurring human monoclonal
antibodies specific to the COVID-19 S1 (S-RBD)
protein15,16,17,18,19,20 were analyzed for their pathogenic
potential, with the in vitro assay as described above. The
results showed that all antibodies except one (85.7%)
did not bind to the healthy A549 cells. Neverthless, two
(28.6%) antibodies of B38 and REGN10987
significantly bound to the damaged A549 cells (Figure
1C) and were selected as potential pathogenic
antibodies for further confirmation by the in vivo animal
model. The results of the virus-free animal experiments
showed that the two antibodies alone are highly
pathogenic and induced significant fetal and neonatal
deaths and the injury of multiple organs of mouse pups
born to the dames, as shown in Figures 1-4 and Table 2.
In contrast, another antibody of the seven monoclonal
anti-COVID-19 S1 antibodies, CR3022-b6, served as a
control antibody and did not induce significant injury in

vo (Figures 1-4 and Table 2). The data indicated that
the in vitro assay is useful for rapid screening of
potential pathogenic antibodies, and the virus-free
animal model is helpful for confirmation of the
pathogenicity of these particular antibodies. It should be
noted that the effect of a pathogenic antibody on the
mouse fetus could be reduced if the antibody binds to
the mother’s tissues.
A pathogenic antibody can be induced during a highly
pathogenic infection, such as the COVID-19 infection.
The discovery of pathogenic antibodies and their
ADAA mechanism may solve the mystery of the
possible mechanisms of pathogenesis (MOP) of serious
infectious diseases, serious complications, and sequela
of a viral infection, particularly of a highly pathogenic
viral infection such as the COVID-19 infection. This
may also explain the cause of cytokine storms and
cytokine release syndrome (CRS), and infection-related
autoimmune diseases (including those suffered by
COVID-19 long haulers26), infection- relating cancers,
and other possible disorders inducible by pathogenic
antibodies. The diseases or conditions caused by
pathogenic antibodies further include abortion,
postpartum labor, still birth and neonatal death of
pregnant females related to an infection.
A new pathogenic mechanism of viral infections
The in vitro and in vivo data of the current study support
a new MOP of highly pathogenic viruses such as the
COVID-19 virus. The MOP includes: 1) a highly
pathogenic respiratory virus such as the COVID-19
virus causes the initial, primary injury such as local
inflammation and cellular damage with missing sialic
acids of its target organ, such as lungs, typically within
week one of the infection; 2) anti-viral antibodies,
including pathogenic antibodies, elevate from week
one. The pathogenic antibodies bind to the damaged or
the inflammatory cells of the target organ (e.g., lungs)
(Figure 8) as well as to other organs with similar injuries
(e.g. kidney, brain and heart); 3) the antibody binding
activates and misleads the immune response to attack
the self cells or tissues (ADAA), and induces further
damage (the secondary injury); 4) the secondary injury
persistently adds further damage to the primary injury,
creating a snowball effect, and causes serious
conditions such as ARDS, cytokine storms, and even
death as the antibodies reach peak levels from week one
to weeks 2-3 (Figure 8); and 5) the self-attacking
immune responses (ADAA) misled by the pathogenic
antibodies can be persistent, and can accumulate after
viral clearance and cause autoimmune diseases as long
as the antibodies continue to exist.
The primary injury is limited, short, and decreases as the
virus is cleared, as seen in regular influenza infections.
That means the virus itself is not sufficient to cause
serious conditions such as ARDS, cytokine storms, and
death. On the other hand, the secondary injury caused
by the pathogenic antibodies is longer, broader, and
additive because antibodies persist much longer than
viruses and can bind nonspecifically to other
inflammatory tissues or organs besides lungs. Thus, the
superposition of the ADAA reactions caused by
pathogenic antibodies can lead to serious conditions
such as ARDS, cytokine storm, and death.
The new MOP can explain why the majority of patients
with serious respiratory viral infections such as a
COVID-19 infection or a highly pathogenic influenza
infection died after week one, especially at weeks 2-3 of
the infection course3,27
, as that matches the time period
of antibody peak levels. The new MOP can also explain
why the majority of severe or lethal infections of the
1918 influenza pandemic happened to the young27
,
because younger people could induce higher levels of
anti-viral antibodies, including pathogenic antibodies.
Similarly, certain pathogenic antibodies inducible by
other infectious pathogens, such as influenza viruses
may also cause serious adverse reactions or
autoimmune diseases through this MOP (study
ongoing).
Cells or tissues vulnerable to pathogenic antibodies
As shown in Figure 6, the highly pathogenic
REGN10987 antibody bound to the majority of human
fetal tissues and inflamatory tissues, as well as certain
cancer tissues. A common feature of those tissues,
including the cancer tissues, is that they consist of
actively proliferating cells. Therefore, those cells and
inflamatory tissues are vulnerable to pathogenic
antibodies, and their interaction with the pathogenic
antibodies (ADAA) can be the cause of 1) serious
infections, particularly highly pathogenic viral
infections such as the COVID-19 infection; 2) serious
complications of infections such as ARDS, cytokine
storm, or cytokine release syndrome (CRS); and 3)

infection-relating inflammation such as pneumonia and
kidney failure (Figures 1-4). Further, unmatured fetal
cells or tissues are vulnerable to pathogenic antibodies
(Figure 6A). Thus, pathogenic antibodies, through
ADAA, may be the cause of abortions, postpartum
labors, still births and neonatal deaths of pregnant
females (Figure 1B and 1C).
Pathogenic antibodies and autoimmune diseases
Many autoimmune diseases are related to viral
infections28, yet the pathogenic mechanisms have
remained unclear so far. The current study discloses, for
the first time, that most inflammatory tissues are
vulnerable to pathogenic antibodies and ADAA (Figure
6B). Chronic inflammation is a feature of most
autoimmune diseases. When an infection occurrs,
antibodies including pathogenic antibodies are induced
and last from months to half a year. The pathogenic
antibodies can readily bind to the pre-existing
vulnerable inflammatory tissues of an autoimmune
disease, and mislead immune responses to attack the
body’s own tissues. This ADAA process can be
repetitive and additive as antibodies elevate and induces
significant reactions. The occurrence time and
pathogenic course of an autoimmune disease caused by
pathogenic antibodies and ADAA can be short or long,
depending on the amount of vulnerable cells or tissues
and the amount of pathogenic antibodies. The
pathogenic antibodies generally persist for months to
half a year, and thus the autoimmune disease can occur
during that period, especially during the period of
antibody peak levels.
COVID-19 long haulers have been reported and the
causes remain a mystery26. The current study provides a
possible pathogenic mechanism of COVID-19 long
haulers. Despite the virus being cleared in the recovered
COVID-19 patients, the anti-viral antibodies remained
and could exist for months to half a year or longer.
Certain pathogenic antibodies could bind to vulnerable
cells or tissues, such as inflammatory cells induced
during the COVID-19 infection, and cause persistent
adverse reactions such as chronic inflammation of
multiple organs. Thus, with the mechanism of ADAA,
pathogenic antibodies can also be responsible for the
longer term effects of the COVID-19 infection. For
example, a highly pathogenic anti-spike antibody such
as REGN10987 can bind to peripheral nerves and may
cause abnormalities of muscles, vision and taste.
Similarly, the pathogenic antibodies inducible by other
infectious pathogens such as an avian influenza virus
can be responsible for the adverse reactions or
autoimmune diseases caused by the infections such as
Guillain-Barré syndrome (GBS). Additionally, in a
chronic viral infection (e.g., an HIV infection),
pathogenic antibodies can repeatedly stimulate cellular
proliferation for a long time and an infection-related
cancer can occur if the cellular proliferation loses
control.
Better vaccines
It was surprising that when the pathogenic
anti-COVID-19 S1 antibodies was mixed with an equal
amount of the non-pathogenic anti-COVID-19 N
antibodies, the sickness and death rates caused by the
antibody mixture was significantly decreased compared
to the results of the injected anti-COVID-19 S1
antibody alone (Table 2 and Figure 1C). A similar result
was observed with the highly pathogenic REGN10987
as well with an antibody mixture of the REGN10987
and the two non-pathogenic monoclonal antibodies of
CR3022-b6 and CC12.3 (Table 2 and Figure 1C). The
data suggested that co-existence of non-pathogenic
antibodies can reduce the ADAA of pathogenic
antibodies. Thus, a vaccine capable of inducing
multivalent antibodies may be safer, in which at least
one kind of antibody is of the non-pathogenic kind that
induces fewer adverse reactions. One example of such a
vaccine is the traditional inactivated viral vaccine (e.g.
inactivated COVID-19 vaccine) which induces
multivalent antibodies specific for multiple antigens of
a virus. As another example, a recombinant or mRNA
COVID-19 vaccine capable of inducing the antibodies
specific to not only the spike protein but also to the
nucleocapsid proteins, or a non-spike protein of the
SARS-CoV-2 virus may be safer (patent pending).
Despite the mechanism of action being unclear, it is not
likely that the non-pathogenic antibodies affected the
ADA actions of the pathogenic antibodies through
competitive binding since neither the anti-COVID-19
S1 nor the anti-COVID-19 N bind to the same antigens.
Neither the REGN10987 nor the other two
non-pathogenic antibodies bind to the same epitope of
the S1 protein of the COVID-19 virus. We hypothesize
that non-pathogenic antibodies affect the ADAA of

hogenic antibodies through diluting and space
obstructing or interrupting the attachment of pathogenic
antibodies to vulnerable cells or tissues.
Novel clinic interventions based on the new
mechanism of pathogenesis
Based on the new MOP of the highly pathogenic viral
infection inducible by pathogenic antibodies, novel
clinic interventions for treating and preventing a serious
condition of the COVID-19 infection may be developed
through interrupting the binding of the pathogenic
antibodies to host vulnerable cells, tissues, and organs.
For example, the following products and approaches
may be effective for the treatment of a serious
COVID-19 infection: 1) for patients with serious
conditions, therapies capable of removing the
pathogenic antibodies, such as replacing the patient’s
plasma with uninfected healthy human plasma, may be
effective and should be performed as soon as possible; 2)
immunoglobulin products, serum or plasma from not
only recovered patients but also from healthy
individuals may be helpful for symptom relief through
diluting and interrupting the binding of pathogenic
antibodies; and 3) pathogen-derived products such as
viral antigens or antigen fragments, and synthetic
peptides may be effective (neutralizing pathogenic
antibodies) (patent pending).
For the diagnosis of a severe COVID-19 infection,
determination of the levels of anti-COVID-19 spike
antibodies may be important and helpful to predict the
condition of a patient with a serious infection. This is
because the virus can become undetectable after one
week, but the antibodies induced by the virus can
elevate from week one and reach peak levels at weeks
2-3, accompanied by the development of serious
conditions such as ARDS, cytokine storms, and death.
Higher levels of the anti-COVID-19 spike antibodies
may indicate a worsening of the infection.
In summary, our study revealed the roles of
“pathogenic antibodies” in viral infections. These
pathogenic antibodies act through a novel mechanism of
action that we have term “Antibody Dependent
Auto-Attack” (ADAA). In particularly, we explored the
ADAA of highly pathogenic respiratory viral infections,
such as COVID-19. The pathogenic antibodies can be
induced during an infection, bind to vulnerable cells or
tissues such as actively growing cells, and initiate a
persistent self-attack immune response, leading to
serious conditions including ARDS, cytokine storms,
and death. Further, the pathogenic antibodies, through
ADAA, may also be responsible for infection-related
autoimmune diseases, including those experienced by
COVID-19 long haulers. Novel clinical interventions
for diagnosis and treatment, including improved
vaccines based on the ADAA of pathogenic antibodies,
can be developed. In addition, the new concept and the
mechanism of ADAA explored by this study may also
be applicable to other infectious diseases, such as highly
pathogenic influenza infections (study ongoing).
Methods
Production of human anti-SARC-CoV-2 spike
monoclonal antibodies
Seven naturally occurring human monoclonal
antibodies specific to the receptor binding domain
(RBD) of the spike protein one (S1) of the
SARS-CoV-2 virus have been reported by
others15,16,17,18,19,20
. The seven monoclonal antibodies
were reproduced for research use only (HuaAn McAb
Biotechnology) according to the gene sequences from
the NCBI crystal structure site (Table 1). The features
and information of the antibodies are listed in Table 1.
Paired heavy chain and light chain plasmids of
anti-Spike human antibody were transiently transfected
into HEK-293FE cells at a mass ratio of 1:2 with
polyetherimide (Polysciences). Transfected cells were
suspension-cultured in a 5% CO2 containing
atmosphere at 37°C and the condition medium (Gibco)
was refreshed 8 hours after transfection. After 7 days,
the supernatants were centrifuged at 10000r per min
(rpm) and purified with Protein A prepacked column
(Senhui Microsphere Technology). Purified antibodies
were quantified by Nanodrop or BCA Quantification
Kit (Beyotime).
Antibody quality control was performed using an
antigen down ELISA. 1 g/ml antigens of COVID-19
Spike-RBD-mFc (HuaAn McAb Biotechnology) were
coated on ELISA plate at 4℃ for overnight. The plate
was blocked with 1% BSA and coated with anti-spike
human antibody as first antibody for 1 hour at 37℃
successively. Uncombined free antibodies were washed
with TBST, the secondary anti-human IgG-HRP

bcam) were added onto the plate, and the plate was
incubated at 37℃ for 30 minutes. Binding affinity of the
anti-spike human antibodies were analyzed with the
signature of OD450 nm absorption.
Anti-COVID19 N protein antibody production
Two months old New Zealand white rabbits were
subcutaneously immunized with 250 μg of purified
COVID19-N protein ((HuaAn McAb Biotechnology).
The rabbits received 3 booster injections at 2-week
intervals with 500 g purified COVID19-N protein.
Serum titer of anti-COVID19-N antibodies were
validated by an antigen down ELISA after each
immunization. Rabbit serum were then harvested,
centrifuged at 10,000 rpm for 10 minutes and purified
with Protein A prepacked column (Senhui Microsphere
Technology). Purified antibodies were quantified by
Nanodrop or BCA Quantification Kit (Beyotime).
Removal of endotoxin from antibody solutions
Antibody solutions were treated with 1% v/v Triton
X-114 in ice for 10 minutes. The solutions were then
incubated at 37°C for 5 minutes, whereupon two phases
formed. The antibody solutions were centrifuged at
12,000 rpm for 5 minutes at room temperature, and
carefully aspirate the upper aqueous phase.
Endotoxin-free antibodies were quantified by BCA
Quantification Kit (Beyotime).
Other antibodies
The rabbit polyclonal antibodies specific for the
recombinant spike one (S1) proteins of the
SARS-CoV-2 virus, the recombinant spike proteins of
SARS-CoV virus, and the mouse monoclonal antibody
specific for the recombinant nucleocapsid (N) proteins
of the SARS-CoV virus were purchased from Bioss
Antibodies (Beijing).
Digestion of A549 cells with neuraminidase
The cells of human lung epithelium cell line A549 were
washed once with the digestion buffer for
neuraminidase (Roche), the cells were centrifuged at
2000 rpm for 5 minutes, and the supernatant was
discarded. The digestion buffer was consisted of 50 mM
of sodium acetate, 3% BSA, and 2 mM of CaCl2 in PBS
(pH5.5-6.0). The cells were resuspended with the
digestion buffer and divided to multiple tubes, each tube
contained about 106
of cells in 200 l of the digestion
buffer containing 50 U of neuraminidase (Roche). The
tubes were incubated at 37°C for one hour. Then the
cells were washed with PBS once and proceeded for
flow cytometry assay. A549 cells without the treatment
of neuraminidase were used as controls.
Flow cytometry
A549 cell with or without the treatment of
neuraminidase were tested for the binding of
anti-coronavirus antibodies as mentioned above. Each
2×105
of cells in 200 l of 1%BSA-PBS were incubated
in ice with each antibody at a concentration of 0.5
mg/ml for one hour, washed once with PBS. The cells
were resuspended with 200 l of 1%BSA-PBS and 0.25
mg/ml of either PE-labeled goat anti-human IgG
(Abcam) or FITC-labeled goat anti-rabbit IgG
(SouthernBiotech), incubated in ice for 30 minutes, and
washed once with PBS. The cells were resuspended
with 200 l of PBS and detected with a flow cytometer
of Accuri 6 (BD Biosciences). The fluorescent labeled
wheat germ agglutinin (WGA), which specifically binds
to sialic acid (Vector), was used as a control (Figure
1A).
A timed-pregnant mouse model
A timed-pregnant mouse model without viral infection
was developed using the anti-coronavirus antibodies as
mentioned above, to evaluate the pathogenic action of
anti-coronavirus antibodies. The animal experiments
were performed at the Center of Laboratory Animals of
Hangzhou Normal University. The protocol for the
animal experiment was approved by the Laboratory
Animal Welfare and Ethics Committee of Hangzhou
Normal University. The CALAS No. is 2020244. The
animal experiments were performed three times.
Animal SPF-grade C57BL/6J pregnant mice at
pregnancy (embryonic) day E13-E14 were purchased
from Shanghai SLAC Laboratory Animal Co., Ltd. The
animals were randomly divided into groups as needed,
two pregnant mice for each group at every experiment.
Antibody injection The purified and endotoxin-free
IgG of the anti-coronavirus antibodies used for the
animal model include rabbit polyclonal anti-COVID-19
S1, anti-COVID-19 N, anti-SARS-CoV S, mouse
monoclonal anti- SARS-CoV N, and the human
monoclonal anti-COVID-19 S1 or S-RBD antibodies of
B3815, REGN1098717, CC12.318, and CR3022-B620
.
Two dosages of each antibody IgG were injected

intraperitoneally (IP) into timed-pregnant mice twice
every three days at pregnancy (embryonic) day of E15
(about 26-28 g) and E18 (about 30-32 g) respectively
(Figure 2A). For each polyclonal antibody, 50 μg
(microgram) for the first dose (about 2.0 mg/kg) and 60
μg for the second dose (about 2.0 mg/kg) were
administrated. For each monoclonal antibody, 40 μg for
the first dose (about 1.5 mg/kg) and 50 μg for the second
dose (about 1.5 mg/kg) were administrated. In addition,
the rabbit polyclonal antibody mixture consisted of 50
μg of the anti-COVID-19 S1 and 50 μg of the
anti-COVID-19 N, and the human monoclonal antibody
mixture consisted of 40 μg of the REGN10987, 20 μg of
the CC12.3, and 20 μg of the CR3022-B6 were
administered, respectively. The body weight of the
pregnant mice was measured every day before and after
the antibody injection. The mouse pups were born at
about E20-E21 and the healthy status including clinical
signs of the newborn mouse pups were observed and
recorded (Figure 2B). The experiment was ended at day
1-2 post birth.
Sample collection At the end of the day, the blood
samples were collected from newborn mouse pups,
incubated at 4℃ for overnight, centrifuged at 3000 rpm
for 5 minutes, and the supernatant was transferred to a
new tube. The isolated sera were stored at -80℃ for
cytokine detection. Lungs, hearts, brains, kidneys,
livers, and intestines were collected from at least 3
mouse pups, fixed in formalin for 48-72 hours, went
through gradient alcohol dehydration and embedded in
paraffin, and tissue sections were processed.
HE and immunofluorescent staining The mouse tissue
sections of lungs, hearts, brains, kidneys, livers, and
intestines were dewaxed and stained with
hematoxylin-eosin (HE) for histology evaluation. For
an immunofluorescent staining, the dewaxed sections
were incubated at room temperature with the secondary
antibodies of PE-labeled goat anti-human IgG (Abcam)
or FITC-labeled goat anti-rabbit IgG (SouthernBiotech)
for one hour, washed three times with PBS, and
examined under an immunofluorescent microscope
(Leica).
Tissue array Human tissue array slides consisted of
various human fetal tissues (BE01015), or mutiple
human diseased tissues of respiratory (LUD151),
cardiovesvular (HE1001), urinary (BC07014) and
digestive (BCC000128) system were purchased from
US Biomax (Rockville, MD). 4-8 g of biotin-labeled
REGN10987 antibody was incubated with each of the
tissues array slide at room temperature for one hour,
washed off the free antibody, stained with FITC-labeled
strepavidin for 30 minutes at room temperature, washed
three times and examined under an immunofluorescent
microscope (Leica).
Acknowledgement
We thank Dr. Haifeng Bao for his valuable advice on
the development of the in vitro cellular assay, Dr.
Xiaohui Zhou from Fudan University for reviewing the
manuscript. The study was supported by funding from
Hangzhou HuaAn PuChu Investment Limited
Partnership.
Competing Interests
H.W. is the shareholder of Huirui Biopharma, X.L. and
Y.C. are shareholders of HuaAn McAb Biotechnology,
J.L. is a shareholder of Biolynx Technology. There are
patent applications pending related to this work.
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Despre vaccinarea bebelușilor

Dacă se merge pe vaccinare cu arn messenger , atunci nu știu dacă efectele vaccinurilor vor fi benefice copiilor, deci pentru familiile abia închegate decizia de a face această terapie , este o loterie, in care practic cei ce o acceptă își aleg viitorul, constrânși de un sistem birocratic în care statul de drept este anulat de decizia guvernanților, vorba lui Radu Banciu „niște papă lapte”. Adică practic este ca și cum ne-am arunca cu o parașută care nu știm dacă se va deschide în timp util. Dumnezeu să ne ocrotească și să insufle Duhul Sfânt cadrelor medicale care să sfătuiască românii să ia decizia cea mai bună când se vor confrunta cu vaccinarea obligatorie a copiilor. 🙏👼

Vax covid și sindromul Guillain Barr

https://m.activenews.ro/covid-dezvaluiri-covid/Studii-Dovezi-tot-mai-multe-ca-vaccinurile-anti-COVID-19-sunt-legate-de-un-risc-crescut-de-dezvoltare-a-sindromului-Guillain-Barr%C3%A9-185657

Starea postvaccinare

Ce a pățit un preot-călugăr din Grecia după ce s-a injectat cu o doză de vaccin!

#VaxxedOrthodoxPriestDescribingItsDemonicStatesOfMind
Gânduri puternice de desnădejde și părere de rău, stări demoniace, atacuri de panică, vedea negru, nu avea deloc liniște, nu putea dormi, nu mai simțea Harul din Altar, se simțea complet dezumanizat!
După cum am spus – e foarte posibil ca Semnul Fiarei să fie compus din 7 doze – exact ca o carte ce e compusă din 7 capitole. O persoană vaccinată are Semnul Fiarei în ea, însă nu în totalitate, astfel că îndemnul pt oricine e de a nu mai primi și alte doze.
Însă acum diavolul s-a șmecherit! Să presupunem că întreaga cantitate de ser aferentă pt 7 doze e de 300 de mililitri. Dacă omul a primit doar – să zicem, o parte din cantitatea totală, restul îl va putea primi din mâncare, băutură, sau chiar de la alte persoane înțepate.
Ce vreau să zic e că nu doar de ac tre’ să vă feriți, ci și de orice altă formă de infectare!_RealEducation

– Air Vax – ARNm livrat direct în plămâni – nu este nevoie de un jab –

https://wp.me/pazewS-1sP

Measles, Mumps, Rubella And Varicella Vaccine For Children Shows Nanobot Swarms, Quantum Dots And Self Assembly Hydrogel

https://anamihalceamdphd.substack.com/p/measles-mumps-rubella-and-varicella?utm_source=substack&utm_medium=email

The childhood MMR vaccine is loaded with nanobots. They are so small that on my highest magnification you can barely see them, but they are clearly there. I tried to go up to 4000x with my Oil objective but could not visualize them. I took many videos and if you look at the entirety of the documentation it is clearly stunning. The MMRV vax is supposed to be stored at -56F. Thawed it looks exactly like the C19 bioweapon. Filaments do assemble and large areas of hydrogel clots. Without a cover slip the self assembly is much more visible. This is given to 9 month old babies, then again at 15months, and then at 6 years of age. This is the 5th childhood vaccine I looked at. It all looks the same to me, it is loaded with self assembly nanotechnology. Almost makes me wonder if they just use the same ingredients just put a different label on it. Any doctor or individual who has ever been called an antivaxxer needs to get these articles ( which I will put all of them together on one post, I have a couple more “ vaccines” to go) and sue anyone who have accused them. The Big Pharma Criminals, the medical societies, medical boards, physicians and healthcare providers who get kickbacks called “Pay for Performance” – the more they shoot children up with this. The schools and other agencies that are mandating this are all complicit in poisoning our future generation. This is literally a criminal enterprise. Undisclosed clot forming chemicals and nanotechnology are in these shots. Any doctor with a conscience needs to get a darkfield microscope and replicate this work. If you have a soul left, you cannot poison one more child with this. Ever again. Parents who love their children, you cannot buy into this vaccine propaganda again. NOBODY can justify injecting this material into babies

You can see that the liquid is dense and many layers of activity are seen including larger hydrogel pieces. I wanted to show the miniscule swarming in the background that is clearly involved in self assembly. A human red blood cells has about a diameter of 6.8 micrometers. I would say these small nanobots are at least 1000 times smaller than that.

Larger pieces of hydrogel can be seen moving in the extremely busy background

The entire drop was moving towards the center, clearly coordinated intelligently to build a large hydrogel like clot. In this video you can see 100x magnification with clear movement. It looks just like Insulin that I filmed.

Here you can see after about 45 minutes how much of this has already assembled and how much coordinated movement there is

Here is what this looks like after about 70 minutes