UPDATE 02. May 2020: COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level

PROLOGUE: As assumed earlier, the contagion dubbed SARS-CoV-2 is rather a self-replicating neurotoxic bio-chemical agent than just a 'virus' and can be used as weapon. Any government, which does not immediately engage in tracing the origin of this lab-fabricated pathogen and enables a still not yet founded but urgently required Independent International Tribunal to find the real truth of the pandemic and those responsible, must be seen as what it then is: An accomplice and partner in crimes against humanity.

Severe brain damage possible even with mild coronavirus symptoms

MRI scan of brainAccording to British neurologists, COVID-19 can cause serious damage to the brain and central nervous system. Such damage can lead to psychosis, paralysis and strokes, which are often detected in their late stages.

By DW - 09. July 2020

There are numerous signs that the novel coronavirus SARS-CoV-2 not only attacks the lungs and respiratory tract, but also other organs on a massive scale.It can severely affect the heart, vessels, nerves, kidneys, and skin. 

British neurologists have now published shocking details in the journal "Brain," which suggests SARS-CoV-2 can cause severe brain damage — even in patients with mild symptoms or those in recovery. Often this damage is detected very late or not at all.

Neurologists at the University College London (UCL) diagnosed acute demyelinating encephalomyelitis (ADEM) in nine British COVID-19 patients. This inflammatory disease causes a degenerative destruction of the central nervous system, affecting the myelin sheaths of the nerves in the brain and spinal cord.

Different degrees of damage

Of the 43 patients examined, 12 suffered from inflammation of the central nervous system, 10 from a transient encephalopathy (brain disease) with delirium or psychosis, eight from strokes, and a further eight from problems of the peripheral nerves, mostly with the diagnosis of Guillain-Barré syndrome. This is an immune reaction that attacks the nerves and causes paralysis and is fatal in 5% of cases. A 59-year-old woman died of the complication.

Infografik Erkrankungen der Myelinscheide ENG

Scientists have never before seen another virus attack the brain in the same way COVID-19 does, points out Dr. Michael Zandi. He is a lead author of the study, as well as a consultant at UCL Hospitals. What is unusual is the severe brain damage even in patients with mild symptoms.

Damage often goes unrecognized

The cases now published confirm fears that COVID-19 is causing long-term health problems in some patients. Many patients remain breathless and tired long after their recovery. Other recovering patients suffer from numbness, weakness, and memory problems.

Biologically, ADEM has some similarities to multiple sclerosis, but it is more severe and usually occurs only once. Some patients will be left with a long-term disability, while others will recover well, explains Michael Zandi.

The entire spectrum of brain diseases and long lasting side effects caused by SARS-CoV-2 may not yet have been recorded, said Zandi, because many patients in hospitals are too sick to be examined with brain scanners or other methods.

COVID-19 patients in hospital in Brazil

Neurological damage or late effects are partly not detected or are detected too late due to overload

Neurological damage or late effects are partly not detected or are detected too late due to overload

"We would like to draw the attention of physicians around the world to these complications of the coronavirus," said Zandi. Physicians and medical staff should always consult a neurologist for patients with cognitive symptoms, memory problems, fatigue, numbness, or weakness.

Shocking case studies

Also published were touching individual stories, for example of a 47-year-old woman who suddenly felt headaches and numbness in her right hand after a week of coughing and fever. In the hospital she became fatigued and unresponsive. During an emergency operation, part of her skull had to be removed to relieve the pressure on her swollen brain.

Another 55-year-old patient without any previous mental illness began to behave strangely the day after being discharged from the hospital. For example, she put on and took off her coat several times in a row. She also began to hallucinate — seeing monkeys and lions in her house. Back at the hospital she was given antipsychotic medication.

People in American hospital during the Spanish Flu outbreak of 1918

The Spanish flu was an influenza pandemic that killed between 20 and 50 million people, according to the WHO

The Spanish flu was an influenza pandemic that killed between 20 and 50 million people, according to the WHO

Thousands of cases of brain damage, even with Spanish flu

British neurologists fear that COVID-19 could leave subtle brain damage in some patients, which will only become apparent in the coming years. According to the study, there were similar long lasting side effects discovered in those who recovered from the devastating Spanish flu in 1918, in which up to one million people probably suffered brain damage.

"Of course, we hope that this won't happen, but when you have such a large pandemic affecting such a large part of the population, we have to be vigilant," said Dr. Michael Zandi of the UCL Queen Square Institute of Neurology.

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Delirium, rare brain inflammation and stroke linked to Covid-19

8 July 2020

Neurological complications of Covid-19 can include delirium, brain inflammation, stroke and nerve damage, finds a new UCL and UCLH-led study.

Brain scans

Published in the journal Brain, the research team identified one rare and sometimes fatal inflammatory condition, known as ADEM, which appears to be increasing in prevalence due to the pandemic.

Some patients in the study did not experience severe respiratory symptoms, and the neurological disorder was the first and main presentation of Covid-19.

Joint senior author Dr Michael Zandi (UCL Queen Square Institute of Neurology and University College London Hospitals NHS Foundation Trust) said: “We identified a higher than expected number of people with neurological conditions such as brain inflammation, which did not always correlate with the severity of respiratory symptoms.

“We should be vigilant and look out for these complications in people who have had Covid-19. Whether we will see an epidemic on a large scale of brain damage linked to the pandemic – perhaps similar to the encephalitis lethargica outbreak in the 1920s and 1930s after the 1918 influenza pandemic – remains to be seen.”

The study provides a detailed account of neurological symptoms of 43 people (aged 16-85) treated at the National Hospital for Neurology and Neurosurgery, UCLH, who had either confirmed or suspected Covid-19.

The researchers identified 10 cases of transient encephalopathies (temporary brain dysfunction) with delirium, which corresponds with other studies finding evidence of delirium with agitation. There were also 12 cases of brain inflammation, eight cases of strokes, and eight others with nerve damage, mainly Guillain-Barré syndrome (which usually occurs after a respiratory or gastrointestinal infection).

Most (nine out of 12 cases) of those with brain inflammation conditions were diagnosed with acute disseminated encephalomyelitis (ADEM). ADEM is rare and typically seen in children and can be triggered by viral infections: the team in London normally sees about one adult patient with ADEM per month, but that increased to at least one per week during the study period, which the researchers say is a concerning increase.

The virus causing Covid-19, SARS-CoV-2, was not detected in the cerebrospinal brain fluid of any of the patients tested, suggesting the virus did not directly attack the brain to cause the neurological illness. Further research is needed to identify why patients were developing these complications.

In some patients, the researchers found evidence that the brain inflammation was likely caused by an immune response to the disease, suggesting that some neurological complications of Covid-19 might come from the immune response rather than the virus itself.

The findings add clinical descriptions and detail to another recent study, which also involved Dr Zandi and co-author Dr Hadi Manji (UCL Queen Square Institute of Neurology and UCLH) identifying 153 people with neurological complications from Covid-19.* This paper also confirms the previously reported findings of a higher than expected number of patients with stroke which results from the excessive stickiness of the blood in COVID-19 patients.**

Joint first author Dr Ross Paterson (UCL Queen Square Institute of Neurology) said: “Given that the disease has only been around for a matter of months, we might not yet know what long-term damage Covid-19 can cause.

“Doctors needs to be aware of possible neurological effects, as early diagnosis can improve patient outcomes. People recovering from the virus should seek professional health advice if they experience neurological symptoms,” he added.

Joint first author Dr Rachel Brown (UCL Queen Square Institute of Neurology and UCL Infection & Immunity) said: "Our study advances understanding of the different ways in which Covid-19 can affect the brain, which will be paramount in the collective effort to support and manage patients in their treatment and recovery.”

Joint senior author Dr Hadi Manji said: “Our study amalgamates, for the first time, the clinical presentations of patients with Covid-19 neurological disease with MRI and laboratory features including, in one case, a brain biopsy.

“This now sets up a template for other researchers around the world, facilitating coordinated research to optimise the diagnosis and treatments of these complications, which to date, has proved difficult. In addition, patients are going to require long term follow up.”

The researchers were supported by the National Institute for Health Research UCLH Biomedical Research Centre, Medical Research Council, Alzheimer's Association, and the UK Dementia Research Institute.

Links

Image

  • Brain scan images from the study.

Media contact

Chris Lane

Tel: +44 (0)20 7679 9222

Email: chris.lane [at] ucl.ac.uk

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COVID-19 Is a Vascular Disease: Coronavirus’ Spike Protein Attacks Vascular System on a Cellular Level

By Salk Institute May 2, 2021

SARS-CoV-2 Spike Protein Vascular Endothelial Cells

Representative images of vascular endothelial control cells (left) and cells treated with the SARS-CoV-2 Spike protein (right) show that the spike protein causes increased mitochondrial fragmentation in vascular cells. Credit: Salk Institute

Salk researchers and collaborators show how the protein damages cells, confirming COVID-19 as a primarily vascular disease.

Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that they also play a key role in the disease itself.

The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”

Salk researchers collaborated with scientists at the University of California San Diego on the paper, including co-first author Jiao Zhang and co-senior author John Shyy, among others.

While the findings themselves aren’t entirely a surprise, the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time. There’s been a growing consensus that SARS-CoV-2 affects the vascular system, but exactly how it did so was not understood. Similarly, scientists studying other coronaviruses have long suspected that the spike protein contributed to damaging vascular endothelial cells, but this is the first time the process has been documented.

In the new study, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain any actual virus. Exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model—proving that the spike protein alone was enough to cause disease. Tissue samples showed inflammation in endothelial cells lining the pulmonary artery walls.

The team then replicated this process in the lab, exposing healthy endothelial cells (which line arteries) to the spike protein. They showed that the spike protein damaged the cells by binding ACE2. This binding disrupted ACE2’s molecular signaling to mitochondria (organelles that generate energy for cells), causing the mitochondria to become damaged and fragmented.

Previous studies have shown a similar effect when cells were exposed to the SARS-CoV-2 virus, but this is the first study to show that the damage occurs when cells are exposed to the spike protein on its own.

“If you remove the replicating capabilities of the virus, it still has a major damaging effect on the vascular cells, simply by virtue of its ability to bind to this ACE2 receptor, the S protein receptor, now famous thanks to COVID,” Manor explains. “Further studies with mutant spike proteins will also provide new insight towards the infectivity and severity of mutant SARS CoV-2 viruses.”

The researchers next hope to take a closer look at the mechanism by which the disrupted ACE2 protein damages mitochondria and causes them to change shape.

Reference: “SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2” by Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan and John Y-J. Shyy, 31 March 2021, Circulation Research.
DOI: 10.1161/CIRCRESAHA.121.318902

Other authors on the study are Yuyang Lei and Zu-Yi Yuan of Jiaotong University in Xi’an, China; Cara R. Schiavon, Leonardo Andrade, and Gerald S. Shadel of Salk; Ming He, Hui Shen, Yichi Zhang, Yoshitake Cho, Mark Hepokoski, Jason X.-J. Yuan, Atul Malhotra, Jin Zhang of the University of California San Diego; Lili Chen, Qian Yin, Ting Lei, Hongliang Wang and Shengpeng Wang of Xi’an Jiatong University Health Science Center in Xi’an, China.

The research was supported by the National Institutes of Health, the National Natural Science Foundation of China, the Shaanxi Natural Science Fund, the National Key Research and Development Program, the First Affiliated Hospital of Xi’an Jiaotong University; and Xi’an Jiaotong University.