A couple of Dr.Been videos pointed me at the S1 Spike Protein being causal of Long Covid and directly involved in lung injury. In the lung injury case, mice with a humanized ACE2 were dosed with S1 Spike units and developed lung injury. The implication here is that some folks getting the vaccine may also react similarly.
Then, in Long Covid, another group of doctors have found that the S1 protein expressed on the surface of a monocyte is likely responsible for Long Covid. They mentioned a similar syndrome post vaccination where some folks have a long duration of feeling off, and that this was likely the same mechanism.
The claim is made that they now have an effective treatment for Long Covid.
Has Bruce Patterson Cracked Long COVID?
by Cort Johnson | Jul 21, 2021 | Homepage, long COVID
Bruce Patterson MD is a former Stanford researcher with quite a record. The former Medical Director of Diagnostic Virology at Stanford University Hospitals and Clinics, Patterson has co-authored around 90 papers – most prior to 2011 – at about the time he left the University and created the incellDx diagnostic laboratory. Over the past ten years, incellDx has focused mostly on cancer screening and has produced products to test for HPV, CMV, antibodies, and others. Over the past two years, though, Patterson has jumped back into the publication field, co-authoring 7 papers on COVID-19 with more to come.
In June of 2020, Patterson reported that he’d identified the cause of the so-called “cytokine storm” in COVID-19.
“When we were developing a cytokine quantification assay for possible COVID trials in China, we discovered that infected patients had consistently high levels of CCL5/RANTES in plasma which in some cases was 100 times normal depending on the severity of the disease.”
Patterson and incellDx filed a patent in June 2020 for its CCL5/RANTES diagnostic test for COVID-19, Patterson reported. In October, incellDx reported that it was collaborating on a COVID-19 clinical trial using Pfizer’s CCR5 antagonist Maraviroc – a key part of Patterson’s long-COVID protocol.
Patterson is all over social media. His YouTube interviews and presentations have garnered over 400,000 views over the past year. ABC News just led with a story: “EXCLUSIVE: Lab discovers root cause of confusion, fatigue experienced by COVID ‘long haulers‘
Patterson has become a kind of a sensation … and why not? He’s credible, claims to be studying the largest cohort of long haulers (thousands) in existence, and believes that not only has he found the cause of long COVID, but that he’s put together a treatment regimen that works. No new drugs are needed – everything is off the shelf. It almost couldn’t be better.
How excited are people? One doctor on YouTube is so sure that Patterson has got it right that he recommended that he be nominated for a Nobel Prize. That’s a bit much for a hypothesis and treatment regimen which hasn’t been independently validated yet, but it does portray some of the excitement Patterson has generated.
Patterson, incellDX and the Coronavirus
As noted, it all began in the summer of 2020 when Patterson and incellDX found abnormal levels of cytokines – signaling fire in the body. Patterson’s first COVID-19 paper in May 2020 found a “profound elevation of plasma IL-6 and CCL5 (RANTES)” in 10 critically ill COVID-19 patients. It was followed in January 2021 by a paper showing that a COVID patient with a poor T-cell response was still shedding the virus 90 days after becoming infected. Next, Patterson and his team found that a CCL5 blocker called leronlimab might be a good drug to try in COVID.
Patterson’s two major papers, “Immune-Based Prediction of COVID-19 Severity and Chronicity Decoded Using Machine Learning“, and “Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection” – the second an unreviewed preprint – showed up in June of this year.
Immune Cells and Cytokines
On the face of it, the first paper didn’t seem revolutionary at all. This type of study – which assessed the immune cell subsets and 14 cytokines – has been done many times in chronic fatigue syndrome (ME/CFS). (In a talk, Patterson noted that he’d winnowed down the cytokines from about 150 possible factors to 14.) The study involved a mishmash of 224 acute COVID-19 and long-haul COVID-19 patients and 24 healthy controls.
The study found that CCL5/RANTES, IL-2, IL-4, CCL3, IL-6, IL-10, IFN-γ, and VEGF were all significantly elevated (all P<0.001) while GM-CSF and CCL4 were significantly reduced in COVID patients in general.
Next, they used machine learning to develop immunotypes pertaining to each type of COVID patient and found long-haul COVID patients were characterized by increased IFN-γ and IL-2, and reduced CCL4 production.
skipping down a bit it is the “2nd Paper” that’s what this posting is about:
The second paper, “Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) Up to 15 Months Post-Infection“, tied their hypothesis together.
As noted, it wasn’t just the monocytes – it was a particular kind of monocyte – that was increased in both acute and long COVID-19.
First, the group looked for evidence that COVID-19 had infected the monocytes in both acute and long-COVID patients and found evidence of some infection but not a lot. COVID-19 replication does not appear to be the problem.
When they used antibodies to look for evidence of coronavirus proteins in the monocytes, though, they found them – in spades. Seventy-three percent of the “non-classical” monocytes in long-COVID patients carried the coronavirus proteins. (They used another test – Ultra-High-Performance Liquid Chromatography – to largely confirm the results.)
These types of monocytes have often been thought to be anti-inflammatory, but recent studies show that they can, in some situations, produce pro-inflammatory cytokines. They’re mostly involved in “trash cleanup”, and the antiviral response. Interestingly, they appear to be unique in the patrolling behavior they exhibit around the blood vessels.
The authors believe these monocytes were drawn to coronavirus-infected cells in the blood vessels, where they ingested them, and then put a coronavirus protein on their surface to alert the immune system. The problem in long COVID occurs when they are drawn to the blood vessels and injure them, or cause the blood vessels to inappropriately dilate.
These nonclassical monocytes are the only monocytes to carry the CX3CR1 receptor, which when it binds to fractalkine, turns on an anti-apoptotic protein that allows the monocytes to survive longer than usual. It also causes the monocytes to revert from their anti-inflammatory state, and start pumping out pro-inflammatory cytokines.
These are important steps as most monocytes die within a few days, and having very long-lived (up to at least 16 months) coronavirus protein-carrying monocytes is a crucial aspect of Patterson’s hypothesis. Patterson also needs these monocytes to attack the blood vessel walls.
CX3CR1 is also an important player in getting the monocytes to engage in their vascular patrols, and deleting CX3CR1 has been shown to reduce their patrolling behavior.
Monocytes carrying the SARS protein and endothelial cells are producing high levels of CCL5/RANTES – a chemokine that draws the monocytes cells to the endothelial cells. Patterson reported that CCL5/RANTES was upregulated in 80% of long haulers. Once at the endothelial cells, the monocytes bind to them via fractalkine – a kind of immune Velcro.
There’s more at the link about mechanism. Let’s skip on down to treatment:
Successfully treating long COVID is. Patterson, an MD, reported that they started treating long-COVID patients in September 2020. Patterson’s protocol has two main goals:
Use CCR5 antagonists to reduce CCL5/RANTES levels, and therefore prevent the monocytes from getting to the blood vessels.
Damp down the CX3CR1/fractalkine pathway in order to turn off the long term monocyte survival mechanism that’s allowing them to survive longer than usual. Over time, the monocytes carrying the coronavirus protein will die off.
The treatment protocol is remarkably brief – just 4-6 weeks. First, immune labs are taken and then 3 drugs are given. (The fact that none of these drugs have been used in ME/CFS should remind us how vast the medical drug toolkit is and how many possibilities it holds.)
CCR5 antagonist – Maraviroc (Selzentry (US), Celsentri (EU)) is in an antiretroviral drug used in combination with other drugs to treat HIV. (HIV can use the CCR5 receptor to enter the cell). Its efficacy against the coronavirus is also being explored. Maraviroc also stops monocytes from moving around the body in response to CCL5/RANTES – a chemokine which is produced in endothelial cells. Maraviroc comes with plenty of warnings, including a black box one, but Patterson says its is safe – and has two papers coming out on it. Most long haulers are on for 2-4 weeks and the longest has been 8 weeks. Maraviroc, he said, was incredibly effective in relieving tinnitus and brain fog and typically did do so in 3-5 days. He said “we see it (tinnitus) a lot, and treat it a lot and are very good at eliminating it.”
Statins – by inhibiting fracktalkine, it stops the monocyte cells from attaching to endothelial cells on the blood vessels.
Ivermectin -an immunomodulator and anti-parasitic drug is used because of its persistent antiviral properties. It also affects cell membranes. A meta-review of 11 randomized Ivermectin COVID-19 trials found a significant reduction in hospitalization and and 56% reduction in death. Many of the trials were not peer-reviewed, and a wide range of doses was used. A placebo-controlled Ivermectin COVID-19 study is underway at the University of Oxford.
Here’s the Dr. Been Videos.
Some of Dr. Been’s audio is a bit garbled, but the rest is fine. This is the one about Long Haulers. One hour, 24 minutes:
Spike Proteins In Immune Cells – Dr. Bruce Patterson Discusses COVID Long Haul
567,348 views Streamed live on Jun 25, 2021
Drbeen Medical Lectures
Dr. Bruce Patterson’s team has discovered that the S1 pieces of the spike proteins persist in the monocytes resulting in immune dysregulation and long-haul syndrome. Let’s discuss these findings with him.
Dr. Patterson’s site: https://covidlonghaulers.com/
Then the other video on how the S1 Spike bit causes lung injury in mice which human ACE2 enzyme. 26 minutes:
Researchers Show How SARS-COV-2 Spike Protein Causes Acute Lung Injury in Mice
137,347 views Streamed live on Sep 1, 2021
Drbeen Medical Lectures
First study in mice demonstrates that S1 part of the spike protein in combination with hACE2 enzyme triggers cytokine like storm and acute lung injury. Let’s review this study.
Long Haul Post Vaccine?
I’d not heard of “Post Vaccine Long Haul” but it looks like for some folks “it’s a thing”:
Long Haul Post-Vaccine Syndrome: Share Your Experience
By Dr. Brimah -August 17, 2021
by Dr. Perry Brimah M.D., M.S. Twitter: @DrPerryBrimah
Long haul post-vaccine syndrome deals with a variety of symptoms that have been reported post Covid-19 vaccine. Some patients are reported to have presented with symptoms which resemble acute Covid-19 infections and others have presented with symptoms seen in patients suffering from Long haul Covid. Long haul post-vaccine syndrome may present in patients several months after taking Covid vaccine shots. According to leading physicians dealing with the syndrome, it is manageable and is treated similar to Long haul Covid. The suspected culprit in both syndromes is the ‘spike protein.’
Covid Virus Spike Protein
Covid-19 virus’ pathogenicity is courtesy of its spike protein. Upon entrance into the body, the spike protein attaches to ACE2 (angiotensin converting enzyme 2) receptors in the cell membranes (Pillay, 2020). ACE2 receptors of epithelial cells lining the airways are a first target of the virus upon inhalation. Upon attachment, the spike protein gets activated and changes from a ‘pre-fusion’ shape to a ‘post-fusion’ state where it is like a spear that pokes through the cell membrane and allows the viral genetic material entrance to your cells to replicate.
Long Haul Covid
Long haul covid or Long-COVID or COVID long-haulers according to a new review can present with as many as 55 long term symptoms. The most common of which are “fatigue (58%), headache (44%), attention disorder (27%), hair loss (25%), and dyspnea (24%)…Diseases such as stroke and diabetes mellitus were also present.” Psychiatric problems like dementia and insomnia are also included. Smell and taste deficiency may persist as also cough and lung abnormalities. Autoimmune problems where the body fights itself is also part of this plethora of presentations. Weight loss, palpitations, renal failure, mood disorders, throat pain and sputum, myocarditis, arrhythmia, OCD, intermittent fever, digestive problems are some more.
The precise cause of Long-COVID and Long-Post-Vaccine is being investigated but it may be due to organ damage or persistent autoimmune or inflammatory damage after the infection. Another recent study found Epstein Bar virus reactivated in 73% of long haulers and blamed this for the chronic fatigue, raynaud’s phenomenon and other related symptoms.
I’ve seen an assertion that post vaccination various endogenous suppressed viruses are able to reactivate. Shingles outbreaks, for example.
IF In fact Long Covid is due to just the S1 protein on monocytes, and both the vaccine and the disease can cause that to happen, then being vaccinated alone will be a big problem for some folks.
I note in passing that Robert Felix of Iceagenow.com / Iceagenow.info died after a sudden resurgence of an autoimmune illness that had been in remission, and that this started about 2 months after he was vaccinated. He did not believe his illness was related, due to the passage of many weeks after the vaccination. But not all reactions are immediate… It looks like his web site is now gone, but I found a copy on the Wayback Machine: http://web.archive.org/web/20210828042903/https://iceagenow.info/
All Cause Mortality numbers must be compared pre and post vaccination campaigns to have any clue how much damage is being done by turning people into S1 Spike Protein factories.