I have been listening to Dr Bruce Patterson and his hypothesis on what causes Long Covid. He claims to be able to prevent the formation of the mico clots in patients early in the illness with a particular protocol and claims that he has a 80% success rate in treating Long Covid.
In this video he also makes a number of references to ME as he has used 50 ME patients in his research. He doesn't appear to be of the opinion that micro clots will be a major feature of ME as he claims there isn't much vascular inflammation. I am puzzled by his use of statins in ME as, in my experience, they cause a major relapse.
I have made notes as I listened and will paste them below if anyone is interested in the outline of the talk.
Dr Bruce Patterson on Long Covid and ME
Bruce Patterson is both a former Stanford researcher and Medical Director of Diagnostic Virology at Stanford University Hospitals and Clinics, He 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 two years Patterson has concentrated on publishing and has co-authored seven
papers on COVID-19 with more publications due.
In June of 2020, Patterson reported that he’d identified the cause of the so-called
cytokine storm in COVID-19.
Quote,
“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. In October, IncellDx reported that it was collaborating on a
COVID-19 clinical trial using the CCR5 antagonist
Maraviroc which is part of Patterson’s LC protocol.
Patterson’s first
Covid paper in May 2020 found a “profound elevation of plasma IL-6 and CCL5 (RANTES)” in ten seriously ill Covid 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, Leronlimab ,might be an appropriate medication to use 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” were released summer 2021.
According to Patterson:
Long Covid is a vascular inflammation caused by the S1 protein in the white blood cells.
In more than 8000 patients treated so far, disruption of these mechanisms with CCR5 antagonists and statins has resulted in a profound improvement in more than 80%
A similar pathology may exist in the Covid vaccine injured and those with ME, Fibro, and Lyme.
Investigating Cytokines in Long Covid. The same Cytokine pattern has not shown up in ME but it is caused by many different viruses and other triggers so to be expected. IL 6 and IL 8 are more common in ME than LC. He believes ME can be treated with the same antiretroviral though i.e. Maraviroc. VEGF is high in Long Covid and is the marker for polyneuropathy. It is low in ME (!) (despite neuropathy in about 1/3….another cause?)
He used 14 biomarkers: found a Long Covid profile. There was a cytokine flip when patients 'flipped' from Covid into Long Covid.
Found signature for platelet activation in early stages which triggers the clots that are part of the pathogenesis of LC.
None of the 13 000 LC patients had micro clots nor the 1000 severe acute patients after using CCR5 antagonist as it reduces platelet activation and reduced vascular inflammation. Says that the same vascular inflammation is not present in ME.
The Covid vaccine-injured also have a Long Covid profile but have less IL 6, VEGF. Less severe than LC. When treated with CCR5 med. they respond in 2-4 weeks instead of 6-8 weeks for Long Covid because they have fewer severity markers (cytokines)
Used 50 ME patients from Kaplin and overlaid their cytokine pattern over those for LC and vaccine-triggered LC. They had even higher LC indices (cytokines) than LC. The ME patients responded well to Maravirov and statins. (!) Did not have the degree of vascular inflammation seen in LC.
ME patients have an immune profile like the Post Vaccine Long Covid but have high IL 6 and, to a lesser degree, IL 8. Post Vaccine LC also have less VEGF like ME, so don't have polyneuropathy???
How the blood vessels become inflamed in LC
There are 3 types of monocytes: classical, intermediary, and nonclassical. It is the nonclassical that takes the S protein to the blood vessels and is responsible for the damage. His second paper proposes that these monocytes responded to the initial infection by taking pieces of virus and displaying them on their surface which attracted an immune attack.
Why do Monocytes, which normally only survive for two days, in LC survive for much longer?
- Patterson suggests that an inadequate immune response to the virus by T cells resulted in large numbers of monocytes being recruited to fight off the virus.
- Monocytes usually only survive a couple of days but Patterson proposed that an interaction with fractalkine gave them very much longer lifespans and caused them to start creating proinflammatory cytokines.
- They appear to emit high levels of CCL5/RANTES – a chemokine that directs them to the endothelial cells in the blood vessels where it is thought they create inflammation which results in dilation of the blood vessels
The LC symptoms, he believes, are caused by inflammation in different blood vessels across the body and brain.
Since exercise mobilizes these monocytes, this process is exacerbated when people with long COVID exercise.
USE OF MARAVIROC
It is a CCR5 antagonist and antiretroviral medication and it appears to be effective against Covid. Maraviroc also stops monocytes from moving around the body in response to CCL5/RANTES – the chemokine produced in endothelial cells. Most LC patients are on for 2-4 weeks and it can be as long as two months. It particularly relieves tinnitus and brain fog and in only three to five days.
Statins – work in LC by inhibiting fractalkine thus preventing monocyte cells from attaching to endothelial cells on the blood vessels.
He has found both S1, S2 peptides in post-vaccination LC and a potential for mutant S1 peptides. He discusses the implication for this in a paper that is shortly to be published.
The increased level of VEGF in LC correlates with polyneuropathy and the sensation of head fullness which is notable in LC and it also causes vasodilation. The vasodilation results in the brain fog, tinnitus, and headache. Is caused by the monocytes binding to the endothelium. It is the same in Lyme Disease where the monocytes carry the infection.
Patterson thinks monocytic reservoirs of infection established early in people who later developed LC. Treatment with steroids in the acute stage might inadvertently have allowed those reservoirs in monocytes to be established
The role of Fractalkine in vascular inflammation.
Monocytes damage blood vessels and cause inflammation. Increases production of IFN gamma and Type 1 immune response. (This is from a 2013 publication.)
'This interferon-gamma and its TH1 collaborator interleukin 2 are the numerators of our LC index' So it is the reason why there is elevated INF gamma, interleukin 2 in the vascular endothelium. Important to block these with statins. Use this to judge the success of therapy.
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 increases the longevity of monocytes. It also causes the monocytes to revert from their anti-inflammatory state, and to commence producing pro-inflammatory cytokines.
These are crucial 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 critical aspect of Patterson’s hypothesis. He believes these attack the blood vessel walls.
CX3CR1 is also an important player in getting the monocytes to engage in vascular patrols, and
deleting CX3CR1 has been shown to reduce their patrolling behaviour.
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 states that CCL5/RANTES was upregulated in 80% of Long Covid. Once at the endothelial cells, the monocytes bind to them with fractalkine.
Antiretroviral lowers LC index…it is a very, very potent approach to decreasing destructive cytokines such as TNF alpha.
VEGF causes blood vessel growth….and results in polyneuropathy. 85% of LC have high VEGF.
Important to target cytokines and not symptoms for treatment. They are the root cause.
In ME there is chronic viral infection and need anti-viral.
In Covid, there is a huge decrease in CD8 cells which results in the reactivation of all herpes viruses.
Patterson found that an LC patient was still infected with active Covid 90 days after the start of infection.
High IL 6 results in joint and muscle pain.
He has written a post-vaccine LC paper and one on post Lyme which will soon be published.
