Bruce Patterson Long Hauler Protocol: Has Bruce Patterson Cracked 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 screening7 papers on COVID-19
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.
The monocyte binding also triggers the production of VEGF – which Patterson reports is elevated in almost all long haulers. VEGF then dilates the blood vessels causing, Patterson thinks, feelings of fullness in the head, migraines, and perhaps cognitive problems.
The many different symptoms that arise depend on where in the body the blood vessels – including those in the brain – get hit.
He also believes that monocytic reservoirs of infection were established early in people who later became long haulers. Those COVID-19 patients treated with steroids might inadvertently have allowed those reservoirs to be established. (If true, that’s something that the NIH-funded studies should readily pick up.)