What is Spikeopathy?

Prevalence of Long Covid 

Post-COVID Condition / Long COVID

Best estimates across population studies suggest:

• ~10–30% of people infected with SARS-CoV-2 experience persistent symptoms beyond the acute phase
• This places tens of millions globally under the Long COVID umbrella.

Public health bodies and research programs (including National Institutes of Health RECOVER) treat this as a mass-disabling condition.
How many of these are “spike-mediated”?
This is unknown—and exactly why measurement matters.
Current evidence suggests:
Some subset of people with PASC show circulating or tissue-associated viral antigens, including spike
Not all people with PASC do
Not all studies agree on pathogenic significance
Translation: spikeopathy is likely a phenotype or sub-phenotype, not the entirety of Long COVID.
The Pathophysiology of Spikeopathy

1) Viral Antigen Persistence (Central Hypothesis)
Multiple peer-reviewed studies have reported:
Detectable SARS-CoV-2 antigens (including spike or S1) months after infection in subsets of patients
Evidence of viral persistence in tissues (GI tract, brain, etc.) in some autopsy and biopsy studies
Persistent antigen → chronic immune stimulation
Chronic stimulation → inflammation, endothelial injury, autoimmunity, autonomic dysfunction

2) Endothelial Dysfunction & Vascular Injury
Spike protein has been shown in vitro and in vivo to:
Interact with ACE2-expressing endothelial cells 
Promote endothelial activation/dysfunction of the heart, vessels, and lymphatic system
Disrupt nitric oxide signaling and vascular tone
Downstream effects
-Impaired microcirculation
-Oxygen delivery problems
-Exercise and orthostatic intolerance
-Chest pain, headaches, brain fog, dysautonomia

3) Immune Dysregulation & Autoimmunity
Observed in subsets of patients:
Population shifts and depletion of  T-cells
Persistent cytokine signaling
Autoantibodies and chronic immune system irritation

4) Microclotting & Impaired Fibrinolysis
Some groups have described:
Fibrin amyloid microclots
Platelet hyperactivation
Impaired clot breakdown
Increased maternal hemorrhage and altered blood clotting cascades

5) Autonomic Nervous System Disruption (Dysautonomia)
Common clinical manifestations:
POTS-like symptoms
Orthostatic intolerance
Palpitations
Temperature dysregulation
Neuroinflammation
Spike-mediated immune effects are one possible contributor, not the sole cause.

Why the Field Is Stuck (and Why Measurement Is the Bottleneck)
Right now:
PASC is diagnosed clinically
Routine labs are often normal and standard therapeutics ineffective
Studies disagree because:
-different assays
-different timing
-different phenotypes lumped together