The science
The mechanism that connects infection, immunity and some of the diseases we still struggle to explain.
When a microbe looks like us, the immune system can mistake us for the microbe.
We are exposed to far more pathogens than we ever register. When part of one resembles part of us, the immune response it triggers can also recognise our own tissue, and the damage can continue after the infection has cleared.1
An infection, often silent, triggers an immune response against the pathogen.
Part of a pathogen molecule, a protein segment or a sugar structure, resembles a molecule of our own.
Antibodies or T cells raised against the pathogen also bind the human molecule. In a susceptible host, tolerance breaks and tissue is damaged.
Molecular mimicry has been demonstrated in several autoimmune and post-infectious diseases. These are four of the most studied cases, each with its primary source.6
| Disease | Pathogen · molecule | Human target | Type | What was shown | Source |
|---|---|---|---|---|---|
| Rheumatic fever | Streptococcus pyogenesM protein | Cardiac myosin | Protein | Antibodies and T cells from patients cross-react with streptococcal M protein and cardiac myosin. | [2] |
| Guillain–Barré syndrome | Campylobacter jejuniLipo-oligosaccharide | GM1 ganglioside, peripheral nerve | Carbohydrate | Immunisation with the bacterial molecule reproduced the neuropathy in an animal model. | [3] |
| Systemic lupus erythematosus | Epstein–Barr virusEBNA1 | Ro and Sm autoantigens | Protein | The earliest lupus autoantibodies cross-react with EBNA1, and immunisation induced lupus-like autoimmunity in animals. | [4] |
| Multiple sclerosis | Epstein–Barr virusEBNA1 | GlialCAM, central nervous system | Protein | Antibodies from patients' cerebrospinal fluid bind both with high affinity, and EBNA1 immunisation worsened disease in a mouse model. | [5] |
Neural Omega turns resemblances between proteins into hypotheses that can be tested, with a method that keeps what computation finds apart from what evidence confirms.
Neural Omega grew out of its own bioinformatics research into molecular mimicry: proteome-wide comparisons between pathogen and human proteins, in search of the resemblances that matter to the immune system. That work remains the foundation of our approach.
Patient, clinician, researcher, pharma: each meets molecular mimicry at a different point. One line of inquiry, read from four points of view.
Mimicry begins long before a diagnosis: an early, silent infection and, sometimes years later, symptoms of still uncertain cause. That sequence can only be studied if the patient's history is recorded over time.
In consultation, the clinician works with symptoms, tests and scores spread across specialties, and needs reliable references at the point of care.
Research turns individual histories into patterns: which exposures, in which people, before which disease. That takes consented, longitudinal data and studies designed to answer the question.
At proteome scale, resemblances between pathogen and human proteins number in the thousands. Computation finds them; each one that holds up becomes a therapeutic hypothesis and the first step of discovery.
Molecular mimicry is where our work begins. These are the research directions it opens, and where the right partners join early.7
A systematic map of the pathogen exposures that may drive autoimmunity: a data layer still to be built.
Understanding how pathogen mutations reshape molecular mimicry, and what that could mean for risk before it reaches a clinic.
Turning the phenomenon into therapeutic hypotheses at the earliest point in the discovery chain, together with pharma partners.
Neural Omega grew out of its own research into molecular mimicry, and every product carries that question forward. Research groups, clinicians and pharma partners are welcome to answer it with us.