Soma · Disease Ontology
Morbus is the human disease ontology, taxonomy, and model inside Persona. It organizes disease knowledge without assuming that every inherited clinical category is a clean natural kind — working from the hypothesis that many diseases are better understood as intersecting processes than as single objects.
15 interactive exemplars below · shareable via URL hash
Rather than starting from organ systems or specialty boundaries, Morbus organizes disease first by whether it is defined by a relatively identifiable cause, by emergent physiological dysregulation over time, or by both at once.
Pathology is chiefly organized around a relatively identifiable initiating cause.
Physical injury
Deficiency
Chemical exposure
Infectious disease
Hereditary disease
Pathology emerges from complex dysregulation of physiological systems over time.
Cardiovascular
Metabolic / endocrine
Neurological
Degenerative
Neoplastic
Immunological / inflammatory
Cause and physiology are both essential; one disease may belong to multiple explanatory layers.
Infection plus host response
Gene plus physiology
Environment plus regulation
Immune plus tissue ecology
Treatment effect
Beneath the top-level frame, Morbus separates the layers that get collapsed when a disease is treated as one object. A single condition is built from several of these primitives at once.
A condition treated as a recognizable, nameable whole.
A co-occurring cluster of features without a single settled cause.
The unfolding mechanism by which function is disrupted.
The initiating cause or causes that set the process in motion.
A predisposing condition that raises the probability of disease.
The structural change visible at the level of tissue.
The pathway, mutation, or signalling change underneath.
The characteristic immune response or dysregulation involved.
Failure of epithelial, vascular, or other protective barriers.
The microbial community whose shifts shape the condition.
A downstream condition arising from the primary disease.
Change in the disease produced by intervention.
Harm caused by medical care itself.
The condition as felt and narrated by the person living it.
The working hypothesis of Morbus is that one condition is simultaneously anatomical, molecular, immunological, developmental, ecological, environmental, and social. Explore how key human diseases decompose along each axis rather than being forced into a single legacy category.
| Disease | Anat | Etiol | Mol | Imm | Barr | Eco | Dev | Soc | Exp |
|---|---|---|---|---|---|---|---|---|---|
| Inflammatory Bowel Disease | Gastrointestinal tract, ileum and colon | Polygenic risk plus environmental triggers | NOD2 mutation, IL-23 / Th17 signalling pathways | Dysregulated mucosal immune response | Compromised intestinal epithelial barrier | Altered gut microbiome (dysbiosis) | Onset often in adolescence / young adulthood | Western diet, urbanization, antibiotic exposure | Relapsing-remitting pain, fatigue, social stigma |
| Type 2 Diabetes | Pancreas, skeletal muscle, liver, adipose tissue | Genetic susceptibility + chronic positive energy balance | IRS-1 serine phosphorylation, GLUT4 downregulation | Chronic low-grade macrophage-driven tissue inflammation | Intestinal permeability leading to endotoxemia | Altered gut microbiota diversity | Progressive accumulation of metabolic strain with age | Ultra-processed food environments, sedentary labor | Dietary anxiety, neuropathic pain, fear of failure |
| Tuberculosis | Pulmonary parenchyma, alveolar macrophages | Infection with Mycobacterium tuberculosis | Mycolic acid wall, ESX-1 secretion system | Th1 cell-mediated immunity & granuloma formation | Alveolar epithelial barrier disruption | Host nutritional status and pulmonary microbiome | Latency phase vs. active reactivation | Overcrowded housing, poverty, poor ventilation | Chronic cough, isolation, treatment fatigue |
| Alzheimer's Disease | Hippocampus, neocortex, cerebral vasculature | APOE4 allele, aging, cardiovascular disease | Abeta42 aggregation, hyperphosphorylated tau | TREM2 microglial activation, astrogliosis | Blood-brain barrier breakdown, glymphatic failure | Gut-brain metabolic axis, systemic lipid state | Long prodromal plaque accumulation (20+ years) | Cognitive reserve, air pollution, social isolation | Identity erosion, caregiver burden, memory loss |
| Traumatic Brain Injury | Cerebral cortex, diffuse axonal pathways, meninges | Mechanical impact, deceleration forces | Excitotoxicity, mitochondrial calcium overload | Microglial priming, peripheral cell infiltration | Traumatic blood-brain barrier (BBB) disruption | Systemic autonomic dysfunction, gut dysbiosis | Acute mechanical shock to chronic dementia risk | Sports regulations, infrastructure safety, military exposure | Cognitive fatigue, mood shifts, isolation |
| Post-Traumatic Stress Disorder | Amygdala, hippocampus, medial prefrontal cortex | Exposure to actual or threatened death, injury, or sexual violence | FKBP5, glucocorticoid receptor sensitivity, BDNF | Low-grade systemic inflammation, HPA-axis dysregulation | Blood-brain barrier stress vulnerability | Gut-brain axis, sleep ecology, substance co-use | Childhood trauma increases lifetime risk | War, displacement, intimate partner violence, occupational trauma | Hypervigilance, flashbacks, emotional numbing, moral injury |
| Malaria | Liver, erythrocytes, cerebral microvasculature | Plasmodium falciparum, P. vivax, and related species | PfEMP1 variant surface antigens, hemozoin crystals | Partial acquired immunity after repeated exposure | Blood-brain barrier sequestration in cerebral malaria | Rainfall, temperature, vector habitat, land use | Highest mortality in young children and pregnant people | Bed-net access, health-system reach, poverty, migration | Cyclical fever, anemia, treatment delays, recurrence fear |
| Heart Failure | Left ventricle, atria, coronary arteries, kidneys | Ischemic heart disease, hypertension, valve disease, toxins | BNP/NT-proBNP release, beta-adrenergic desensitization | Cardiac fibrosis, macrophage-mediated remodeling | Capillary leak, pulmonary and gut barrier congestion | Sodium intake, air pollution, sleep-disordered breathing | Adult-onset progression with acute decompensation episodes | Access to diagnostics, medications, cardiac rehabilitation | Breathlessness, fluid limits, hospitalization anxiety |
| Rheumatoid Arthritis | Synovium, small joints of hands and feet, cardiovascular system | Autoimmune dysregulation with genetic and environmental triggers | Anti-CCP antibodies, TNF-alpha, IL-6 pathway activation | Adaptive autoimmunity plus innate inflammatory amplification | Synovial barrier breakdown, endothelial activation | Oral microbiome, gut dysbiosis hypotheses | Peak onset in middle adulthood with chronic course | Work disability, gendered burden, treatment access | Morning stiffness, pain unpredictability, treatment trade-offs |
| COVID-19 | Respiratory epithelium, alveoli, endothelium | SARS-CoV-2 coronavirus infection | ACE2 receptor binding, spike protein variants | Cytokine storm, T-cell exhaustion, autoantibody formation | Alveolar-capillary barrier breakdown | Indoor ventilation, seasonality, co-circulating pathogens | Acute illness with long-COVID sequelae | Global travel, vaccine equity, misinformation | Isolation, breathlessness, grief, uncertainty |
| Sickle Cell Disease | Erythrocytes, bone marrow, spleen, cerebral vessels | HBB gene mutation (HbS) inherited in autosomal recessive pattern | Hemoglobin S polymerization under deoxygenation | Functional asplenia, chronic inflammation | Endothelial activation and microvascular leak | Malaria endemicity and ancestral selection pressure | Symptoms from infancy with cumulative organ injury | Healthcare access, newborn screening, hydroxyurea availability | Unpredictable pain crises, fatigue, stigma |
| Major Depressive Disorder | Prefrontal cortex, amygdala, hippocampus, raphe nuclei | Multifactorial — genetic risk plus adversity and stress | Serotonin, norepinephrine, BDNF pathway dysregulation | Elevated inflammatory cytokines in subsets | HPA-axis hyperactivity, gut-brain signalling | Sleep disruption, substance use, social isolation | First episodes often in adolescence or early adulthood | Poverty, unemployment, discrimination, care access | Emptiness, guilt, hopelessness, slowed cognition |
| Asthma | Bronchi, bronchioles, airway smooth muscle | Atopy, early-life exposures, respiratory infections | IgE signalling, IL-4/IL-13 pathways, mast cell degranulation | Eosinophilic and neutrophilic airway inflammation | Epithelial barrier fragility in airways | Indoor allergens, outdoor air pollution, climate | Often begins in childhood with variable remission | Housing quality, occupational exposures, inhaler access | Breathlessness fear, activity limits, night waking |
| HIV / AIDS | CD4+ T lymphocytes, gut-associated lymphoid tissue | Human immunodeficiency virus (HIV-1 / HIV-2) | Reverse transcriptase, integrase, envelope glycoprotein | Progressive T-cell loss and immune activation | Mucosal barrier disruption in gut | Sexual networks, injection equipment sharing, coinfections | Acute seroconversion to chronic controlled infection | Stigma, criminalization, PrEP/ART access disparities | Disclosure anxiety, pill burden, fear of progression |
| Lung Cancer | Bronchial epithelium, alveoli, pleura | Tobacco smoke, radon, occupational carcinogens, genetics | EGFR, KRAS, ALK, PD-L1 expression | Tumor immune evasion, checkpoint suppression | Disrupted alveolar-capillary interface | Air pollution, occupational dust, radon in homes | Long latency from exposure to diagnosis | Tobacco policy, screening access, occupational protection | Dyspnea, fatigue, prognosis conversations |
15 of 15 exemplars · 9 axes each
A relapsing-remitting inflammatory condition of the gastrointestinal tract, emerging from polygenic risk, barrier disruption, and dysregulated host immune response to gut microbiota.
Simulate how a computational agent queries the database registries of the Digital Halo to aggregate physiological evidence. Click a tab to select a database.
Simulated API Request URL
Querying literature database for clinical trials and review articles linking NOD2 mutations to Crohn's disease susceptibility.
Knowledge Synthesis & Findings
{
"esearchresult": {
"count": "1485",
"retmax": "3",
"idlist": ["38128312", "37992019", "37554318"],
"translationset": [
{ "from": "inflammatory bowel disease", "to": "\"inflammatory bowel diseases\"[MeSH Terms] OR \"inflammatory bowel disease\"[All Fields]" }
]
}
}Existing nosologies are treated as reference mappings rather than the native Morbus hierarchy. ICD-11 in particular is a public reporting crosswalk — a way to translate out, not the structure to organize around.
Many diseases are better understood as intersecting processes rather than single objects. Morbus supports plural classification: one condition may be simultaneously anatomical, molecular, immunological, developmental, ecological, environmental, and social.