| Domain | High-confidence annotation/finding | Suggested ontology identifiers/terms | Evidence type and caveat |
|---|---|---|---|
| Disease identifier/classification | Nipah virus disease is a zoonotic henipavirus infection causing severe acute encephalitis and/or respiratory disease. Confident retrieved identifier: MeSH **D045464 Henipavirus Infections**; specific MONDO ID not confidently established from retrieved evidence, so mark **unknown/not confirmed here**. | MeSH: **D045464 Henipavirus Infections**; Disease label: **Nipah virus infection / disease**; MONDO: **unknown in retrieved sources** | Clinical trial registry-derived MeSH plus recent reviews; MeSH term in trials is broader than Nipah-specific disease, so disease-level normalization should be reviewed separately (pqac-00000008, pqac-00000009, pqac-00000013, pqac-00000018) |
| Pathogen | Cause is **Nipah virus (NiV)**, a negative-sense ssRNA henipavirus in family Paramyxoviridae; major clades/strains discussed are Malaysia and Bangladesh/India lineages. | Pathogen label: **Nipah virus**; Taxon term label acceptable if needed; CHEBI: not applicable | Review/pathobiology evidence; strain nomenclature and clade proposals are evolving, especially for India lineage (pqac-00000001, pqac-00000018, pqac-00000021) |
| Reservoir and spillover ecology | Natural reservoir is **Pteropus fruit bats**; spillover occurs directly via bat-contaminated food (notably raw date palm sap) and indirectly via amplifying hosts such as **pigs**; horses also noted in some outbreaks/reviews. | Host/reservoir terms: **Pteropus bats**, **swine**, **horse**; Exposure term: **raw date palm sap consumption** | Strong epidemiologic consensus; exact reservoir species differs by geography, and not all spillover events involve an intermediate host (pqac-00000001, pqac-00000006, pqac-00000011, pqac-00000030, pqac-00000032) |
| Transmission/risk factors | Major routes: pig-to-human in Malaysia/Singapore, contaminated date palm sap in Bangladesh, and person-to-person spread in Bangladesh/India/Kerala; close patient contact is a major risk factor. | Exposure terms: **zoonotic transmission**, **person-to-person transmission**, **foodborne exposure**, **occupational exposure** | Human outbreak investigations and reviews; route contributions vary strongly by outbreak setting (pqac-00000000, pqac-00000001, pqac-00000003, pqac-00000004) |
| Core phenotype set | Dominant phenotype spectrum: fever, headache, myalgia, cough/shortness of breath, acute encephalitis, confusion, seizures, coma; respiratory disease can be prominent, especially Bangladesh/India clade. | HPO suggestions: **Fever**, **Headache**, **Myalgia**, **Cough**, **Dyspnea**, **Encephalitis**, **Confusion**, **Seizure**, **Coma** | Human clinical reviews and outbreaks; exact frequency by symptom is incompletely standardized across cohorts (pqac-00000003, pqac-00000005, pqac-00000020) |
| Long-term sequelae / QoL | Survivors may develop persistent neurologic disability, including paralysis and oculomotor/neurologic deficits; relapsing or late encephalitis is recognized. | HPO suggestions: **Paralysis**, **Abnormality of eye movement**, **Neurocognitive impairment** | Based on follow-up literature summarized in reviews; precise prevalence and QoL instrument data are limited (pqac-00000005, pqac-00000020, pqac-00000007) |
| Host genes / molecular host factors | **EFNB2** and **EFNB3** are key host entry receptors for NiV G glycoprotein. These are **host susceptibility/entry factors**, **not inherited monogenic causes** of disease. | Gene symbols: **EFNB2**, **EFNB3**; Mechanism labels: **viral receptor activity**, **virus entry into host cell** | Strong mechanistic evidence from virology studies and reviews; no retrieved evidence supports inherited pathogenic variants causing Nipah disease susceptibility (pqac-00000018, pqac-00000019, pqac-00000021) |
| Viral genes and immune evasion | Viral genome encodes N, P, M, F, G, L and accessory **V/W/C** proteins; G mediates receptor binding, F mediates fusion, and V/W/P antagonize interferon pathways. | GO suggestions: **virus entry into host cell**, **membrane fusion**, **negative regulation of type I interferon production**, **suppression by virus of host type I interferon-mediated signaling pathway** | Mostly mechanistic review synthesis from primary experimental work; gene-by-gene effects are largely derived from in vitro/animal systems rather than direct human intervention studies (pqac-00000018, pqac-00000019) |
| Pathophysiology | Upstream-to-downstream chain: respiratory entry → local replication → viremia/leukocyte-associated spread → endothelial and neuronal tropism → vasculitis, thrombosis, syncytia, BBB disruption, encephalitis, pulmonary edema/ARDS. | GO suggestions: **viral process**, **cell-cell fusion**, **vasculitis**, **inflammatory response**, **blood-brain barrier disruption**; CL suggestions: **endothelial cell**, **neuron**, **monocyte**, **natural killer cell**, **T cell** | Combined human pathology, in vitro, and animal-model evidence; BBB and leukocyte “Trojan horse” mechanisms remain incompletely resolved (pqac-00000018, pqac-00000020, pqac-00000021) |
| Affected anatomy and cells | Primary organs/systems: **brain/CNS**, **lung/respiratory tract**, **vascular endothelium**; secondary involvement includes kidney, liver, and heart in severe systemic disease. Key target cells include **neurons**, **vascular endothelial cells**, and probably leukocyte populations during dissemination. | UBERON suggestions: **brain**, **lung**, **blood vessel endothelium**, **kidney**, **liver**, **heart**; CL suggestions: **neuron**, **endothelial cell**, **smooth muscle cell**, **monocyte**, **NK cell**, **CD8-positive T cell** | Human pathology and animal data agree on CNS/lung/endothelium; cell-type ranking outside endothelium/neurons is less certain in humans (pqac-00000018, pqac-00000020, pqac-00000021) |
| Diagnostics | Outbreak diagnosis relies on laboratory confirmation plus clinical/epidemiologic context; recent reviews emphasize need for rapid diagnosis and strengthened diagnostic capacity. Experimental immunoassays using recombinant ephrin-B2 capture have been described. | Diagnostic labels: **RT-PCR**, **serology/ELISA**, **antigen detection**, **contact/exposure history** | Retrieved evidence set gives only partial test-detail coverage; exact specimen hierarchy and reference-standard algorithms are not fully captured here, so formal WHO/CDC lab guidance should be added in production (pqac-00000000, pqac-00000018) |
| Prognosis / statistics | High mortality overall. Recent review summarized **729 cases, 424 deaths (58%)** overall; CFRs are typically **<40% in Malaysia** and often **>70% in Bangladesh/India/Philippines**. 2023 Bangladesh outbreak reported **14 cases, 10 deaths (71%)** in one review. | Prognostic labels: **case fatality rate**, **neurologic sequelae**, **rapid progression** | Aggregated review data; outbreak-specific CFRs depend on strain, detection intensity, and care access, so statistics should be stored with location/year provenance (pqac-00000001, pqac-00000003, pqac-00000004) |
| Treatment status and care | **No licensed therapy or vaccine for humans**. Current care is mainly **supportive/ICU care**; evidence-based priorities for trials are **m102.4** and **remdesivir** for prophylaxis/early treatment. Ribavirin has observational human use but uncertain efficacy and tolerability concerns. | MAXO suggestions: **supportive care**, **intensive care management**, **mechanical ventilation/respiratory support**, **antiviral treatment**, **monoclonal antibody therapy** | Strong expert consensus from 2024 reviews; efficacy evidence for most agents is preclinical or observational, not definitive randomized clinical efficacy (pqac-00000022, pqac-00000023, pqac-00000024, pqac-00000026, pqac-00000029) |
| Prevention / public health | Key preventive measures: avoid **raw date palm sap**, use tree skirts/barriers to prevent bat contamination, infection-control measures for human-to-human spread, surveillance/contact tracing, and community education. | MAXO suggestions: **exposure avoidance counseling**, **infection prevention and control**, **contact tracing**, **behavior change intervention** | Includes interventional prevention trial context; effectiveness depends on local adherence and outbreak ecology (pqac-00000011, pqac-00000012, pqac-00000002) |
| Vaccine clinical development | Human vaccine trials through 2024 include **HeV-sG-V / HenipaVax** Phase 1 (**NCT04199169**, completed, n=192), **mRNA-1215** Phase 1 (**NCT05398796**, completed, n=40), **PHV02** Phase 1 (**NCT05178901**, completed, n=60), and PHV02 prime-boost Phase 1b (**NCT06221813**, completed, n=120). | Intervention labels: **subunit vaccine**, **mRNA vaccine**, **rVSV-vectored vaccine** | ClinicalTrials.gov records are high-confidence for status/design/enrollment; efficacy against clinical disease is not established from these early-phase studies (pqac-00000008, pqac-00000009, pqac-00000013, pqac-00000016) |
| Animal models / comparative biology | Reservoir biology centers on **Pteropus** bats; major models include **Syrian hamster**, **ferret**, **guinea pig**, **swine**, **cat**, and **nonhuman primates**. **African green monkeys** most closely reproduce human disease; hamsters/ferrets are practical for countermeasure triage but incompletely capture all human features. | Model labels: **Pteropus bat**, **Syrian hamster**, **ferret**, **guinea pig**, **pig**, **cat**, **African green monkey**, **marmoset**, **cynomolgus monkey** | Dedicated 2023 model review plus 2024 summaries; route/phenotype details vary by strain and inoculation method, and some companion-animal models are used sparingly for ethical/practical reasons (pqac-00000030, pqac-00000031, pqac-00000033, pqac-00000034, pqac-00000035) |


*Table: This table summarizes high-confidence knowledge-base annotations for Nipah virus disease across identifiers, pathogenesis, clinical features, prognosis, prevention, treatment status, vaccine trials, and animal models. It is designed as a compact curation aid and notes where ontology IDs or evidence remain uncertain.*