Nipah Virus Disease: Comprehensive Disease-Characteristics Report

Executive summary

Nipah virus disease (NVD) is an acute, bat-borne zoonotic infection caused by Nipah virus (NiV), an enveloped negative-sense single-stranded RNA henipavirus. Disease ranges from asymptomatic infection or influenza-like illness to rapidly progressive pneumonia, acute respiratory distress syndrome (ARDS), encephalitis, seizures, coma, and death. The major biological lesion is systemic infection of ephrin-B2/B3-expressing endothelium and neural cells, producing vasculitis, thrombosis, blood–brain-barrier injury, and neuronal infection. Pteropus fruit bats are the reservoir; transmission occurs through contaminated food, infected livestock, and close contact with infected people. Outbreak-specific case-fatality ratios (CFRs) range from approximately 25% to 100%, and an aggregated 2024 review reported 424 deaths among 729 recognized cases (58%). No human vaccine or disease-specific treatment is licensed; supportive intensive care remains standard, while m102.4 and remdesivir are the leading candidates for clinical efficacy trials. (hassan2024nipahvirusdisease pages 11-14, hassan2024nipahvirusdisease pages 9-11, fauscotino2024nipahvirusa pages 3-5, fauscotino2024nipahvirusa pages 7-9, chan2024nipahvirustherapeutics pages 12-14)

The following compact table is intended for direct knowledge-base curation.

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.

1. Disease information

Definition and terminology

NVD is a zoonotic henipavirus infection characterized principally by acute encephalitis and/or severe respiratory disease. Synonyms include Nipah virus infection, Nipah encephalitis, NiV infection, and, less specifically, henipavirus infection. It was first recognized during the 1998–1999 Malaysia–Singapore outbreak; subsequent recurrent outbreaks have occurred mainly in Bangladesh and India, with an equine-associated outbreak in the Philippines. (tan2024asystematicreview pages 1-2, hassan2024nipahvirusdisease pages 11-14)

Identifiers

• MeSH: D045464, Henipavirus Infections—a broader parent concept consistently assigned in the retrieved ClinicalTrials.gov records. (NCT05178901 chunk 1, NCT04199169 chunk 1)
• MONDO: a Nipah-specific MONDO identifier was not reliably returned by the resources accessed and should be curator-verified rather than inferred.
• ICD-10/ICD-11: no specific code was established in the retrieved evidence. Coding generally falls under viral encephalitis or other specified zoonotic viral disease, depending on jurisdiction; production use requires verification against the current national ICD modification.
• OMIM/Orphanet: not applicable as primary sources for a non-Mendelian acute infection; no disease-specific entries were confirmed.

This report synthesizes aggregated disease-level resources, outbreak cohorts, clinical-trial registries, and experimental literature. It is not derived from an individual EHR.

2. Etiology, risk, and protective factors

Cause

The sole necessary causal agent is NiV. Important lineages include NiV-Malaysia and the Bangladesh/India clade. The latter is associated epidemiologically with severe pulmonary involvement, person-to-person transmission, and CFRs often exceeding 70%, whereas Malaysian outbreaks had CFRs below 40%; ascertainment, route, health-system capacity, and viral biology all probably contribute. (tan2024asystematicreview pages 1-2, anish2024pandemicpotentialof pages 2-3)

Exposure risks

• Bangladesh: consumption of raw date-palm sap contaminated by bat saliva or urine; direct caregiving and exposure to respiratory/oral secretions.
• Malaysia/Singapore: occupational contact with infected pigs; 93% of patients in the initial setting reportedly had direct swine contact.
• India/Kerala: zoonotic spillover followed by household or nosocomial transmission; hospital superspreading has occurred.
• Other: contact with infected horses or contaminated meat was implicated in the Philippines.

One review estimated that 51% of recognized Bangladeshi cases followed close contact with another patient. A reported effective reproduction number around 1.46–1.80 should be interpreted cautiously because most transmission chains terminate and superspreading creates marked heterogeneity. (rahman2024riskevaluationand pages 3-4, anish2024pandemicpotentialof pages 1-2, hassan2024nipahvirusdisease pages 9-11, pigeaud2023animalmodelsfor pages 1-2)

Genetic, protective, and gene–environment factors

No validated human germline causal variant, susceptibility locus, protective allele, modifier gene, Mendelian inheritance pattern, or clinically actionable pharmacogenomic association is established. EFNB2 and EFNB3 are host entry factors, not inherited causes. The dominant gene–environment relationship is functional: exposure introduces virus to tissues expressing these receptors. Environmental protection consists of avoiding raw sap, blocking bat access to collection sites, reducing infected-animal contact, and infection-control precautions. A 7,782-participant community protocol evaluated “do not drink raw sap” messaging and sap collection from trees protected by bamboo skirts or banas. (NCT01811784 chunk 1, NCT01811784 chunk 2, fauscotino2024nipahvirusa pages 3-5)

3. Phenotypes

Disease affects all age groups and usually begins acutely after a 4–14-day incubation period, although longer incubations have occasionally been reported. Early fever, headache, myalgia, vomiting, cough, and dyspnea can progress over hours to days to altered consciousness, seizures, encephalitis, and coma; coma may develop within 24–48 hours after major neurological deterioration. Severity and respiratory prominence vary by lineage and outbreak. (chan2024nipahvirustherapeutics pages 1-4, anish2024pandemicpotentialof pages 2-3)

Survivors may have substantial dependence, impaired mobility, cognition, communication, or employment. However, recent disease-specific EQ-5D, SF-36, or PROMIS estimates were not found; quality-of-life effects are chiefly inferred from neurological disability studies. (chan2024nipahvirustherapeutics pages 1-4, chan2024nipahvirustherapeutics pages 12-14, saha2024recentadvancesof pages 6-7)

4. Genetic and molecular information

NVD is not a genetic disorder. Therefore causal human genes, ACMG-classified pathogenic variants, allele frequencies, chromosomal abnormalities, anticipation, mosaicism, founder effects, and carrier frequency are not applicable.

The approximately 18.2-kb viral genome encodes structural proteins N, P, M, F, G, and L; RNA editing/alternative expression from the P locus produces V, W, and C. G is the attachment protein, F mediates membrane fusion, M coordinates assembly/egress through phosphatidylserine and PI(4,5)P2 interactions, and L is the RNA-dependent RNA polymerase. V/W/P antagonize interferon production or STAT-dependent signaling; C contributes to budding. (fauscotino2024nipahvirusa pages 3-5, brown2023immunopathogenesisofnipah pages 5-7)

Relevant human genes are EFNB2 and EFNB3, whose products act as viral receptors. Deep mutational scanning published in 2023 engineered an EFNB2 decoy that retained henipavirus-G binding while reducing Eph-receptor binding, illustrating a potential therapeutic rather than inherited-disease mechanism.

No reproducible human disease-associated DNA methylation, histone modification, structural variant, or clinically actionable epigenetic signature was established in the evidence reviewed.

5. Environmental and infectious-agent information

The primary non-genetic determinants are ecological and behavioral: bat habitat overlap, date-palm-sap harvesting, livestock intensification, occupational swine exposure, unsafe caregiving, inadequate personal protective equipment, and delayed recognition in resource-constrained settings. Smoking, alcohol, exercise, and ordinary diet have no established disease-specific causal role apart from consumption of contaminated raw foods. (rahman2024riskevaluationand pages 3-4, tan2024asystematicreview pages 1-2, NCT01811784 chunk 1)

Agent: Nipah virus, genus Henipavirus, family Paramyxoviridae. The virus requires maximum-containment laboratory practices for live-virus work. Pteropus bats shed virus through saliva and urine without the fulminant disease seen in spillover hosts. (NCT01811784 chunk 1, pigeaud2023animalmodelsfor pages 1-2)

6. Mechanism and pathophysiology

Causal chain

1. Attachment and fusion: NiV-G binds EFNB2/EFNB3; conformational activation of trimeric F drives fusion at the plasma/endosomal membrane.
2. Local replication: respiratory epithelial infection produces syncytia and inflammatory mediators; severe cases develop alveolar hemorrhage, edema, and ARDS.
3. Immune evasion: V/W/P suppress type-I interferon production or signaling, including STAT pathways; W also suppresses inflammatory mediators including CCL4, CCL5, and TNF-α in experimental systems.
4. Dissemination: free virus and leukocyte-associated virus enter blood. T cells, natural-killer cells, and monocytes have been implicated experimentally.
5. Endotheliotropism: infection of vascular endothelial cells causes multinucleated syncytia, necrotizing vasculitis, permeability, thrombosis, and microinfarction.
6. Neuroinvasion: hematogenous endothelial infection, disrupted blood–brain barrier, leukocyte-associated transport, olfactory routes, and direct neuronal spread are plausible, nonexclusive mechanisms.
7. Clinical injury: neuronal infection plus ischemic/perivascular lesions causes encephalitis, seizures, coma, and persistent deficits; systemic vascular disease contributes to renal, hepatic, and cardiac injury. (fauscotino2024nipahvirusa pages 3-5, saha2024recentadvancesof pages 6-7, anish2024pandemicpotentialof pages 2-3)

Suggested annotations include GO: virus entry into host cell; membrane fusion; viral genome replication; negative regulation of type-I interferon signaling; inflammatory response; cell–cell fusion, and cell types endothelial cell, neuron, bronchiolar epithelial cell, alveolar type-II cell, smooth-muscle cell, monocyte, NK cell, and CD8-positive T cell. Smooth-muscle cells can support prolonged high-titer replication without obvious cytopathic effect in vitro, so infection does not invariably equal tissue destruction.

Molecular profiling and advanced technology

Bulk immune-expression studies report TNF-α, IL-1β, IL-6, IL-8, CXCL10, and G-CSF perturbation, but validated diagnostic transcriptomic, proteomic, metabolomic, or lipidomic signatures are not established. No mature human single-cell atlas, spatial-transcriptomic map, integrated clinical multi-omics classifier, or validated genome-wide CRISPR dependency panel was identified. These should be marked insufficient evidence, not negative findings. (saha2024recentadvancesof pages 6-7)

7. Anatomical structures affected

Primary systems are the CNS, respiratory tract, and systemic vasculature. Suggested UBERON labels are brain, cerebral blood vessel, blood–brain barrier, lung, bronchial epithelium, pulmonary alveolus, blood vessel endothelium, kidney, liver, and heart. Major lesions include encephalitis with necrosis/perivascular cuffing, pulmonary edema and hemorrhage, endothelial syncytia, vasculitis, and thrombosis. Kidney, liver, and heart are secondary systemic targets. Disease is diffuse rather than consistently unilateral; lateralization is not characteristic. (fauscotino2024nipahvirusa pages 3-5, saha2024recentadvancesof pages 6-7, pigeaud2023animalmodelsfor pages 2-4)

Subcellular annotations include plasma membrane (G–receptor attachment and fusion), endosome (F trafficking/activation), cytoplasm (replication complex), and plasma-membrane lipid domains (M-mediated assembly). There is no established primary mitochondrial, lysosomal, or nuclear storage defect.

8. Temporal development

Onset is acute or subacute in children and adults rather than congenital or age-dependent. A pragmatic sequence is incubation → febrile/prodromal illness → respiratory or neurological deterioration → encephalitis/ARDS and multiorgan injury → death or recovery with possible neurological sequelae. The critical treatment window is probably before high viral burden, encephalitis, and irreversible vascular/neural injury. (chan2024nipahvirustherapeutics pages 1-4, chan2024nipahvirustherapeutics pages 12-14)

Most disease is self-limited through death or recovery, not chronically replicative lifelong disease. Nevertheless, persistent viral foci or delayed inflammatory/reactivation phenomena may produce relapsing or late-onset encephalitis months to years later. Spontaneous clinical remission occurs in survivors; no therapy-induced remission rate has been established.

9. Inheritance, epidemiology, and population

No inheritance pattern, penetrance, carrier state, anticipation, or genetic counseling indication applies. Population risk is exposure-driven.

The 2024 global review synthesized 97 articles and found almost annual outbreaks in Bangladesh. Aggregate counts in another clinical review were 729 recognized cases and 424 deaths (58%). Country/outbreak CFRs varied from approximately 25% to 100%; mortality was generally below 40% in Malaysia and above 70% in Bangladesh, India, and the Philippines. The 2023 Bangladesh outbreak had 14 cases and 10 deaths (71%); Kerala’s September 2023 outbreak had six cases and two deaths. Kerala’s 2018 event included 23 infections (18 confirmed and five probable) and 21 deaths. (tan2024asystematicreview pages 1-2, anish2024pandemicpotentialof pages 1-2, hassan2024nipahvirusdisease pages 11-14, hassan2024nipahvirusdisease pages 9-11)

Because NiV is episodic and geographically focal, stable prevalence and annual incidence per 100,000 are not meaningful globally. Surveillance limitations likely cause underascertainment. No consistent sex ratio is established; occupational exposure produced male predominance in some swine-associated cohorts. All ages can be affected. (rahman2024riskevaluationand pages 3-4, chan2024nipahvirustherapeutics pages 1-4)

10. Diagnostics

Diagnosis requires epidemiological suspicion plus laboratory confirmation. Recommended outbreak testing includes:

• Real-time RT-PCR for viral RNA from respiratory/throat or nasal swabs, blood/serum, urine, and cerebrospinal fluid as clinically appropriate; timing and local reference-laboratory protocols matter.
• Serology, especially NiV-specific IgM/IgG ELISA or neutralization, for later disease or retrospective confirmation.
• Virus isolation only in appropriately equipped high-containment laboratories.
• MRI may show multifocal small ischemic or inflammatory brain lesions; EEG and CSF studies support encephalitis assessment but are not pathogen-specific.
• Histopathology may show necrotizing vasculitis, thrombosis, endothelial syncytia, and neuronal/endothelial viral antigen.

Experimental ephrin-B2-capture ELISA and lateral-flow formats can distinguish NiV/HeV antigen in research settings, but they are not replacements for validated public-health assays.

Clinical differentials include Japanese encephalitis, herpes simplex encephalitis, other arboviral encephalitides, bacterial meningitis, cerebral malaria, influenza/COVID-19 and other severe viral pneumonias, toxic-metabolic encephalopathy, and stroke. Exposure history, combined respiratory–neurological disease, clustering, and NiV-specific testing are discriminating.

Human genetic testing—WGS, WES, panels, CMA, karyotype, FISH, mitochondrial, or repeat-expansion testing—is not indicated for etiologic diagnosis. There is no population newborn or carrier screening. During outbreaks, contact identification, symptom surveillance, and targeted molecular testing constitute secondary prevention.

11. Outcome and prognosis

Mortality is high and usually occurs during acute encephalitic, respiratory, or multiorgan disease. Conventional five- or ten-year survival estimates are not applicable. Poor prognostic features plausibly include severe encephalopathy, coma, seizures, respiratory distress, high viral burden, and delayed supportive care, although validated bedside prognostic models are lacking. (chan2024nipahvirustherapeutics pages 1-4, anish2024pandemicpotentialof pages 2-3)

Survivors can recover substantially but remain at risk for paralysis, cognitive/sensory/motor deficits, oculomotor dysfunction, psychiatric or functional consequences, and late encephalitis. There is no validated prognostic molecular biomarker. Viral RNA burden, inflammatory mediators, and neutralizing-antibody responses remain research measures rather than approved prognostic tests. (chan2024nipahvirustherapeutics pages 1-4, saha2024recentadvancesof pages 6-7)

12. Treatment

Current standard

There is no licensed NiV-specific drug or human vaccine. Management consists of isolation and infection prevention, oxygen and ventilatory support, fluid/electrolyte management, hemodynamic and renal support, seizure treatment, treatment of secondary infections, nutrition, pressure-injury prevention, and rehabilitation. Suggested MAXO labels include supportive care, intensive-care management, mechanical ventilation, anticonvulsant therapy, renal replacement therapy, physical therapy, occupational therapy, and speech therapy. (chan2024nipahvirustherapeutics pages 4-6, fauscotino2024nipahvirusa pages 7-9)

Investigational agents

• m102.4: human monoclonal antibody targeting the G–EFNB2/B3 interface. A Phase 1 study in 40 healthy volunteers found no serious adverse events and a placebo-like safety profile; headache was most common. Post-exposure protection has been demonstrated in ferrets and nonhuman primates. MAXO: monoclonal-antibody therapy. (chan2024nipahvirustherapeutics pages 6-8)
• Remdesivir: nucleotide-analog viral polymerase inhibitor. It protected African green monkeys when given early; one review reported 67% survival with early dosing. Compassionate-use Kerala observations are uncontrolled and too small for efficacy inference. MAXO: antiviral therapy. (anish2024pandemicpotentialof pages 9-10, kallon2024therapeuticadvancementin pages 6-7)
• Ribavirin: observational Malaysian data suggested a 36% relative mortality-risk reduction, but confounding is substantial and African-green-monkey efficacy was absent. Fatigue, headache, hyperbilirubinemia, and hemoglobin reduction caused all eight recipients in one post-exposure series to discontinue therapy. (fauscotino2024nipahvirusa pages 7-9, chan2024nipahvirustherapeutics pages 6-8)
• Favipiravir: RNA-polymerase inhibitor giving 100% survival in one hamster regimen; no demonstrated human efficacy. (kallon2024therapeuticadvancementin pages 6-7)
• Other antibodies, including h5B3.1, nAH1.3, HENV-26, and HENV-32, remain preclinical.

The clearest 2024 expert assessment was that only m102.4 and remdesivir had sufficient evidence to prioritize for trials, alone or in combination, for prophylaxis or early treatment. This is a prioritization judgment, not proof of clinical efficacy. PK/PD optimization and pre-positioned adaptive outbreak protocols are essential. (chan2024nipahvirustherapeutics pages 12-14, chan2024nipahvirustherapeutics pages 1-4)

Vaccine trials and recent development

• HeV-sG-V/HenipaVax, Hendra soluble-G subunit with alum: Phase 1, NCT04199169, completed, 192 adults; 10-, 30-, and 100-µg schedules. (NCT04199169 chunk 1)
• PHV02, live attenuated rVSV-ΔG-EBOV-GP-NiV-G: NCT05178901, Phase 1, completed, 60 adults; NCT06221813, Phase 1b prime–boost study, 120 adults, begun January 2024. (NCT05178901 chunk 1, NCT06221813 chunk 1)
• mRNA-1215, lipid-nanoparticle mRNA encoding a secreted prefusion-stabilized F/G immunogen: NCT05398796, Phase 1, 40 adults, two doses at 10–100 µg. (NCT05398796 chunk 1, NCT05398796 chunk 2)

These studies address safety and immunogenicity, not clinical disease prevention. Gene therapy, cell therapy, surgery, and genotype-guided treatment are not applicable.

13. Prevention

Primary prevention: avoid raw date-palm sap and fruit contaminated by bats; boil/pasteurize sap; cover collection sites with bat-exclusion skirts; use gloves and respiratory/eye protection when handling sick livestock; improve farm biosecurity and separate pigs from bat-attracting fruit trees. (NCT01811784 chunk 1)

Secondary prevention: rapid case recognition and RT-PCR confirmation, immediate isolation, contact tracing and active monitoring, safe specimen handling, appropriate PPE, and targeted testing. Healthcare-associated superspreading makes ventilation, hand hygiene, droplet/contact precautions, and escalation to airborne precautions for aerosol-generating procedures especially important. (anish2024pandemicpotentialof pages 1-2)

Tertiary prevention: aggressive organ support, seizure control, prevention of aspiration and secondary infection, and long-term neurological rehabilitation.

There is no licensed immunization or established antiviral prophylaxis. m102.4 and remdesivir prophylaxis remain investigational. Community engagement and One Health surveillance of humans, bats, livestock, food production, and land-use change are authoritative priorities. (tan2024asystematicreview pages 1-2, chan2024nipahvirustherapeutics pages 12-14)

14. Other species and natural disease

Pteropus fruit bats—including Pteropus medius in South Asia—are principal reservoirs. Pigs were amplification hosts in Malaysia/Singapore; 93% of patients in the original setting had direct infected-swine contact. Horses were implicated in the Philippines. Infection or serological evidence has also occurred in dogs and cats near outbreaks. Breed-specific VBO associations and orthologous “disease genes” are not applicable. (anish2024pandemicpotentialof pages 2-3, pigeaud2023animalmodelsfor pages 1-2)

Cross-species susceptibility is facilitated by conservation of EFNB2/B3. Spillover hosts develop much more severe respiratory, neurological, and vascular disease than reservoir bats. Swine are both veterinary disease hosts and epidemiologically important amplifiers, making livestock vaccination and surveillance potentially valuable One Health interventions.

15. Model organisms

• Syrian golden hamster: intranasal challenge emphasizes pneumonia/respiratory disease; intraperitoneal challenge produces dose-dependent lung, brain, kidney, hemorrhagic, and vascular lesions. It recapitulates most major human features but not myocarditis consistently. Practical for antiviral/vaccine screening. (anish2024pandemicpotentialof pages 2-3)
• Ferret: develops acute respiratory, neurological, and systemic disease and is widely used for antibody and vaccine evaluation. It is more expensive and less immunologically tractable than rodents and does not reproduce every human lesion. (pigeaud2023animalmodelsfor pages 34-35, mishra2024advancementsinnipah pages 11-12)
• Guinea pig: useful for histopathology, but disease reproducibility and translational fidelity are weaker.
• Swine: biologically relevant amplifier-host model for transmission and livestock vaccines; requires both humoral and cellular immunity for protection. Husbandry and containment constrain sample size. (pigeaud2023animalmodelsfor pages 35-36)
• Cats/dogs: susceptible and historically useful, but companion-animal ethics, inconsistent recapitulation, and superior alternatives limit routine use. (pigeaud2023animalmodelsfor pages 24-26)
• African green monkey: most faithful model of human pulmonary, vascular, and neurological disease; used for remdesivir, antibody, vaccine, aerosol, intratracheal, and intranasal studies. Limitations are cost, small cohorts, ethics, and BSL-4 requirements. (pigeaud2023animalmodelsfor pages 35-36, pigeaud2023animalmodelsfor pages 2-4)
• Common marmoset: intranasal/intratracheal NiV-B challenge caused 4/4 lethality, pulmonary edema, systemic vasculitis, hyperventilation, lethargy, anorexia, and hind-limb tremor after 8–11 days. Its small size permits larger NHP cohorts, but brain lesions were limited and immunological reagents are sparse. (pigeaud2023animalmodelsfor pages 24-26)
• Cynomolgus and squirrel monkeys: reproduce portions of respiratory and neurological disease, but vasculitis and brain pathology can be less pronounced than in humans. (pigeaud2023animalmodelsfor pages 35-36, pigeaud2023animalmodelsfor pages 24-26)

No standard transgenic, knockout, humanized, zebrafish, Drosophila, yeast, organoid, or iPSC model has supplanted challenge models. Model outcomes depend strongly on viral strain, dose, route, and age, so cross-study efficacy comparisons require standardized challenge stocks and endpoints.

Evidence limitations and authoritative interpretation

The evidence base is constrained by small, unpredictable outbreaks, limited access to acute specimens, BSL-4 requirements, nonrandomized compassionate treatment, and heterogeneous case definitions. Consequently, outbreak CFRs should retain year/location provenance; animal protection must not be presented as demonstrated human efficacy; and host entry genes must not be misclassified as causal germline genes. The 2024 systematic review’s abstract accurately summarizes the central development gap: many countermeasures protect animals, but only a small number have entered human trials. (tan2024asystematicreview pages 1-2, chan2024nipahvirustherapeutics pages 4-6)

Key recent sources and URLs

1. Tan FH et al. A systematic review on Nipah virus: global molecular epidemiology and medical countermeasures development. Virus Evolution. Published July 2024. https://doi.org/10.1093/ve/veae048. (tan2024asystematicreview pages 1-2)
2. Hassan MZ et al. Nipah virus disease: what can we do to improve patient care? Lancet Infectious Diseases. Published July 2024. https://doi.org/10.1016/S1473-3099(23)00707-7. (hassan2024nipahvirusdisease pages 11-14)
3. Faus-Cotino J et al. Nipah Virus: A Multidimensional Update. Viruses. Published January 2024. https://doi.org/10.3390/v16020179. (fauscotino2024nipahvirusa pages 3-5, fauscotino2024nipahvirusa pages 7-9)
4. Anish TS et al. Pandemic potential of the Nipah virus and public health strategies adopted during outbreaks. PLOS Global Public Health. Published December 2024. https://doi.org/10.1371/journal.pgph.0003926. (anish2024pandemicpotentialof pages 1-2)
5. Pigeaud DD et al. Animal Models for Henipavirus Research. Viruses. Published September 2023. https://doi.org/10.3390/v15101980. (pigeaud2023animalmodelsfor pages 34-35)
6. Chan XHS et al. Nipah Virus Therapeutics: A Systematic Review to Support Prioritisation for Clinical Trials. medRxiv preprint, posted March 2024. https://doi.org/10.1101/2024.03.11.24304091. Its recommendations require the additional caution appropriate to a preprint. (chan2024nipahvirustherapeutics pages 1-4)

References

1. (hassan2024nipahvirusdisease pages 11-14): Md Zakiul Hassan, Tahmina Shirin, Syed M Satter, Mohammed Z Rahman, Josephine Bourner, Ashleigh Cheyne, Els Torreele, Peter Horby, and Piero Olliaro. Nipah virus disease: what can we do to improve patient care? Jul 2024. URL: https://doi.org/10.1016/s1473-3099(23)00707-7, doi:10.1016/s1473-3099(23)00707-7. This article has 26 citations and is from a highest quality peer-reviewed journal.

2. (hassan2024nipahvirusdisease pages 9-11): Md Zakiul Hassan, Tahmina Shirin, Syed M Satter, Mohammed Z Rahman, Josephine Bourner, Ashleigh Cheyne, Els Torreele, Peter Horby, and Piero Olliaro. Nipah virus disease: what can we do to improve patient care? Jul 2024. URL: https://doi.org/10.1016/s1473-3099(23)00707-7, doi:10.1016/s1473-3099(23)00707-7. This article has 26 citations and is from a highest quality peer-reviewed journal.

3. (fauscotino2024nipahvirusa pages 3-5): Javier Faus-Cotino, Gabriel Reina, and Javier Pueyo. Nipah virus: a multidimensional update. Viruses, 16:179, Jan 2024. URL: https://doi.org/10.3390/v16020179, doi:10.3390/v16020179. This article has 46 citations.

4. (fauscotino2024nipahvirusa pages 7-9): Javier Faus-Cotino, Gabriel Reina, and Javier Pueyo. Nipah virus: a multidimensional update. Viruses, 16:179, Jan 2024. URL: https://doi.org/10.3390/v16020179, doi:10.3390/v16020179. This article has 46 citations.

5. (chan2024nipahvirustherapeutics pages 12-14): Xin Hui S Chan, Ilsa L Haeusler, Bennett J K Choy, Md Zakiul Hassan, Junko Takata, Tara P Hurst, Luke M Jones, Shanghavie Loganathan, Elinor Harriss, Jake Dunning, Joel Tarning, Miles W Carroll, Peter W Horby, and Piero L Olliaro. Nipah virus therapeutics: a systematic review to support prioritisation for clinical trials. MedRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.11.24304091, doi:10.1101/2024.03.11.24304091. This article has 4 citations.

6. (NCT05178901 chunk 1): A Phase 1 Study to Evaluate Safety & Immunogenicity of RVSV-Nipah Virus Vaccine Candidate PHV02 in Healthy Adult Subjects. Public Health Vaccines LLC. 2022. ClinicalTrials.gov Identifier: NCT05178901

7. (NCT04199169 chunk 1): Safety and Immunogenicity of a Nipah Virus Vaccine. Auro Vaccines LLC. 2020. ClinicalTrials.gov Identifier: NCT04199169

8. (NCT05398796 chunk 1): Dose Escalation, Open-Label Clinical Trial to Evaluate Safety, Tolerability and Immunogenicity of a Nipah Virus (NiV) mRNA Vaccine, mRNA-1215, in Healthy Adults. National Institute of Allergy and Infectious Diseases (NIAID). 2022. ClinicalTrials.gov Identifier: NCT05398796

9. (tan2024asystematicreview pages 1-2): Foo Hou Tan, Asif Sukri, Nuryana Idris, Kien Chai Ong, Jie Ping Schee, Chong Tin Tan, Soon Hao Tan, Kum Thong Wong, Li Ping Wong, Kok Keng Tee, and Li-Yen Chang. A systematic review on nipah virus: global molecular epidemiology and medical countermeasures development. Virus Evolution, Jul 2024. URL: https://doi.org/10.1093/ve/veae048, doi:10.1093/ve/veae048. This article has 38 citations and is from a peer-reviewed journal.

10. (anish2024pandemicpotentialof pages 2-3): Thekkumkara Surendran Anish, Reghukumar Aravind, Chandni Radhakrishnan, Nivedita Gupta, Pragya D. Yadav, Jerin Jose Cherian, Rima Sahay, Shubin Chenayil, Anoop Kumar A. S., Anitha Puduvail Moorkoth, Ashadevi, Velichapat Ramakrishnan Lathika, Shamsudeen Moideen, Sekhar Lukose Kuriakose, Kalathil Joseph Reena, and Thomas Mathew. Pandemic potential of the nipah virus and public health strategies adopted during outbreaks: lessons from kerala, india. PLOS Global Public Health, 4:e0003926, Dec 2024. URL: https://doi.org/10.1371/journal.pgph.0003926, doi:10.1371/journal.pgph.0003926. This article has 26 citations and is from a peer-reviewed journal.

11. (NCT01811784 chunk 1): Community Intervention to Prevent Nipah Spillover. International Centre for Diarrhoeal Disease Research, Bangladesh. 2012. ClinicalTrials.gov Identifier: NCT01811784

12. (pigeaud2023animalmodelsfor pages 1-2): Declan D. Pigeaud, Thomas W. Geisbert, and Courtney Woolsey. Animal models for henipavirus research. Viruses, 15:1980, Sep 2023. URL: https://doi.org/10.3390/v15101980, doi:10.3390/v15101980. This article has 40 citations.

13. (rahman2024riskevaluationand pages 3-4): Md. Ashrafur Rahman, Yeasna Shanjana, Sydney Cronmiller, Donovan Zong, Rob Davis, Julianne Ernest, Jonah Nguyen, Amanda Rawa, Marie Roke Thomas, and Md. Rabiul Islam. Risk evaluation and mitigation strategies for potential outbreaks of nipah virus infection: evidenced by the recent incidences in southeast asian countries. Health Science Reports, Dec 2024. URL: https://doi.org/10.1002/hsr2.70239, doi:10.1002/hsr2.70239. This article has 4 citations and is from a peer-reviewed journal.

14. (chan2024nipahvirustherapeutics pages 1-4): Xin Hui S Chan, Ilsa L Haeusler, Bennett J K Choy, Md Zakiul Hassan, Junko Takata, Tara P Hurst, Luke M Jones, Shanghavie Loganathan, Elinor Harriss, Jake Dunning, Joel Tarning, Miles W Carroll, Peter W Horby, and Piero L Olliaro. Nipah virus therapeutics: a systematic review to support prioritisation for clinical trials. MedRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.11.24304091, doi:10.1101/2024.03.11.24304091. This article has 4 citations.

15. (saha2024recentadvancesof pages 6-7): Sagnik Saha, Manojit Bhattacharya, Sang-Soo Lee, and Chiranjib Chakraborty. Recent advances of nipah virus disease: pathobiology to treatment and vaccine advancement. Journal of microbiology, 62:811-828, Sep 2024. URL: https://doi.org/10.1007/s12275-024-00168-3, doi:10.1007/s12275-024-00168-3. This article has 8 citations and is from a peer-reviewed journal.

16. (brown2023immunopathogenesisofnipah pages 5-7): Brent Brown, Tanya Gravier, Ingo Fricke, Suhaila A. Al-Sheboul, Theodor-Nicolae Carp, Chiuan Yee Leow, Chinua Imarogbe, and Javad Arabpour. Immunopathogenesis of nipah virus infection and associated immune responses. Immuno, 3:160-181, Apr 2023. URL: https://doi.org/10.3390/immuno3020011, doi:10.3390/immuno3020011. This article has 19 citations.

17. (anish2024pandemicpotentialof pages 9-10): Thekkumkara Surendran Anish, Reghukumar Aravind, Chandni Radhakrishnan, Nivedita Gupta, Pragya D. Yadav, Jerin Jose Cherian, Rima Sahay, Shubin Chenayil, Anoop Kumar A. S., Anitha Puduvail Moorkoth, Ashadevi, Velichapat Ramakrishnan Lathika, Shamsudeen Moideen, Sekhar Lukose Kuriakose, Kalathil Joseph Reena, and Thomas Mathew. Pandemic potential of the nipah virus and public health strategies adopted during outbreaks: lessons from kerala, india. PLOS Global Public Health, 4:e0003926, Dec 2024. URL: https://doi.org/10.1371/journal.pgph.0003926, doi:10.1371/journal.pgph.0003926. This article has 26 citations and is from a peer-reviewed journal.

18. (chan2024nipahvirustherapeutics pages 4-6): Xin Hui S Chan, Ilsa L Haeusler, Bennett J K Choy, Md Zakiul Hassan, Junko Takata, Tara P Hurst, Luke M Jones, Shanghavie Loganathan, Elinor Harriss, Jake Dunning, Joel Tarning, Miles W Carroll, Peter W Horby, and Piero L Olliaro. Nipah virus therapeutics: a systematic review to support prioritisation for clinical trials. MedRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.11.24304091, doi:10.1101/2024.03.11.24304091. This article has 4 citations.

19. (NCT01811784 chunk 2): Community Intervention to Prevent Nipah Spillover. International Centre for Diarrhoeal Disease Research, Bangladesh. 2012. ClinicalTrials.gov Identifier: NCT01811784

20. (anish2024pandemicpotentialof pages 1-2): Thekkumkara Surendran Anish, Reghukumar Aravind, Chandni Radhakrishnan, Nivedita Gupta, Pragya D. Yadav, Jerin Jose Cherian, Rima Sahay, Shubin Chenayil, Anoop Kumar A. S., Anitha Puduvail Moorkoth, Ashadevi, Velichapat Ramakrishnan Lathika, Shamsudeen Moideen, Sekhar Lukose Kuriakose, Kalathil Joseph Reena, and Thomas Mathew. Pandemic potential of the nipah virus and public health strategies adopted during outbreaks: lessons from kerala, india. PLOS Global Public Health, 4:e0003926, Dec 2024. URL: https://doi.org/10.1371/journal.pgph.0003926, doi:10.1371/journal.pgph.0003926. This article has 26 citations and is from a peer-reviewed journal.

21. (NCT06221813 chunk 1): Study to Evaluate Safety and Immunogenicity of a Prime-Boost Regimen of rVSV-Nipah Virus Vaccine Candidate PHV02 in Healthy Adult Subjects. Public Health Vaccines LLC. 2024. ClinicalTrials.gov Identifier: NCT06221813

22. (pigeaud2023animalmodelsfor pages 34-35): Declan D. Pigeaud, Thomas W. Geisbert, and Courtney Woolsey. Animal models for henipavirus research. Viruses, 15:1980, Sep 2023. URL: https://doi.org/10.3390/v15101980, doi:10.3390/v15101980. This article has 40 citations.

23. (pigeaud2023animalmodelsfor pages 35-36): Declan D. Pigeaud, Thomas W. Geisbert, and Courtney Woolsey. Animal models for henipavirus research. Viruses, 15:1980, Sep 2023. URL: https://doi.org/10.3390/v15101980, doi:10.3390/v15101980. This article has 40 citations.

24. (pigeaud2023animalmodelsfor pages 24-26): Declan D. Pigeaud, Thomas W. Geisbert, and Courtney Woolsey. Animal models for henipavirus research. Viruses, 15:1980, Sep 2023. URL: https://doi.org/10.3390/v15101980, doi:10.3390/v15101980. This article has 40 citations.

25. (pigeaud2023animalmodelsfor pages 2-4): Declan D. Pigeaud, Thomas W. Geisbert, and Courtney Woolsey. Animal models for henipavirus research. Viruses, 15:1980, Sep 2023. URL: https://doi.org/10.3390/v15101980, doi:10.3390/v15101980. This article has 40 citations.

26. (chan2024nipahvirustherapeutics pages 6-8): Xin Hui S Chan, Ilsa L Haeusler, Bennett J K Choy, Md Zakiul Hassan, Junko Takata, Tara P Hurst, Luke M Jones, Shanghavie Loganathan, Elinor Harriss, Jake Dunning, Joel Tarning, Miles W Carroll, Peter W Horby, and Piero L Olliaro. Nipah virus therapeutics: a systematic review to support prioritisation for clinical trials. MedRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.11.24304091, doi:10.1101/2024.03.11.24304091. This article has 4 citations.

27. (kallon2024therapeuticadvancementin pages 6-7): Mary K. Kallon, Daniel Maada Mami, Emmanuel Tom Mami, Mariam Romba, M. Patrick Andrew, and M. Sylvester Martain. Therapeutic advancement in treatment and prevention of nipah viral infection: a review. Asian Journal of Research in Infectious Diseases, 15:51-65, Apr 2024. URL: https://doi.org/10.9734/ajrid/2024/v15i4343, doi:10.9734/ajrid/2024/v15i4343. This article has 5 citations.

28. (NCT05398796 chunk 2): Dose Escalation, Open-Label Clinical Trial to Evaluate Safety, Tolerability and Immunogenicity of a Nipah Virus (NiV) mRNA Vaccine, mRNA-1215, in Healthy Adults. National Institute of Allergy and Infectious Diseases (NIAID). 2022. ClinicalTrials.gov Identifier: NCT05398796

29. (mishra2024advancementsinnipah pages 11-12): Gayatree Mishra, Vishal Prajapat, and Debasis Nayak. Advancements in nipah virus treatment: analysis of current progress in vaccines, antivirals, and therapeutics. Immunology, 171:155-169, Sep 2024. URL: https://doi.org/10.1111/imm.13695, doi:10.1111/imm.13695. This article has 78 citations and is from a peer-reviewed journal.

Artifacts

• Edison artifact artifact-00