Rift Valley Fever — Disease Characteristics Research Report

Target: Rift Valley Fever (RVF) · MONDO:0017880 · Category: Infectious · Synonym: RVF Causal agent (not a host gene): Rift Valley fever virus (RVFV) — an enveloped, tri‑segmented, negative‑/ambisense ssRNA virus, genus Phlebovirus (now Phlebovirus riftense), family Phenuiviridae, order Bunyavirales (NCBITaxon:11588). RVF is a zoonotic arboviral disease, not a Mendelian disorder; it has no causal human gene. The "causal gene(s): not recorded / OMIM: not recorded" fields in the template are therefore expected and correct — the pathogenesis is driven by the viral genome, whose S‑segment NSs protein is the principal virulence determinant.

A well‑curated dismech entry already exists (kb/disorders/Rift_Valley_Fever.yaml); this report is organized to validate and extend it.

1. Disease Information

RVF is a mosquito‑borne, zoonotic viral disease primarily of domestic ruminants (sheep, cattle, goats) in Africa and the Arabian Peninsula, with humans infected as epizootic spillover hosts. In animals it causes "abortion storms" and high neonatal mortality; in humans the great majority of infections are a self‑limiting febrile illness, with a minority progressing to one of three severe syndromes: (i) viral hemorrhagic fever with hepatic necrosis, (ii) delayed retinitis, and (iii) meningoencephalitis (Ikegami & Makino, Viruses 2011, PMID 21666766; Bird et al., JAVMA 2009, PMID 19335238).

Key identifiers: MONDO:0017880; ICD‑11 1D49 (Rift Valley fever); ICD‑10 A92.4; MeSH D012295 ("Rift Valley Fever"); the agent is NCBITaxon:11588. There is no OMIM entry (not a heritable human disorder). Synonyms/alternative names: RVF; enzootic hepatitis (historical, in livestock).

Data provenance: Information is derived from aggregated, disease‑level resources — outbreak investigations, hospital case series, serosurveys, WHO/CDC/OIE (WOAH) surveillance, and virological reviews — not individual‑patient EHR records.

2. Etiology

Disease causal factor — infectious. The sole cause is infection with RVFV. Transmission to humans is by (a) bites of infected mosquitoes — floodwater Aedes spp. (notably Aedes mcintoshi/ochraceus), which maintain the virus transovarially in desiccation‑resistant eggs and are the presumed reservoir, and Culex spp. (e.g. Cx. pipiens, Cx. tritaeniorhynchus), which amplify epidemics; and (b) direct contact with blood, body fluids, tissues, and aborted fetal material of viraemic livestock during slaughter, butchering, birthing, and veterinary handling, including aerosol exposure (Pepin et al., Vet Res 2010, PMID 21188836; Linthicum et al., Annu Rev Entomol 2016, PMID 26497313).

Environmental / behavioural risk factors (the dominant axis for this disease): - Heavy rainfall and flooding (El Niño/Southern Oscillation–linked) that flood dambo habitats and produce explosive mosquito emergence — the single strongest epidemic driver; satellite NDVI/rainfall anomalies can predict outbreaks (Anyamba et al., PNAS 2009, PMID 19144928; Linthicum et al., Science 1999, PMID 10411503). - Occupational contact with livestock — herders, pastoralists, abattoir/slaughterhouse workers, veterinarians (identified as risk factors in the Kenya 2006–07 investigation: "Of these, 52 (26%) had severe RVF disease characterized by hemorrhagic manifestations or death" — Anyangu et al., Am J Trop Med Hyg 2010, PMID 20682902). - Consumption/handling of sick animals; drinking raw milk; sheltering animals in the home. - Male sex and adult age (occupational exposure pattern).

Protective factors: Avoidance of contact with viraemic animal tissues, personal protective equipment at slaughter, vector avoidance, and livestock vaccination (indirect human protection by suppressing amplification). No human protective genetic variant is established. There is biological rationale (and mouse/in‑vitro data) that an intact type I interferon response is protective, since the viral NSs protein exists specifically to defeat it, but a validated human genetic protective locus is not available.

Gene–environment interactions: Not applicable in the human‑Mendelian sense. The relevant "G×E" is viral‑genotype × ecological: NSs/NSm virulence determinants interacting with vector ecology and rainfall.

3. Phenotypes

Human RVF is clinically staged: a common self‑limiting febrile phase, and uncommon severe syndromes. Severe disease affects roughly 1–3% of infections in population terms (up to ~8% attack rates reported), but hospital series are heavily biased toward severe cases.

Severity / progression characteristics: Onset is acute after a short incubation of ~2–6 days (range up to ~1 week). Most patients recover in 4–7 days. The three severe syndromes are largely temporally distinct: the hemorrhagic‑hepatic form appears 2–4 days into illness; retinitis is delayed 1–3 weeks and often follows apparent recovery; encephalitis can accompany a second febrile phase. Macular retinitis is the leading cause of permanent morbidity in survivors.

Supporting quotes (verified): Al‑Hazmi et al. (Saudi Arabia 2000, prospective series of 165 hospitalized patients): "Sixteen patients had retinitis and 7 patients had meningoencephalitis" (Clin Infect Dis 2003, PMID 12539063); overall in that series 56/165 (33.9%) died and hemorrhagic manifestations occurred in 32 (19.4%).

Quality‑of‑life impact: Dominated by permanent visual impairment from macular/paramacular retinitis (central scotoma), and by neurological sequelae in encephalitic survivors (focal deficits, cognitive impairment). No disease‑specific EQ‑5D/SF‑36 instrument is established for RVF; impact is reported qualitatively in case series.

4. Genetic / Molecular Information

No human causal or susceptibility gene is established (no OMIM, no ClinVar/HGMD entries — expected for an arboviral zoonosis). The relevant genetics is viral:

• Genome: three negative‑sense/ambisense RNA segments. L encodes the RdRp (L protein); M encodes a polyprotein yielding the glycoproteins Gn and Gc plus the non‑structural NSm and a 78‑kDa protein; S uses an ambisense strategy to encode the nucleoprotein (N) and the non‑structural NSs (Bouloy & Weber, Open Virol J 2010, PMID 20517490; Ikegami & Makino 2011, PMID 21666766).
• NSs — principal virulence factor (analogous to a viral "oncogene‑like" effector). It forms nuclear filaments and defeats innate immunity by three documented mechanisms:
• Suppression of host general transcription by sequestering the p44/TFIIH subunit and degrading TFIIH p62 → shutoff of interferon‑β induction (Le May et al., Cell 2004, PMID 14980221; Billecocq et al., J Virol 2004, PMID 15479799).
• Promoting post‑transcriptional degradation of PKR (dsRNA‑activated protein kinase), relieving translational block (Ikegami et al., PLoS Pathog 2009, PMID 19197350; Habjan et al., J Virol 2009, PMID 19570864).
• Downregulation of IFN‑β at the promoter level via repression of the host SAP30/YY1 complex.
• NSm is anti‑apoptotic and supports vector infection; deletion attenuates (Won et al., J Virol 2007, PMID 17596309).
• Attenuating viral variants: the naturally attenuated Clone 13 carries a large in‑frame deletion in the NSs ORF (Muller et al., Am J Trop Med Hyg 1995, PMID 7872449) — the molecular basis of a leading veterinary vaccine.

Functional consequence: NSs is a gain‑of‑virulence / immune‑antagonist; its loss (Clone 13, MP‑12 partially) is loss‑of‑function → attenuation. Modeled in dismech as pathway‑state modifier: DECREASED on type I IFN induction (GO:0032480), which is correct — there is no host variant to carry functional_impact_category.

Epigenetics / chromosomal abnormalities: Not applicable (host). RVFV biology is RNA‑segment‑based; reassortment between co‑infecting strains is the principal source of genetic novelty (analogous to influenza), documented in field isolates.

5. Environmental Information

• Climatic: Excess rainfall/flooding (ENSO‑linked), elevated NDVI, and dambo/pan flooding drive mosquito emergence and epizootics (Anyamba et al., PNAS 2009, PMID 19144928).
• Ecological/agricultural: Irrigation schemes and dam construction (e.g. the 1987 Mauritania outbreak after the Diama dam on the Senegal River) create permanent vector habitat.
• Occupational/lifestyle: Livestock husbandry, slaughter, and consumption/handling of sick animals (Section 2).
• Infectious agent (CHEBI/NCBITaxon): RVFV, NCBITaxon:11588. Vectors: Aedes spp. and Culex spp. (Culicidae). Amplifying hosts: Bovidae (NCBITaxon:9895), especially Ovis aries (NCBITaxon:9940), Bos taurus (NCBITaxon:9913), Capra hircus (NCBITaxon:9925).

Suggested exposure terms (ECTO): exposure via mosquito bite; occupational exposure to animal blood/tissue; aerosol exposure. (Verify exact ECTO CURIEs at binding time per dismech-terms — do not bind from memory.)

6. Mechanism / Pathophysiology

Ordered causal chain

1. Inoculation of RVFV (mosquito bite or mucocutaneous/aerosol contact with viraemic tissue) → leads to local replication in dermal/regional cells.
2. Viral replication → leads to expression of NSs, which suppresses host transcription and type I IFN induction and degrades PKR (demonstrated in vitro and in mouse models; PMID 14980221, 19197350).
3. Defeat of the interferon response → results in uncontrolled early replication and high‑titre viraemia with hepatotropic dissemination (viraemia magnitude correlates with severity — inferred correlation from human/animal data).
4. Viraemia → leads to preferential infection of hepatocytes and Kupffer cells, producing midzonal→massive hepatic necrosis (the pathological hallmark of fatal RVF).
5. Branch 4a (hepatic): Hepatocellular necrosis → results in release of transaminases and impaired synthesis of clotting factors, and → leads to jaundice.
6. Branch 4b (vascular): Systemic infection + cytokine response → leads to endothelial activation and increased vascular permeability (the rate‑limiting lesion shared with other viral hemorrhagic fevers).
7. Impaired hepatic factor synthesis + endothelial injury + platelet consumption → results in consumptive coagulopathy / DIC → thrombocytopenia and hemorrhage → multi‑organ failure and death in the severe hemorrhagic form.
8. Delayed branch (ocular): 1–3 weeks after the acute phase, a largely immune‑mediated retinitis (vasculitis, retinal hemorrhage, macular edema) develops → leads to permanent vision loss when the macula scars. (Immune‑mediated mechanism is inferred from its post‑viraemic timing, not demonstrated by biopsy.)
9. Delayed branch (neurological): days–weeks later, neuroinvasion produces meningoencephalitis → encephalitis with headache, confusion, focal deficits.

Supporting detail by category

• Molecular pathways: RIG‑I/MAVS → IRF3/IRF7 → IFN‑β induction (antagonized by NSs); PKR–eIF2α translational control (antagonized); JAK‑STAT ISG signaling (blunted downstream of IFN suppression). GO: GO:0032480 (negative regulation of type I IFN production), GO:0019079 (viral genome replication), GO:0039548 (suppression by virus of host IRF3 activity, conceptually), GO:0060337 (type I interferon signaling pathway).
• Cellular processes: hepatocyte apoptosis/necrosis (GO:0097284 hepatocyte apoptotic process), endothelial activation, inflammation/cytokinemia, neuronal infection.
• Protein dysfunction: NSs‑driven degradation of TFIIH p62 and PKR; glycoprotein Gn/Gc mediate entry (receptor candidates include LRP1, DC‑SIGN for dendritic cells — Ganaie et al., Cell 2021, PMID 34320407 identified LRP1 as an RVFV entry receptor).
• Tissue damage mechanisms: direct viral cytopathology (liver), immunopathology (retina), vascular leak and DIC (hemostatic failure).
• Cell types (CL): hepatocyte CL:0000182; Kupffer cell CL:0000091; endothelial cell CL:0000115; dendritic cell CL:0000451; neuron CL:0000540.

Molecular profiling

Transcriptomic/proteomic data exist largely from animal models and cell lines (mouse, rat, NHP challenge; GEO deposits for RVFV‑infected hepatocytes/macrophages). Human multi‑omics is limited by the sporadic, outbreak‑based nature of cases. CRISPR screens identified host entry/replication factors including LRP1 (PMID 34320407). Note evidence‑source discipline: these are predominantly MODEL_ORGANISM / IN_VITRO, not human clinical.

7. Anatomical Structures Affected

• Primary organ: Liver (UBERON:0002107) — hepatocytes and Kupffer cells; the principal target in fatal disease.
• Vascular system / blood (UBERON:0000178; endothelium UBERON:0001986) — the hemostatic/vascular lesion.
• Eye / retina (UBERON:0000970 eye; UBERON:0000966 retina; macula UBERON:0004862) — delayed retinitis, typically bilateral but can be asymmetric; macular involvement causes permanent loss.
• Central nervous system / brain (UBERON:0000955; meninges UBERON:0002360) — meningoencephalitis.
• Spleen (UBERON:0002106) — replication site.
• Body systems: hepatobiliary, cardiovascular/hematologic, nervous, ocular.
• Subcellular (GO CC): viral replication is cytoplasmic; NSs filaments are nuclear (GO:0005634 nucleus) — a distinctive feature; Golgi (GO:0005794) for glycoprotein maturation and budding.

8. Temporal Development

• Incubation: ~2–6 days (up to ~1 week) after exposure.
• Onset: acute.
• Course: Most cases are self‑limited (recovery ~4–7 days). Severe syndromes follow distinct windows: hemorrhagic‑hepatic at day 2–4; retinitis at 1–3 weeks (often after apparent recovery); encephalitis days–weeks later, sometimes as a biphasic fever.
• Critical period for intervention: the early viraemic phase (supportive escalation, isolation); there is no licensed antiviral, so timing is about supportive intensity and complication surveillance (serial ophthalmologic and neurological evaluation).
• Epidemic tempo at population level: explosive, rainfall‑driven epizootic/epidemic peaks over weeks to a few months, then quiescence (inter‑epidemic maintenance in Aedes eggs).

9. Inheritance and Population

Not genetic — no inheritance pattern, penetrance, carrier frequency, founder effect, or consanguinity role applies.

Epidemiology: - Geographic distribution: sub‑Saharan and North Africa, Madagascar, Egypt, and the Arabian Peninsula (Saudi Arabia/Yemen since 2000 — the first spread outside Africa). Repeated large outbreaks: Egypt 1977–78; Kenya 1997–98 and 2006–2007; Saudi Arabia/Yemen 2000; Mauritania (recurrent, incl. 2010, 2015, 2020); Mayotte; Niger 2016; Mauritania/Mali. - Human burden is epidemic, not steady‑endemic. During the Kenya 2006–07 outbreak WHO reported, verbatim: "From 30 November 2006 to 12 March 2007, a total of 684 cases including 155 deaths (case‑fatality ratio, 23%) of RVF was reported in Kenya." (WHO DON, 2007). - Case‑fatality: community‑/population‑wide ~0.5–2%; hospitalized/severe series much higher (e.g. Saudi Arabia 2000 series 33.9%; Kenya 2006–07 ~23%; Tanzania 2007 ~28%; Mauritania 2022 letter ~49%). Large serosurveys imply up to ~180,000 mild/asymptomatic infections in the Kenya outbreak region, confirming the hospitalized CFR is upward‑biased (Nguku et al., Am J Trop Med Hyg 2010, PMID 20682901). - Demographics: higher incidence in adult males reflecting occupational animal contact; no ethnic genetic predisposition.

10. Diagnostics

• Molecular: RT‑PCR / real‑time RT‑PCR on serum during the viraemic phase — the mainstay of early confirmation (Bird et al., J Clin Microbiol 2007, PMID 17913929 describes a diagnostic RT‑PCR assay).
• Serology: IgM capture ELISA (recent infection) and IgG ELISA / seroconversion; plaque‑reduction neutralization (PRNT) as reference. Antigen‑detection ELISA is used in animals.
• Virus isolation: possible in BSL‑3+ settings from serum/tissue (RVFV is a high‑containment select agent; isolation is restricted to appropriately biosafe laboratories).
• Supportive laboratory findings: elevated AST/ALT (often markedly), thrombocytopenia, leukopenia then leukocytosis, coagulopathy (prolonged PT/aPTT, elevated D‑dimer, DIC), hyperbilirubinemia; LOINC‑codable analytes (ALT, AST, platelet count, PT, fibrinogen, bilirubin).
• Histopathology: hepatic midzonal necrosis with Councilman‑like acidophilic bodies and minimal inflammatory infiltrate; immunohistochemistry/IHC for viral antigen.
• Imaging/functional: ophthalmologic exam and fluorescein angiography/OCT for retinitis; neuroimaging/EEG and CSF analysis (lymphocytic pleocytosis) for encephalitis.
• Clinical criteria / case definition: WHO/CDC outbreak case definitions combine acute febrile illness in an epizootic setting with laboratory confirmation.
• Differential diagnosis: other viral hemorrhagic fevers (Crimean‑Congo HF, Ebola/Marburg, yellow fever, dengue), leptospirosis, severe malaria, Q fever, brucellosis, typhoid, viral hepatitis.

11. Outcome / Prognosis

• Mild/uncomplicated RVF: full recovery in days; excellent prognosis.
• Hemorrhagic‑hepatic form: high mortality (hospital series 10–50%); death from hepatic failure, hemorrhage, DIC, and multi‑organ failure.
• Ocular form: often permanent central vision loss when the macula is involved; ~50% of patients with macular retinitis retain a permanent deficit. Rarely fatal.
• Encephalitic form: significant mortality and frequent neurological sequelae in survivors.
• Prognostic factors: magnitude/duration of viraemia, degree of transaminase elevation, thrombocytopenia/DIC, presence of hemorrhage, encephalopathy, and hepatorenal failure predict death (Kenya and Saudi series). No validated molecular prognostic biomarker beyond viral load and hepatic/hemostatic markers.

12. Treatment

• No licensed specific human antiviral or therapeutic. Management is supportive (NCIT:C15747 Supportive Care): fluid/electrolyte management, correction of coagulopathy, transfusion support, organ‑failure management, and management in an appropriate isolation/high‑containment setting for hemorrhagic cases.
• Investigational antivirals: ribavirin has in‑vitro and animal activity but no proven human benefit and raises concern for CNS disease in some models; favipiravir (T‑705) shows activity in rodent models (favipiravir: Caroline et al. / Scharton et al., Antimicrob Agents Chemother 2014, PMID 24395232). These remain experimental.
• Ocular/neurological: corticosteroids are used empirically for severe immune‑mediated retinitis/encephalitis, without controlled‑trial support.
• Vaccines: no licensed human vaccine. Candidates include the inactivated TSI‑GSD‑200 (investigational, used for at‑risk laboratory/veterinary personnel under special protocols), the live‑attenuated MP‑12, and the chimpanzee‑adenovirus‑vectored ChAdOx1 RVF, which has entered early‑phase human trials (Warimwe/Jenner Institute programme). Veterinary vaccines are established and central to control: the live Smithburn strain, the inactivated vaccine, and Clone 13 (NSs‑deletion) and MP‑12.
• Treatment strategy: early recognition in an outbreak, supportive escalation, complication surveillance (serial ophthalmologic/neurologic review), and strict infection control. (NCIT suggestions at binding: C15747 Supportive Care; C15986 Pharmacotherapy only if an agent is used off‑label; C15313 is not applicable.)

13. Prevention

• Primary prevention (the core of RVF control):
• Livestock vaccination ahead of predicted outbreaks (Smithburn / Clone 13 / inactivated) to suppress amplification — the keystone intervention.
• Early warning / forecasting using rainfall and NDVI satellite anomalies to pre‑position response (Anyamba et al., PMID 19144928).
• Vector control (larval source reduction, insecticides) during high‑risk periods; personal protection (repellents, bed nets).
• Safe animal‑handling practices — PPE at slaughter/birthing, avoiding contact with abortus material, avoiding raw milk, and movement restrictions/slaughter bans during epizootics.
• Secondary prevention: outbreak surveillance (sentinel herds, human case detection) and rapid laboratory confirmation for early response.
• Tertiary prevention: complication surveillance and supportive care to limit mortality and permanent sequelae.
• Public health / One Health: integrated human–animal–environment surveillance, abattoir regulation, and community health education; environmental management of irrigation/dam habitats.
• Prophylaxis: investigational human vaccination restricted to high‑risk laboratory and veterinary personnel.

14. Other Species / Natural Disease

• Species affected (natural amplifying/clinical hosts): domestic ruminants are most susceptible — sheep (Ovis aries, NCBITaxon:9940) and goats (Capra hircus, NCBITaxon:9925) most severely, cattle (Bos taurus, NCBITaxon:9913); also camels (Camelus dromedarius). Wild ruminants and rodents show infection/seropositivity; buffalo and some wildlife amplify.
• Natural disease in animals: characteristic "abortion storms" (near‑100% abortion in pregnant ewes) and very high mortality in newborn lambs/kids (often >90%), with hepatic necrosis — more severe than typical human disease. This is of major veterinary and economic importance (Bird et al., JAVMA 2009, PMID 19335238).
• Comparative pathology: liver is the shared primary target across species; neonatal animals and humans both show massive hepatic necrosis, but the abortifacient effect is an animal‑specific hallmark.
• Transmission / zoonotic potential: strongly zoonotic; humans are incidental dead‑end hosts (viraemia insufficient for onward mosquito transmission). Cross‑species susceptibility spans many mammals.
• OMIA: RVF is catalogued as an infectious (non‑Mendelian) condition of livestock rather than an OMIA Mendelian trait.

15. Model Organisms

• Mouse (Mus musculus): the principal small‑animal model; wild‑type mice are highly susceptible, developing early hepatic necrosis and, in survivors, delayed encephalitis — recapitulating the biphasic human severe disease. Type I IFN‑receptor knockout (IFNAR⁻/⁻) mice are uniformly, rapidly susceptible, confirming the IFN axis NSs targets (Bouloy et al., J Virol 2001, PMID 11152510).
• Rat (Rattus norvegicus): strain‑dependent susceptibility (Lewis vs Wistar‑Furth) models hepatic vs encephalitic outcomes.
• Non‑human primates (rhesus macaque, marmoset, common marmoset): model hemorrhagic and febrile disease for vaccine/therapeutic testing.
• Induced/genetic models: the attenuating NSs‑deletion (Clone 13) and MP‑12 reverse‑genetics systems are core tools; recombinant RVFV with NSs/NSm deletions dissect virulence.
• In vitro: hepatocyte and macrophage/dendritic‑cell lines; CRISPR screens (host factor LRP1, PMID 34320407).
• Phenotype recapitulation / limitations: mice over‑recapitulate lethality relative to average human infection; NHP are closest to human disease but scarce; retinitis — the signature human sequela — is poorly modeled in rodents, a key translational gap (relevant to any dismech FAILS_TO_RECAPITULATE / HUMAN_MODEL_MISMATCH annotation for the ocular node).
• Resources: MGI (mouse), RGD (rat), and the RVFV reverse‑genetics literature.

Citation notes and evidence‑discipline flags

• Verified exact quotes (safe to use as dismech snippet: after re‑fetching the source into references_cache/): the WHO Kenya statement ("From 30 November 2006 to 12 March 2007, a total of 684 cases including 155 deaths (case‑fatality ratio, 23%)"); Al‑Hazmi ("Sixteen patients had retinitis and 7 patients had meningoencephalitis", PMID 12539063); Kenya risk‑factor study ("Of these, 52 (26%) had severe RVF disease characterized by hemorrhagic manifestations or death").
• PMIDs cited from the established literature (confirm each with just fetch-reference PMID:… before binding — do not enter a snippet unverified): 21666766 (Ikegami & Makino 2011), 19335238 (Bird 2009), 21188836 (Pepin 2010), 20517490 (Bouloy & Weber 2010), 14980221 (Le May 2004), 19197350 (Ikegami 2009 PKR), 19570864 (Habjan 2009), 12539063 (Al‑Hazmi 2003), 14523773 (Madani 2003), 20682901 / 20682902 (Kenya 2006‑07 series), 19144928 (Anyamba 2009), 10411503 (Linthicum 1999), 34320407 (Ganaie 2021 LRP1), 24395232 (favipiravir), 11152510 (Bouloy 2001 IFNAR mouse), 7872449 (Muller 1995 Clone 13).
• Per‑CLAUDE.md: this is a microbial/infectious entry — on binding, ensure ≥1 NCBITaxon infectious_agent and ≥1 transmission route (already present), and consider conformance to the viral_hemorrhagic_fever_syndrome module (already used for the viraemia and vascular‑leak nodes). Model‑organism evidence (mouse/NHP) must be graded MODEL_ORGANISM and not stand alone for human phenotypes.

Sources (web): - Frontiers in Immunology 2022 — RVFV/host innate immunity review (PMC9813963) - WHO Disease Outbreak News — RVF Kenya 2007 - Nguku et al., Kenya 2006‑07 outbreak investigation (PMC2913492) - Al‑Hazmi et al. 2003, Saudi Arabia series (qxmd/PMID 12539063) - Epidemiologic and clinical aspects of the Tanzania 2007 RVF outbreak (ILRI) - "The challenging management of Rift Valley fever in humans" (Javelle et al.)

This report mirrors and is consistent with the existing kb/disorders/Rift_Valley_Fever.yaml entry; the main extensions beyond the current entry are the ocular/encephalitic timing detail, the LRP1 entry receptor (PMID 34320407), favipiravir/ribavirin investigational status, the vaccine landscape (Clone 13, MP‑12, ChAdOx1 RVF), and the retinitis modeling gap worth recording as a HUMAN_MODEL_MISMATCH.

Reference Validation

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All extracted references resolved successfully.

Term Validation

Checked with linkml-term-validator 0.4.5, through the ols: adapter.

Terms the report names something else

These identifiers resolve, so nothing about them looks wrong, and the ontology calls them something unrelated to what the report calls them. That usually means the identifier is not the one the sentence needs:

• NCBITaxon:11588 (3 mentions) - the report calls it "Bunyavirales"; NCBITaxon calls it Rift Valley fever virus
• UBERON:0002107 (1 mention) - the report calls it "Liver", "Primary organ: Liver"; UBERON calls it liver

Obsolete terms

These terms are real but deprecated. Citing one is not a fabrication; it does mean the report is naming something the ontology has retired:

• HP:0001146 (obsolete Pigmentary retinal degeneration) (1 mention) - replaced by HP:0000580

Terms named inconsistently

The report gives these identifiers more than one name of its own:

• UBERON:0002107 - called "Liver", "Primary organ: Liver"