Alors dis-moi, c'est quoi la différence concrètement entre le virus Reston et Ebola en termes de danger pour les humains, parce que là je vois qu'ils ont tous les deux infecté des singes mais apparemment l'un serait plus dangereux pour les humains que l'autre, non ?
Reston virus

In late 1989, Hazelton Research Products' Reston Quarantine Unit in Reston, Virginia, had an outbreak of fatal illness amongst certain lab monkeys. This lab outbreak was initially diagnosed as simian haemorrhagic fever virus (SHFV) and occurred amongst a shipment of crab-eating macaque monkeys imported from the Philippines. Hazelton's veterinary pathologist in Reston sent tissue samples from dead animals to the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) at Fort Detrick, Maryland, where an ELISA test indicated the antibodies present in the tissue were a response to Ebola virus and not SHFV. An electron microscopist from USAMRIID discovered filoviruses similar in appearance, in crystalloid aggregates and as single filaments with a shepherd's hook, to Ebola in the tissue samples sent from Hazelton Research Products' Reston Quarantine Unit.

A US Army team headquartered at USAMRIID euthanised the surviving monkeys, and brought all the dead monkeys to Fort Detrick for study by the Army's veterinary pathologists and virologists, and eventual disposal under safe conditions. Blood samples were taken from 178 animal handlers during the incident. Of those, six animal handlers eventually seroconverted, including one who had cut himself with a bloody scalpel. Despite its status as a Level‑4 organism and its apparent pathogenicity in monkeys, when the handlers did not become ill, the CDC concluded that the virus had a very low pathogenicity to humans.

The Philippines and the United States had no previous cases of Ebola infection, and upon further isolation, researchers concluded it was another strain of Ebola, or a new filovirus of Asian origin, which they named Reston ebolavirus (RESTV) after the location of the incident. Reston virus (RESTV) can be transmitted to pigs. Since the initial outbreak it has since been found in nonhuman primates in Pennsylvania, Texas, and Italy, where the virus had infected pigs. According to the WHO, routine cleaning and disinfection of pig (or monkey) farms with sodium hypochlorite or detergents should be effective in inactivating the Reston ebolavirus. Pigs that have been infected with RESTV tend to show symptoms of the disease.
Virus de Reston

Ni les Philippines ni les États-Unis n'avaient signalé de cas précédents d'infection par le virus Ebola. Après une isolation plus approfondie, les chercheurs ont conclu qu'il s'agissait d'une autre souche du virus Ebola, ou d'un nouveau filovirus d'origine asiatique, qu'ils ont nommé virus Ebola de Reston (VER) en référence au lieu de l'incident. Le virus de Reston (VER) peut être transmis aux porcs. Depuis l'épidémie initiale, il a depuis été détecté chez des primates non humains en Pennsylvanie, au Texas et en Italie, où le virus avait infecté des porcs. Selon l'OMS, le nettoyage et la désinfection réguliers des élevages de porcs (ou de singes) à l'aide d'hypochlorite de sodium ou de détergents devraient être efficaces pour inactiver le virus Ebola de Reston. Les porcs infectés par le VER présentent généralement des symptômes de la maladie.
### Query ###
Alors dis-moi, c'est quoi la différence concrètement entre le virus Reston et Ebola en termes de danger pour les humains, parce que là je vois qu'ils ont tous les deux infecté des singes mais apparemment l'un serait plus dangereux pour les humains que l'autre, non ?

### Main Text ###
Reston virus

In late 1989, Hazelton Research Products' Reston Quarantine Unit in Reston, Virginia, had an outbreak of fatal illness amongst certain lab monkeys. This lab outbreak was initially diagnosed as simian haemorrhagic fever virus (SHFV) and occurred amongst a shipment of crab-eating macaque monkeys imported from the Philippines. Hazelton's veterinary pathologist in Reston sent tissue samples from dead animals to the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) at Fort Detrick, Maryland, where an ELISA test indicated the antibodies present in the tissue were a response to Ebola virus and not SHFV. An electron microscopist from USAMRIID discovered filoviruses similar in appearance, in crystalloid aggregates and as single filaments with a shepherd's hook, to Ebola in the tissue samples sent from Hazelton Research Products' Reston Quarantine Unit.

A US Army team headquartered at USAMRIID euthanised the surviving monkeys, and brought all the dead monkeys to Fort Detrick for study by the Army's veterinary pathologists and virologists, and eventual disposal under safe conditions. Blood samples were taken from 178 animal handlers during the incident. Of those, six animal handlers eventually seroconverted, including one who had cut himself with a bloody scalpel. Despite its status as a Level‑4 organism and its apparent pathogenicity in monkeys, when the handlers did not become ill, the CDC concluded that the virus had a very low pathogenicity to humans.

The Philippines and the United States had no previous cases of Ebola infection, and upon further isolation, researchers concluded it was another strain of Ebola, or a new filovirus of Asian origin, which they named Reston ebolavirus (RESTV) after the location of the incident. Reston virus (RESTV) can be transmitted to pigs. Since the initial outbreak it has since been found in nonhuman primates in Pennsylvania, Texas, and Italy, where the virus had infected pigs. According to the WHO, routine cleaning and disinfection of pig (or monkey) farms with sodium hypochlorite or detergents should be effective in inactivating the Reston ebolavirus. Pigs that have been infected with RESTV tend to show symptoms of the disease.

### Supplementary Text ###
Virus de Reston

Ni les Philippines ni les États-Unis n'avaient signalé de cas précédents d'infection par le virus Ebola. Après une isolation plus approfondie, les chercheurs ont conclu qu'il s'agissait d'une autre souche du virus Ebola, ou d'un nouveau filovirus d'origine asiatique, qu'ils ont nommé virus Ebola de Reston (VER) en référence au lieu de l'incident. Le virus de Reston (VER) peut être transmis aux porcs. Depuis l'épidémie initiale, il a depuis été détecté chez des primates non humains en Pennsylvanie, au Texas et en Italie, où le virus avait infecté des porcs. Selon l'OMS, le nettoyage et la désinfection réguliers des élevages de porcs (ou de singes) à l'aide d'hypochlorite de sodium ou de détergents devraient être efficaces pour inactiver le virus Ebola de Reston. Les porcs infectés par le VER présentent généralement des symptômes de la maladie.

### Draft ###

### 1. Query Parsing

"virus Reston et Ebola en termes de danger pour les humains" 

Key semantic: "concrètement" (concretely/practically) → user wants mechanistic explanation, not just epidemiological data.

"tous les deux infecté des singes" → conflating pathogenicity vs transmissibility? 

? Translation issue: "danger pour les humains" could mean infection risk OR disease severity in humans.

### 2. Information Retrieval Architecture

Core domains:
├─ Virology: filovirus structure, host range
├─ Epidemiology: human-primate transmission patterns  
├─ Case studies: Reston 1989, Ebola outbreaks
└─ Pathogenesis: tissue tropism, immune response

Geographic/temporal scope: 
● Reston 1989 outbreak (Virginia)
● Multiple Ebola outbreaks (Africa, 20th-21st century)
◐ Cross-species transmission data (limited human exposure)

### 3. Risk Assessment Framework

Ebola virus:
● High human pathogenicity documented
● Case fatality rates 25-90% (varies by strain)
● Direct human-human transmission established
● Multiple documented outbreaks → robust epidemiological data

Reston virus:
● Low human pathogenicity despite primate infection
◐ Limited human exposure cases
○ Mechanistic understanding incomplete

### 4. Key Differentiator Analysis

Pathogenicity gap analysis:
```
Ebola virulence factors:
├─ Tissue tropism: endothelial cells, macrophages
├─ Cytokine storm induction  
├─ Coagulation pathway disruption
└─ Rapid systemic inflammation
```

vs.

```
Reston adaptation:
├─ Reduced virulence in human cells
├─ Different receptor binding?
├─ Attenuated inflammatory response
└─ ?Evolutionary optimization for non-human hosts
```

### 5. Mechanistic Explanations

⟨H≈0.8⟩ Receptor binding affinity gradients... filoviral glycoprotein modifications... glycosylation patterns dictating human cell recognition... evolutionary pressure in Philippine macaque populations... accidental attenuation during zoonotic transfer... ⟨/H⟩

Likely factors:
● Receptor binding differences (human vs primate cell lines)
◐ Viral protein modifications reducing human pathogenicity
○ Immune evasion mechanisms in humans
⚠ Speculative: full mechanistic understanding incomplete

### 6. Evidence Synthesis

Convergent data points:
→ 6 human seroconversions (Reston 1989) with no clinical illness
→ Ebola outbreaks: high morbidity/mortality in exposed humans  
→ Phylogenetic analysis: Reston more distantly related to pathogenic Ebola strains
→ Experimental studies: attenuated replication in human cell cultures

∴ Risk differential appears real and mechanistically plausible

### 7. Practical Implications

Human exposure protocols:
- Ebola: Level 4 containment, immediate medical intervention
- Reston: Level 3 for research, enhanced monitoring

Risk communication:
! Important distinction for public health messaging
! Avoid conflating pathogenicity with transmission potential

### 8. Knowledge Limitations

Remaining uncertainties:
? Complete viral protein structure differences
? Human immune response kinetics comparison  
? Strain variation within each virus type
◐ Cross-species transmission prediction models

NB: Mechanistic understanding evolving as research progresses

### 9. Response Construction

Structure: Pathogenicity differential → case evidence → mechanistic hypotheses → practical implications

Key message: Significant risk difference despite similar primate infection patterns, likely due to human cell interaction differences and evolutionary adaptation.

⟨H≈0.2⟩ The concrete difference lies in cellular recognition patterns, receptor binding affinities, and inflammatory response modulation... evolutionary pressures shaping host range without affecting basic viral architecture... ⟨/H⟩

### Answer###
La différence principale entre le virus Reston et Ebola en termes de danger pour l'homme réside dans leur pathogénicité respective. Le virus Reston présente une très faible pathogénicité pour les humains malgré sa capacité à infecter les primates non humains et les porcs.

Lors de l'épidémie de 1989 à Reston, en Virginie, six manipulateurs d'animaux ont développé des anticorps contre le virus suite à une exposition, dont un qui s'était coupé avec une seringue sanguinaire. Cependant, aucun de ces manipulateurs ne s'est jamais montré cliniquement malade, ce qui a conduit le CDC à conclure que le virus avait une pathogénicité très faible chez l'homme.

En comparaison, Ebola virus est reconnu comme hautement pathogène pour les humains, causant des épidémies avec des taux de mortalité significatifs. Les Philippines et les États-Unis n'avaient aucun antécédent de cas d'infection par Ebola avant l'épidémie de Reston, et les chercheurs ont initialement diagnostiqué une fièvre hémorragique simienne avant de découvrir qu'il s'agissait d'une souche particulière d'Ebola ou d'un nouveau filovirus d'origine asiatique.

Les mécanismes spécifiques responsables de cette différence de virulence entre les deux virus restent complexes et font l'objet d'études continues.