Side-by-side comparison
| HFRS | HPS | |
|---|---|---|
| Full name | Hemorrhagic fever with renal syndrome | Hantavirus pulmonary syndrome |
| Geography | Asia, Europe, eastern Russia | Americas — North & South |
| Causative species | Hantaan, Seoul, Puumala, Dobrava-Belgrade | Sin Nombre, Andes, Bayou, Black Creek Canal, Choclo |
| Primary organ | Kidneys, with bleeding diathesis | Lungs, with cardiogenic shock |
| Hallmark symptom | Acute kidney injury + petechial rash | Sudden pulmonary edema |
| Case-fatality ratio | 0.4–15% (depends on species) | 25–40% |
| Antiviral evidence | Ribavirin reduces mortality if given early | Ribavirin not effective; supportive care only |
| Vaccine availability | Inactivated vaccines licensed in China & Korea | No licensed vaccine |
| Person-to-person spread | No | Andes virus only (~12% of cases) |
Why the same virus family causes such different diseases
All hantaviruses share the same basic genome architecture and a similar tropism for endothelial cells. The split between HFRS and HPS reflects which capillary beds the particular species preferentially infects. Old World hantaviruses target renal capillaries, producing kidney injury and the classical hemorrhagic phenotype. New World hantaviruses target pulmonary capillaries, producing the catastrophic pulmonary edema of HPS. Recent research suggests this difference is mediated by host receptor preference and innate-immune evasion strategies.