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Hantavirus infections in humans can lead to two distinct but severe clinical syndromes: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), also known as hantavirus cardiopulmonary syndrome (HCPS). Both diseases are caused by different hantavirus species and are characterized by vascular dysfunction, increased capillary permeability, and thrombocytopenia. The clinical presentation varies significantly depending on the infecting virus species, the geographic region, and host immune factors.
Figure 1. Overview of orthohantavirus pathogenicity and virulence mechanisms. (Khaiboullina et al., 2025)
HFRS is primarily caused by Old World hantaviruses, including Hantaan virus (HTNV), Seoul virus (SEOV), Puumala virus (PUUV), and Dobrava-Belgrade virus (DOBV). The disease is endemic in Asia and Europe, with tens of thousands of cases reported annually. Hantaan virus and Dobrava-Belgrade virus infections tend to produce the most severe forms of HFRS, with case fatality rates of 5 to 15%, while Puumala virus typically causes a milder form known as nephropathia epidemica (NE), with a fatality rate below 1%.
HFRS typically progresses through five distinct clinical phases, each with characteristic symptoms and laboratory findings. The incubation period ranges from 2 to 4 weeks after exposure. Not all patients progress through every phase, and the severity varies widely.
Table 1. Clinical Phases of Hemorrhagic Fever with Renal Syndrome (HFRS)
| Phase | Duration | Key Symptoms | Laboratory Findings |
| Febrile | 3-7 days | High fever, headache, myalgia, abdominal pain, facial flushing | Thrombocytopenia begins; proteinuria |
| Hypotensive | Hours to 2 days | Hypotension, shock, nausea, vomiting, abdominal tenderness | Platelet nadir; rising hematocrit; leukocytosis |
| Oliguric | 3-7 days | Oliguria or anuria, renal failure, hemorrhagic manifestations (petechiae, ecchymosis, hematuria) | Elevated creatinine and BUN; hematuria; proteinuria |
| Diuretic | Days to weeks | Polyuria, fluid and electrolyte imbalances, risk of dehydration | Improving renal function; electrolyte abnormalities |
| Convalescent | Weeks to months | Gradual recovery of renal function, fatigue | Normalizing laboratory values |
Figure 2. Schematic representation of HFRS pathogenesis and immune response dynamics. (Jiang et al., 2023)
The clinical severity of HFRS is influenced by the infecting virus species. Hantaan virus and Dobrava-Belgrade virus cause the most severe forms, with prominent hemorrhagic manifestations, acute kidney injury requiring dialysis, and significant mortality. Seoul virus infections are generally moderate, while Puumala virus causes the mildest form (nephropathia epidemica), characterized by fever, abdominal pain, and transient renal impairment. The primary reservoir host of Puumala virus, Myodes glareolus (the bank vole), is widely distributed across Europe, making PUUV the most common cause of hantavirus disease on the continent.
View more Hantavirus Antigens
HPS, also referred to as hantavirus cardiopulmonary syndrome (HCPS), is primarily caused by New World hantaviruses, including Sin Nombre virus (SNV), Andes virus (ANDV), and several other species found throughout the Americas. HPS is characterized by rapid onset of pulmonary edema, respiratory failure, and cardiogenic shock, with a significantly higher case fatality rate (35 to 50%) compared to HFRS.
Figure 3. Clinical manifestations of HFRS across various nosologic forms. (Tkachenko et al., 2025)
Unlike HFRS, HPS progresses through three main phases with a more rapid and catastrophic clinical course. The disease can advance from initial symptoms to life-threatening respiratory failure within 24 to 48 hours.
Table 2. Clinical Phases of Hantavirus Pulmonary Syndrome (HPS)
| Phase | Duration | Key Symptoms | Clinical Findings |
| Prodromal (Febrile) | 3-6 days | Fever, headache, myalgia, dizziness, chills, gastrointestinal symptoms (nausea, vomiting, diarrhea, abdominal pain) | Non-specific; mimics influenza or gastroenteritis |
| Cardiopulmonary | Hours to days | Dyspnea, tachypnea, cough, hypotension, non-cardiogenic pulmonary edema, cardiogenic shock | Bilateral pulmonary infiltrates; thrombocytopenia; elevated hematocrit; metabolic acidosis |
| Diuretic / Convalescent | Days to weeks | Rapid diuresis, resolving pulmonary edema (in survivors) | Improving oxygenation; hemodynamic stabilization |
Andes virus (ANDV), carried by the reservoir host Oligoryzomys longicaudatus in South America, is unique among hantaviruses for its documented ability to transmit directly between humans. This person-to-person transmission has been observed in Argentina and Chile, particularly among close contacts of infected patients. ANDV-associated HPS has a case fatality rate of approximately 30 to 40%, and outbreaks have been reported in rural communities where human-rodent contact is common.
Despite the different clinical presentations of HFRS and HPS, both syndromes share key pathological features driven by hantavirus-induced vascular dysfunction:
Increased vascular permeability: Hantavirus infection of endothelial cells causes disruption of intercellular junctions, leading to plasma leakage, tissue edema, and hypotension. This is mediated by the interaction of viral glycoproteins with host integrin receptors, particularly beta-3 integrins, on endothelial and platelet surfaces.
Thrombocytopenia: Platelet counts drop significantly during the acute phase of both HFRS and HPS, contributing to hemorrhagic manifestations. The mechanism involves both direct platelet activation by viral glycoproteins and immune-mediated platelet destruction.
Immune-mediated damage: The host immune response plays a central role in disease pathogenesis. CD8+ T cells and cytokine cascades (including TNF-alpha, IL-6, and IFN-gamma) contribute to vascular leakage and tissue damage. The severity of disease correlates more closely with the magnitude of the immune response than with viral load.
Figure 4. Hantavirus-induced immune response and cytokine dysregulation in HFRS pathogenesis. (Jiang et al., 2023)
Several factors influence the severity of hantavirus disease. The infecting virus species is the primary determinant, with HTNV, DOBV, SNV, and ANDV causing more severe disease than PUUV or SEOV. Host genetic factors also play a significant role: specific HLA haplotypes have been associated with increased disease severity, and individuals with certain immune response gene polymorphisms may experience more severe clinical courses. Age is another risk factor, as older patients and those with pre-existing conditions tend to have worse outcomes. Delayed diagnosis and supportive care also contribute to increased mortality.
References
| Target | Cat. No. | Product Name | Size | Species Reactivity | Application | Detection Sample | |
| Hantavirus | DEIABL10 | Mouse Anti-Hantavirus ELISA Kit | 48T 2 | Mouse | Qualitative | Serum | Inquiry |
| DEIA2203 | Human Hantavirus Hantaan ELISA Kit | 96T | Human | Qualitative | Serum | Inquiry | |
| DEIA-JY2451 | Mouse Hantavirus (HV) Antibody ELISA Kit | 96T | Mouse | Qualitative | Serum | Inquiry | |
| DEIA-JY2467 | Rat Hantavirus (HV) Antibody ELISA Kit | 96T | Rat | Qualitative | Serum | Inquiry | |
| DEIA2203L | Human Hantavirus Nucleoprotein (HVNP) IgG/IgM ELISA Kit | 96T | Human | Qualitative | Serum | Inquiry | |
| DEIA-NS2660 | Hantavirus IgG ELISA Kit | 96T | Human | Qualitative | Serum or plasma (citrate or heparin) | Inquiry | |
| DEIA-NS2661 | Hantavirus IgM ELISA Kit | 96T | Human | Qualitative | Serum or plasma (citrate or heparin) | Inquiry | |
| DEIA595 | Hantavirus Dobrava/Hantaan IgG/IgM ELISA Kit | 96T | Human | Qualitative | Human serum | Inquiry | |
| DEIA596 | Hantavirus (Puumala) IgG/IgM ELISA Kit | 96T | Human | Qualitative | Serum | Inquiry |
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