Hantavirus infection history and symptoms
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Basir Gill, M.B.B.S, M.D.[2] Furqan M M. M.B.B.S[3]
Overview
Hantavirus infection produces two major clinical syndromes: hemorrhagic fever with renal syndrome (HFRS), caused by Old World hantaviruses endemic in Europe and Asia, and hantavirus cardiopulmonary syndrome (HCPS), also called hantavirus pulmonary syndrome (HPS), caused by New World hantaviruses endemic in the Americas.[1] Although HFRS and HCPS are recognized as distinct clinical entities, they share overlapping symptoms, signs, and pathogenic alterations, with increased vascular permeability central to the pathogenesis of both syndromes.[1] The initial symptoms of hantavirus infection may include sudden fever, prostration, myalgia, and abdominal discomfort.[2] Pulmonary and hemorrhagic symptoms may arise in severe disease, and virtually all patients with HCPS and more than half of patients with HFRS have respiratory symptoms such as hypoxia and radiological findings on chest x-rays or CT scans.[1]
History and Symptoms
History
Patients usually present with a history of a flu-like illness. History of rodent or rodent dropping contact may be helpful.[3] Hantavirus infection should be considered in patients who reside in or have recent (5–50 days before symptom onset) travel history to an endemic region, presenting with persistent fever (>48 hours), headache, myalgia, gastrointestinal manifestations (abdominal pain, vomiting, diarrhea), and a marked decrease in platelet count.[1]
Incubation Period
The incubation period ranges from 7 to 39 days in HCPS and 14 to 28 days (up to 6 weeks) in HFRS.[1][4]
Exposure History
Key historical features to elicit include:
Domestic, recreational, or occupational activities in areas with wild rodents (e.g., hiking, camping, agricultural work, opening or cleaning structures such as cabins, sheds, or barns that have been unoccupied by humans but inhabited by rodents)[2][5]
Laboratory or pet rat exposure (particularly for Seoul virus)[1]
In Andes virus (ANDV)-endemic regions, close contact with an infected patient in the previous 40 days (particularly sexual contact or sleeping in the same room) should also be considered a risk factor, as ANDV is the only hantavirus with documented person-to-person transmission[1]
Common Symptoms
The common symptoms of hantavirus infection are:[2]
- Sudden fever
Less Common Symptoms
In severe disease (cardiopulmonary or hemorrhagic fever), hantavirus infection can cause the following symptoms:[2][1]
- Dry cough
- Rapidly increasing dyspnea
- Inflammatory symptoms of the eye
- Acute myopia (found in up to 70% of patients infected with Puumala virus, caused by thickening of the lens)[1][5]
Symptomatic Stages of Hantavirus Cardiopulmonary Syndrome
On the basis of symptoms, hantavirus cardiopulmonary syndrome (HCPS) is divided into the following stages. Approximately one-third of patients do not progress beyond the prodromal phase and enter the convalescent phase directly.[6] More than half of Sin Nombre virus (SNV) and ANDV infections are severe, whereas Choclo virus is associated with a milder form for which less than 10% of patients develop respiratory failure, and shock is rare.[1]
Prodromal or febrile stage (2–7 days): It may include[3][2][1][6]
- Abdominal discomfort (can be intense and confused with acute abdomen)
- Conjunctival injection and retro-ocular pain
- Characteristic absence of upper respiratory tract symptoms (cough, sore throat, nasal congestion) during this phase[6]
- Thrombocytopenia is the key early laboratory finding (80–95% of patients have platelet count <150,000/μL)[6]
Cardiopulmonary phase (2–4 days): Cardiopulmonary failure usually develops within 8–24 hours of onset of this phase.[6] It may include[3][2][1]
- Non-cardiogenic pulmonary edema
- Cardiogenic shock (myocardial depression)
- Most deaths occur within the first 24 hours after hospital admission[1]
Diuretic/Polyuric phase (2–3 days):
- Onset of diuresis
- Clinical improvement
- Rapid reversal of endothelial cell barrier deregulation in survivors[1]
Convalescent phase (months to years):
- Impaired cognitive function
- Reduced midexpiratory flows, increased residual volume, and reduced diffusion capacity are common but resolve in most patients within 3 years[7]
- 61.9% of ANDV survivors report incomplete recovery at 3–6 months; motor dysfunction and palpitations are more frequent in ECMO survivors[8]
Laboratory Findings in HCPS
| Parameter | Finding | Clinical Significance |
|---|---|---|
| CBC / Peripheral blood smear | Thrombocytopenia (platelet count <150,000/μL); leukocytosis with left shift; absence of toxic granulation in neutrophils; immunoblasts >10% of total leukocyte population | Presence of ≥4 of 5 peripheral blood criteria (thrombocytopenia, hemoconcentration, absence of toxic granulation, left shift, immunoblasts >10%) has a sensitivity of 96% and specificity of 99% for hantavirus infection[1][6] |
| Hematocrit / Hemoglobin | Hemoconcentration (hematocrit >50% in men, >48% in women) | Reflects plasma leakage; elevated hematocrit is a prognostic marker for severity[1] |
| Creatinine / Liver enzymes | Mild elevation of plasma creatinine and transaminases; increased lactate dehydrogenase (LDH) | Renal involvement can also occur in HCPS[1] |
| Electrolytes | Hyponatremia | Common finding during the cardiopulmonary phase[1] |
| Urinalysis | Proteinuria | Positive quantitative proteinuria at hospital admission has been linked to mortality[1] |
| Platelet count (prognostic) | >115,000/μL at admission: lower risk of severe HCPS; <40,000/μL: increased mortality | Useful for risk stratification at presentation[1] |
Imaging Findings in HCPS
Chest radiograph: Usually normal during the prodrome; bilateral infiltrates develop rapidly with a mixed interstitial and alveolar pattern, and pleural effusions in the cardiopulmonary phase[1]
CT chest: Marked bilateral septal thickening, ground-glass opacities, and pleural effusions[1]
Symptomatic Stages of Hantavirus Hemorrhagic Fever with Renal Syndrome
On the basis of symptoms, hemorrhagic fever with renal syndrome (HFRS) caused by hantavirus infection has classically been divided into five stages. However, the course and severity of infection varies among individuals and hantavirus type; in milder cases (e.g., nephropathia epidemica caused by Puumala virus), the clinical phases may be less identifiable or may overlap. In the majority of patients, the classic clinical distinction into five phases is unclear.[1][9] Among confirmed HFRS cases in Europe, between 30% and 50% are hospitalized, often due to severe symptoms or suspicion of bacterial infection.[1]
Febrile phase (~7 days): It may include[2][10][11][1]
- Abdominal discomfort and back pain
- Conjunctival injection and facial flushing
Hypotensive/Hemorrhagic phase (1–2 days): It may include[1][11]
- Flushing of the face
- Bleeding from mucous membranes (epistaxis, menorrhagia, metrorrhagia, gastrointestinal bleeding), although fatal bleeding is rare[1]
- Cold skin
- Hemorrhagic manifestations are more frequent in severe HFRS (caused by HTNV and DOBV); in PUUV, a third of patients have mild hemorrhages[1]
Oliguric phase (3–5 days; occurs in ~50% of HFRS cases; median onset day 6):[1][9]
- Decreased urine output (oliguria or anuria) which may result in renal failure
- Hypertension (rebound)
- Complications of renal insufficiency (hyperkalemia, metabolic acidosis, uremia)
- Pulmonary edema may develop
- Resolution of petechiae and flushing
- Increased serum creatinine and urea concentrations observed 5–9 days after disease onset[1]
Polyuric (Diuretic) phase (median onset day 9; present in 91% of patients; median duration 7 days):[9]
- Onset of diuresis
- Clinical improvement
- Electrolyte abnormalities may occur during massive diuresis
Convalescent phase (weeks to months):
- Hyposthenuria
Laboratory Findings in HFRS
| Parameter | Finding | Frequency / Timing |
|---|---|---|
| Thrombocytopenia | Decreased platelet count | 95% of patients; median duration 4 days[9] |
| ALT elevation | Elevated liver transaminases | 87% of patients[9] |
| CRP | Elevated | 99% of patients; median duration 7 days[9] |
| Procalcitonin | Elevated | 91% of patients; median duration 3 days[9] |
| Creatinine | Elevated | 94% of patients; median duration 9 days; onset 5–9 days after symptom onset[9][1] |
| GFR | Diminished | 87% of patients[9] |
| Leukocytosis | Elevated white blood cell count | 55% of patients; median duration 2 days[9] |
| Proteinuria and hematuria | Present on urinalysis | Common; supports clinical suspicion of HFRS[1] |
| Albumin | Decreased plasma albumin concentration | Due to plasma leakage[1] |
| Hemoglobin | Elevated | Due to plasma leakage and hemoconcentration[1] |
Organ-Specific Manifestations
Ocular Manifestations
Ocular symptoms are very common in acute PUUV-HFRS, found in up to 70% of patients.[1][5] A total of 87% had reduced visual acuity, 78% had myopic shift, 88% had decreased intraocular pressure, and 88% had thickening of the lens.[5] Ocular findings combined with fever, headache, and thrombocytopenia may be pathognomonic for PUUV infection.[5] Blurred vision and transient myopia are caused by thickening of the lens.[1] Patients infected with DOBV have a higher proportion of visual disturbances than those infected with PUUV.[1]
Cardiac Manifestations
Cardiopulmonary involvement with respiratory failure and shock may also occur in HFRS.[1] In a German study of 471 patients with nephropathia epidemica, electrocardiogram (ECG) abnormalities were detected in 18% of patients, with T wave inversion being the most frequent abnormality (n=31), followed by ST segment changes (9 with elevation, 6 with depression).[12] Relative bradycardia was identified in 80% of patients with acute nephropathia epidemica.[12] ECG abnormalities reverted to normal in the majority of patients during follow-up (median 37 months) and were not associated with negative cardiovascular outcome.[12] Sinus bradycardia has a median onset on day 9.5 of illness and is present in 35% of patients.[9] Severe sinus bradycardia (as low as 25/min) has been reported but is generally asymptomatic and resolves spontaneously.[13] In the Balkans, more than half of patients with PUUV and DOBV showed ECG abnormalities and half had pathological pulmonary x-rays with interstitial infiltrates and pleural effusions.[1]
A comprehensive study of 27 hospitalized PUUV patients using echocardiography with speckle tracking strain rate analysis demonstrated significantly higher pulmonary vascular resistance, higher systolic pulmonary artery pressure, lower left ventricular ejection fraction, and impaired left atrial myocardial motion compared to controls. NT-ProBNP concentrations were markedly increased even in the absence of overt ventricular heart failure.[14]
Pulmonary Manifestations in HFRS
Two-thirds of PUUV-infected patients experience respiratory symptoms such as dry cough or dyspnea.[14] Gas diffusing capacity was impaired in most patients, significantly improving at follow-up but still subnormal in 38%.[14] High-resolution CT showed thoracic effusions or pulmonary edema in 46% of patients.[14]
Neurological Manifestations
Headache (97%), blurred vision (40%), and vomiting (31%) are the most common neurological symptoms in PUUV-HFRS.[15] In a review of 811 cases, 1% had severe neurological manifestations including meningism and cerebral hemorrhage (occurring during the first week) and epileptiform seizures and urinary bladder paralysis (developing during the second week).[15] Insomnia (30%, median onset day 6) and vertigo are also reported.[9] PUUV-related central nervous system symptoms have been documented on MRI and EEG, and signs of inflammation and PUUV-IgM in cerebrospinal fluid are common in acute PUUV-HFRS.[5][16] Lethal cases in which the pituitary gland was invaded by PUUV resulting in local hemorrhages and necrosis have been described.[5]
Seoul Virus — Distinct Clinical Presentation
Seoul virus (SEOV) infection is often asymptomatic or mild, with nonspecific symptoms including prominent gastrointestinal symptoms and a distinct elevation of liver enzymes (hepatitis-like picture).[17][18] SEOV infection may present with lymphopenia, thrombocytopenia, and a milder degree of bleeding and renal derangement but severer liver dysfunction compared to Hantaan virus infection.[19] SEOV infection should be considered in febrile patients with lymphopenia, thrombocytopenia, and elevation of liver enzymes despite the absence of hemorrhagic manifestations and renal syndrome.[18]
Long-Term Sequelae
After HFRS
Hypertension (23% at follow-up; new diagnosis in 67% of those affected)[20]
Proteinuria (7% at follow-up)[20]
Hematuria (25% at follow-up; may have long-term consequences)[20]
Hormonal dysfunction (up to 80% of patients with PUUV may have hormonal dysfunction at follow-up, related to hypophyseal involvement)[1]
After HCPS
Transient convalescent pulmonary dysfunction: exertional dyspnea persisting 1–2 years in 43–77% of survivors; reduced midexpiratory flows, increased residual volume, and reduced diffusion capacity are common but resolve in most patients within 3 years[7]
Potential chronic renal sequelae[1]
Retinal hemorrhage, optic neuritis, and sensorineural hypoacusis[1]
61.9% of ANDV survivors report incomplete recovery at 3–6 months; motor dysfunction and palpitations are more frequent in ECMO survivors[8]
Long-term complications of SNV or ANDV infection can be difficult to differentiate from effects of long-term critical care hospitalization and ECMO[1]
Thromboembolic Complications
Like SARS-CoV-2, hantavirus infections may increase the risk for thromboembolic complications such as stroke and myocardial infarction.[1]
Long-Term Renal Outcomes After HFRS
In the largest and longest follow-up study of nephropathia epidemica patients to date (n=156, median follow-up 156 months), chronic kidney disease (CKD) was diagnosed in 8% of participants, hematuria was present in 6%, and hypertension at follow-up was observed in 78% of individuals. However, causality between prior hantavirus infection and hypertension remains uncertain, and the findings do not support increased CKD incidence following acute nephropathia epidemica. PUUV-specific IgG antibodies remained detectable in all participants irrespective of duration of follow-up, with no evidence of reinfection.[21]
Prognostic Factors
Prognostic Factors for Mortality in HCPS
A systematic review and meta-analysis of 25 studies (7284 participants) identified the following prognostic factors associated with increased mortality in New World hantavirus infection with moderate to high certainty of evidence:[22]
- Age >18 years
- Female sex
- Rural residence
- Elevated creatinine levels
- Increased hematocrit
- Signs of bleeding
- Presence of infiltrates on chest radiograph
Additional prognostic markers include:
- Platelet count >115,000/μL at admission: associated with lower risk of progression to severe HCPS[1]
- Platelet count <40,000/μL: associated with increased mortality[1]
- Positive quantitative proteinuria at hospital admission: linked to mortality[1]
- IL-6 and intestinal fatty acid-binding protein (I-FABP) are independent markers of disease severity and fatality, respectively[23]
In the largest US study of HPS (719 patients, 1993–2018), overall mortality was 35.4% and did not differ between age groups (children, adolescents, adults; P = .8). However, the time between symptom onset and death differed significantly by age group: children (0–12 years) lived a median of 2 days (IQR 2–3), adolescents (13–18 years) 4 days (IQR 3–5), and adults 5 days (IQR 4–8; P = .001). The mean highest hematocrit and median highest creatinine level were significantly associated with mortality in those aged 0–18 years but not in adults.[24]
Prognostic Factors for Mortality in HFRS
A meta-analysis of 37 studies (140,295 patients) found that patients who died from HFRS were older and more likely to have comorbid hypertension, diabetes mellitus, and a history of smoking. Significant clinical predictors of death included multiple organ dysfunction syndrome, shock, overlapping disease courses, cerebral edema, cerebral hemorrhage, arrhythmias, heart failure, dyspnea, ARDS, pulmonary infection, liver damage, gastrointestinal bleeding, and acute kidney injury. Laboratory predictors of death included elevated leukocyte count, decreased platelet count, increased lactate dehydrogenase, elevated ALT and AST, prolonged APTT and PT, and low albumin and chloride levels.[25]
In a 14-year ambispective cohort study of 2245 HFRS patients (132 deaths, 5.9% case fatality rate), a validated death risk stratification scale was developed using six predictors: comorbid hypertension, hypotensive shock, hypoxemia, neutrophil count, AST, and APTT. The scale demonstrated areas under the ROC curve >0.9 with sensitivity and specificity >90% in the training cohort and >84% in the validation cohort.[26]
Serum ferritin and procalcitonin have a robust association with HFRS severity and mortality. The AUC of serum ferritin for predicting mortality was 0.853 (95% CI 0.774–0.933), with a sensitivity of 0.933 and specificity of 0.739. CRP is an effective biomarker to assess bacterial co-infection in HFRS.[27]
Hantavirus Infection in Children
The clinical course of HFRS and HCPS in children appears similar to the course in adults.[1] Abdominal pain and vomiting are more common in children with PUUV infection, whereas adults present more frequently with arthralgia and visual disturbances.[28] Acute kidney injury and thrombocytopenia occur at similar frequencies and severity in both groups, and full recovery is expected in all patients with nephropathia epidemica.[28]
The proportion of cases in children varies by region. For HFRS, children and adolescents represent 1.7% of cases in China, 6.0% in Finland, 9.7% in Russia, and 6.9% in Germany. For HCPS, 18.6% of cases in Chile, 8% in the USA, 10% in Brazil, and 9% in Argentina occur in children younger than 16 years.[1] HCPS caused by ANDV occurs in children aged younger than 10 years and in adolescents, whereas SNV infection in children is largely limited to adolescents.[1] The gender distribution in children (1:1) is different from adults (4:1 male:female).[1]
In a US series of 13 pediatric patients (aged 10–16 years) with SNV infection, the most common prodromal symptoms were fever, headache, and cough or dyspnea (100%); nausea or vomiting (90%); and myalgia (80%). All patients had thrombocytopenia (median platelet count 67,000/mm³) and elevated lactate dehydrogenase (median 1243 IU/L). HCPS developed in 12 of 13 patients (92%), and 4 of those 12 died (33% case-fatality ratio). An elevated prothrombin time (≥14 seconds) at admission was predictive of mortality.[29]
Hantavirus Infection in Pregnancy
Hantavirus infection during pregnancy may be confused with HELLP syndrome or pre-eclampsia due to overlapping features including abdominal pain, hypertension, and thrombocytopenia.[1] Clinicians should maintain a high index of suspicion for hantavirus infection in pregnant women presenting with these features in endemic areas, particularly in the third trimester.
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 1.39 1.40 1.41 1.42 1.43 1.44 1.45 1.46 1.47 1.48 1.49 1.50 1.51 1.52 1.53 Vial PA, Ferrés M, Vial C, Valdivieso F, Mertz GJ, Godoy P (2023). "Hantavirus in humans: a review of clinical aspects and management". Lancet Infect Dis. 23 (9): e371–e382. doi:10.1016/S1473-3099(23)00128-7. PMID 37105214 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Jiang H, Zheng X, Wang L, Du H, Wang P, Bai X (2017). "Hantavirus infection: a global zoonotic challenge". Virol Sin. 32 (1): 32–43. doi:10.1007/s12250-016-3899-x. PMID 28120221.
- ↑ 3.0 3.1 3.2 Levy H, Simpson SQ (1994). "Hantavirus pulmonary syndrome". Am J Respir Crit Care Med. 149 (6): 1710–3. doi:10.1164/ajrccm.149.6.8004332. PMID 8004332.
- ↑ Saavedra F, Díaz FE, Retamal-Díaz A, Ciuoderis K, Aguilera-Correa JJ, Rodríguez-Sosa MA, Kalergis AM, Bueno SM (2021). "Immune response during hantavirus diseases: implications for immunotherapies and vaccine design". Immunology. 163 (3): 262–277. doi:10.1111/imm.13322. PMID 33321107 Check
|pmid=value (help). - ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 Vaheri A, Henttonen H, Voutilainen L, Mustonen J, Sironen T, Vapalahti O (2013). "Hantavirus infections in Europe and their impact on public health". Rev Med Virol. 23 (1): 35–49. doi:10.1002/rmv.1722. PMID 23027245.
- ↑ 6.0 6.1 6.2 6.3 6.4 6.5 Llah ST, Mir S, Sharif S, Khan S, Mir MA (2018). "Hantavirus induced cardiopulmonary syndrome: a public health concern". J Med Virol. 90 (6): 1003–1009. doi:10.1002/jmv.25054. PMID 29322515.
- ↑ 7.0 7.1 7.2 Gracia F, Armien B, Simpson SQ, Munoz C, Broce C, Pascale JM, Koster F (2010). "Convalescent pulmonary dysfunction following hantavirus pulmonary syndrome in Panama and the United States". Lung. 188 (5): 387–91. doi:10.1007/s00408-010-9245-4. PMID 20524006.
- ↑ 8.0 8.1 Valenzuela G, Barahona K, Rojas C, Ferrés M, Vial PA (2025). "Beyond ECMO survival: long-term symptom burden and quality-of-life impairment in hantavirus cardiopulmonary syndrome survivors". Viruses. 17 (9): 1241. doi:10.3390/v17091241. PMID 41012669 Check
|pmid=value (help). - ↑ 9.00 9.01 9.02 9.03 9.04 9.05 9.06 9.07 9.08 9.09 9.10 9.11 9.12 9.13 9.14 Pal E, Korva M, Resman Rus K, Fajs L, Strle F, Avšič-Županc T (2018). "Sequential assessment of clinical and laboratory parameters in patients with hemorrhagic fever with renal syndrome". PLoS One. 13 (5): e0197661. doi:10.1371/journal.pone.0197661. PMID 29791494.
- ↑ Lednicky JA (2003). "Hantaviruses. a short review". Arch Pathol Lab Med. 127 (1): 30–5. doi:10.1043/0003-9985(2003)127<30:>2.0.CO;2. PMID 12521363.
- ↑ 11.0 11.1 Sargianou M, Watson DC, Chra P, Papa A, Starakis I, Gogos C, Panos G (2012). "Hantavirus infections for the clinician: from case presentation to diagnosis and treatment". Crit Rev Microbiol. 38 (4): 317–29. doi:10.3109/1040841X.2012.673553. PMID 22553984.
- ↑ 12.0 12.1 12.2 Kitterer D, Greulich S, Grün S, Latus J, Henes J, Birkmeier S, Alscher MD, Braun N, Segerer S (2016). "Electrocardiographic abnormalities and relative bradycardia in patients with hantavirus-induced nephropathia epidemica". Eur J Intern Med. 33: 67–73. doi:10.1016/j.ejim.2016.06.001. PMID 27296590.
- ↑ Pastissier A, Humbert S, Naudion P, Lepiller Q, Mauny F, Behr J, Meaux-Ruault N, Schiele F, Chopard R (2019). "Severe sinus bradycardia in Puumala virus infection". Int J Infect Dis. 79: 75–76. doi:10.1016/j.ijid.2018.11.019. PMID 30503652.
- ↑ 14.0 14.1 14.2 14.3 Rasmuson J, Lindqvist P, Sörensen K, Hedström M, Blomberg A, Ahlm C (2013). "Cardiopulmonary involvement in Puumala hantavirus infection". BMC Infect Dis. 13: 501. doi:10.1186/1471-2334-13-501. PMID 24160911.
- ↑ 15.0 15.1 Alexeyev OA, Morozov VG (1995). "Neurological manifestations of hemorrhagic fever with renal syndrome caused by Puumala virus: review of 811 cases". Clin Infect Dis. 20 (2): 255–8. doi:10.1093/clinids/20.2.255. PMID 7742425.
- ↑ Hautala N, Partanen T, Kubin AM, Kauma H, Hautala T (2021). "Central nervous system and ocular manifestations in Puumala hantavirus infection". Viruses. 13 (6): 1040. doi:10.3390/v13061040. PMID 34072819 Check
|pmid=value (help). - ↑ Clement J, LeDuc JW, McElhinney LM, Reynes JM, Van Ranst M, Lameire N (2019). "Clinical characteristics of ratborne Seoul hantavirus disease". Emerg Infect Dis. 25 (2): 387–388. doi:10.3201/eid2502.181643. PMID 30666956.
- ↑ 18.0 18.1 Lie KC, Aziz MH, Kosasih H, Neal A, Halim CL, Wulan WN, Karyana M, Aman AT (2018). "Case report: two confirmed cases of human Seoul virus infections in Indonesia". BMC Infect Dis. 18 (1): 578. doi:10.1186/s12879-018-3482-1. PMID 30445913.
- ↑ Kim YS, Ahn C, Han JS, Kim S, Lee JS, Lee PW (1995). "Hemorrhagic fever with renal syndrome caused by the Seoul virus". Nephron. 71 (4): 419–27. doi:10.1159/000188762. PMID 8587622.
- ↑ 20.0 20.1 20.2 Latus J, Schwab M, Tacconelli E, Piber FM, Wegener D, Dippon J, Müller S, Zakim D, Segerer S, Kitterer D, Preusch MR, Goeser F, Latus C, Biegger D, Alscher MD, Braun N (2015). "Clinical course and long-term outcome of hantavirus-associated nephropathia epidemica, Germany". Emerg Infect Dis. 21 (1): 76–83. doi:10.3201/eid2101.140861. PMID 25533268.
- ↑ Kraft L, Oberacker T, Schwab A, Alscher MD, Segerer S, Braun N, Latus J (2026). "Clinical course up to 20 years after hantavirus infection". Nephrol Dial Transplant. 41 (5): 859–865. doi:10.1093/ndt/gfaf212. PMID 41070942 Check
|pmid=value (help). - ↑ Tortosa F, Ragusa MA, Neumann I, Padula P, Bellomo C (2026). "Prognostic factors for mortality in patients infected with New World hantaviruses: a systematic review and meta-analysis". BMJ Open. 16 (1): e096313. doi:10.1136/bmjopen-2024-096313. PMID 41592833 Check
|pmid=value (help). - ↑ Maleki KT, García M, Iglesias A, Alonso D, Ciez M, Cuomo R, Frik J, Ferrer F, Fornés L, Fumière J, Gallego V, Gómez Sanchis MV, Iglesias AA, Khoury C, Levis S, López W, Martínez VP, Molinas FC, Palacios A, Pantozzi F, Riera JA, Sabattini MS, Sánchez Z, Sosa Estani S, Toro J, Vázquez C, Ahlm C, Ljunggren HG, Enria D, Klingström J (2019). "Serum markers associated with severity and outcome of hantavirus pulmonary syndrome". J Infect Dis. 219 (11): 1832–1840. doi:10.1093/infdis/jiz005. PMID 30698699.
- ↑ Thorp L, Fullerton L, Whitesell A, Dehority W (2023). "Hantavirus pulmonary syndrome: 1993-2018". Pediatrics. 151 (4): e2022059352. doi:10.1542/peds.2022-059352. PMID 36855865 Check
|pmid=value (help). - ↑ Lu W, Kuang L, Hu Y, Luo D, Ye C, Hou J, Peng H, Luo M, Bai L, Yin D, Jiang Y (2024). "Epidemiological and clinical characteristics of death from hemorrhagic fever with renal syndrome: a meta-analysis". Front Microbiol. 15: 1329683. doi:10.3389/fmicb.2024.1329683. PMID 38638893 Check
|pmid=value (help). - ↑ Hu H, Zhan J, Chen W, Du H, Bai X (2024). "Development and validation of a novel death risk stratification scale in patients with hemorrhagic fever with renal syndrome: a 14-year ambispective cohort study". Clin Microbiol Infect. 30 (3): 387–394. doi:10.1016/j.cmi.2023.11.003. PMID 37952580 Check
|pmid=value (help). - ↑ Che L, Wang Z, Du N, Li Y, Bhatti MZ, Zhao Z, Bhatti MM (2022). "Evaluation of serum ferritin, procalcitonin, and C-reactive protein for the prediction of severity and mortality in hemorrhagic fever with renal syndrome". Front Microbiol. 13: 865233. doi:10.3389/fmicb.2022.865233. PMID 35677912 Check
|pmid=value (help). - ↑ 28.0 28.1 Echterdiek F, Kitterer D, Alscher MD, Segerer S, Braun N, Latus J (2019). "Clinical course of hantavirus-induced nephropathia epidemica in children compared to adults in Germany—analysis of 317 patients". Pediatr Nephrol. 34 (7): 1247–1252. doi:10.1007/s00467-019-04215-9. PMID 30874941.
- ↑ Ramos MM, Overturf GD, Crowley MR, Rosenberg RB, Hjelle B (2001). "Infection with Sin Nombre hantavirus: clinical presentation and outcome in children and adolescents". Pediatrics. 108 (2): E27. doi:10.1542/peds.108.2.e27. PMID 11483837.