Hantavirus infection epidemiology and demographics
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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] Aditya Ganti M.B.B.S. [3]
Overview
Hantavirus infection is a zoonotic disease with a nearly global distribution, caused by viruses of the genus Orthohantavirus (family Hantaviridae).[1] Approximately 200,000 human infections are diagnosed annually worldwide.[2] The two major clinical syndromes are hemorrhagic fever with renal syndrome (HFRS), which is endemic in Europe and Asia, and hantavirus cardiopulmonary syndrome (HCPS), also called hantavirus pulmonary syndrome (HPS), which is endemic in the Americas.[1] A systematic review and meta-analysis of 110 studies (81,815 observations) estimated the global seroprevalence at 2.93% (95% CI 2.34%–3.67%).[3] Many factors influence hantavirus epidemiology and transmission, including climate, environment, social development, ecology of rodent hosts, and human behaviour in endemic regions.[1] HFRS and HCPS are reportable diseases in most countries, but reports largely reflect hospital admissions; from serosurveillance studies in Finland, only around 15% of infected people are diagnosed and reported.[1]
In the United States, from 1993 to 2020, a total of 833 human hantavirus cases were identified, with 94.9% (745/785) occurring in states west of the Mississippi River and 45.7% (359/785) in the Four Corners region.[4] The median age of confirmed HCPS cases is 34 years (range 0–86 years), and 70–80% of cases occur in men.[1]
Epidemiology
Global Burden
Hantavirus infections cause approximately 200,000 human cases annually worldwide.[2][5] China accounts for the majority of global cases, with over 90% of all HFRS cases worldwide.[6] Case fatality rates vary substantially by virus and syndrome: HFRS caused by Hantaan virus, Amur virus, and Dobrava-Belgrade virus carries CFRs of 5–15%, whereas Seoul virus causes moderate disease (CFR 1–2%) and Puumala virus and Saaremaa virus cause mild forms (CFR 1%).[7] HCPS has higher CFRs, ranging from 12–15% for Choclo virus and Laguna Negra virus to 30–45% for Sin Nombre virus, Andes virus, Araraquara virus, and Juquitiba virus.[1]
Incidence by Region
| Region | Syndrome | Approximate Annual Cases | Case Fatality Rate | Primary Virus(es) |
|---|---|---|---|---|
| China | HFRS | 12,800 (mean, 2004–2016) | 1.3% | HTNV, SEOV |
| Russia | HFRS | 7,300 | 0.4% | PUUV, DOBV, HTNV, SEOV |
| European Union | HFRS | 3,100 (mean) | 0.03%–12% (varies by virus) | PUUV, DOBV |
| South Korea | HFRS | 300–600 | 1% (2011–2016) | HTNV, SEOV |
| Americas (total) | HCPS | ~300 | 12%–45% (varies by virus) | SNV, ANDV, others |
| United States | HCPS | ~26 (mean, 2008–2020) | 35.4% | SNV |
Adapted from Vial et al. 2023,[1] Whitmer et al. 2024,[4] and Thorp et al. 2023.[8]
HFRS in Asia
China: A mean of 12,800 HFRS cases (median 11,063; range 8,853–25,041) per year was reported from 2004 to 2016, with a CFR of 1.3% and a decline in incidence over time. A nationwide surveillance study (2008–2020) analysed 111,054 cases across 76 cities.[1][9] Hantaan virus (HTNV) is responsible for most cases, with Seoul virus (SEOV) also circulating.[1]
South Korea: 300–600 cases per year for the past 20 years. The CFR has decreased from 5–7% in the 1950s to 1% from 2011 to 2016.[1]
HFRS in Europe and Russia
European Union: A mean of 3,100 HFRS cases (median 2,897; range 1,831–4,249) are reported per year. Finland reported 43%, Germany 30%, and Sweden 6% of all EU cases.[1]
Case fatality rates vary by virus and region: 0.1% in Finland (PUUV), less than 0.03% in Germany (PUUV), 0.4% in Sweden (PUUV), and 10–12% in the Balkans and southeast Europe (DOBV).[1] DOBV has also been reported in central Europe, including Germany, Poland, Lithuania, and Czech Republic.[1]
Russia: Approximately 7,300 HFRS cases per year, with an overall CFR of 0.4%. Puumala virus is responsible for almost all HFRS cases diagnosed in western Russia. Multiple hantavirus species circulate, including PUUV, two species of DOBV (Sochi virus and Kurkino virus), HTNV, Amur virus, and SEOV.[1]
HCPS in the Americas
Overall: Approximately 300 cases of HCPS are diagnosed per year in the Americas, mainly in Argentina, Brazil, and Chile.[1]
United States: From 1993 to 2020, 833 human hantavirus cases were identified, with 335 cases occurring from 2008 to 2020. Of all US cases, 94.9% (745/785) were detected west of the Mississippi River, with 45.7% (359/785) in the Four Corners region. From 2008 to 2020, 67.7% of New World hantavirus cases were detected between March and August.[4] HPS cases have been reported in 30 states, including most of the western half of the country and some eastern states as well. Over half of the confirmed cases have been reported from areas outside the Four Corners area.[10] About three-quarters of patients with HPS have been residents of rural areas.[10]
California (1993–2020): 89 hantavirus cases were reported in California residents. Fifty-six (63%) were male, mean age was 41.5 years, and 28 (31%) were fatal. Indoor exposure was most common, and more exposures occurred in peridomestic environments than at worksites or recreational areas.[11]
Argentina: A 9-year surveillance study (2009–2017) identified 533 HCPS cases. The Northwest region contributed the largest proportion of cases. Cases clustered predominantly during warmer months, with seasonal patterns more pronounced in tropical regions.[12]
Seoul Virus: A Global Hantavirus
Seoul virus (SEOV) is the only cosmopolitan hantavirus, distributed worldwide together with its reservoir host, the brown rat (Rattus norvegicus).[1] SEOV cases have been reported on all inhabited continents. Most SEOV infections in humans, including those acquired from laboratory or pet rats, appear to be asymptomatic or cause a mild illness that remains undiagnosed.[1]
A 2017 multistate outbreak investigation in the United States identified SEOV infections in people and pet rats across 31 facilities in 11 US states. Seventeen people had SEOV IgM, indicating recent infection; 7 reported symptoms and 3 were hospitalized. All patients recovered. Among facilities with ≥10 rats tested, rat IgG prevalence ranged from 2% to 70% and SEOV RT-PCR positivity ranged from 0% to 70%.[13]
Seroprevalence
A 2024 systematic review and meta-analysis of 110 studies (81,815 observations) estimated global hantavirus seroprevalence by region:[3]
| Region | Number of Studies | Pooled Seroprevalence (95% CI) |
|---|---|---|
| Global | 110 | 2.93% (2.34%–3.67%) |
| Americas | 61 | 2.43% (1.71%–3.46%) |
| Europe | 33 | 2.98% (2.19%–4.06%) |
| Asia | 10 | 6.84% (3.64%–12.50%) |
| Africa | 6 | 2.21% (1.82%–2.71%) |
Adapted from Tortosa et al. 2024.[3]
An inverse correlation of seroprevalence rates and disease severity has been observed: in the USA, Chile, and Argentina where the disease is severe, seroprevalence is low (0.1–2.2%), whereas in Paraguay and Panama, where HCPS is milder, 17–40% and 33%, respectively, are seropositive.[1]
Occupational Seroprevalence
A systematic review and meta-analysis of 42 studies (total workforce of 15,043 individuals) found elevated seroprevalence in occupational groups with high rodent exposure:[14]
| Occupational Group | Pooled Seroprevalence (95% CI) | Odds Ratio vs. Reference (95% CI) |
|---|---|---|
| Farmers | 3.7% (2.2%–6.2%) | 1.875 (1.438–2.445) |
| Forestry workers | 3.8% (2.6%–5.7%) | 2.892 (2.079–4.023) |
Adapted from Riccò et al. 2021.[14]
Other high-risk occupations include military troops (especially those with extended outdoor training), construction and demolition workers, and laboratory workers handling rodents.[1][5]
Seasonality
HCPS
HCPS cases occur mainly in spring and summer in the Americas.[1] In the United States, 67.7% of New World hantavirus cases from 2008 to 2020 were detected between March and August.[4] In Chile, abrupt, localised increases in Oligoryzomys longicaudatus populations (known as ratadas), following blooming and seeding of bamboo species, lead to increased Andes virus infections in rodents and humans.[1]
HFRS
HFRS in China exhibits a dual seasonal pattern dependent on the dominant hantavirus genotype. Hantaan virus-dominant areas (Type I) show one spike every year in the autumn-winter season. Seoul virus-dominant areas (Type II) show one spike in spring. Mixed-type areas (Type III) show dual peaks.[9] In Northern Europe, 3- to 4-year cycles of Myodes glareolus (bank vole) populations drive cyclical Puumala virus epidemics, linked to tree-seed production following warm summers and autumns.[15]
Climate and Environmental Drivers
Hantavirus outbreaks are strongly influenced by ecological and climatic factors that drive rodent population dynamics and human-rodent contact.[1]
Temperature and rainfall are key climatic variables controlling the interannual cycles of hantavirus outbreaks. A 54-year study (1960–2013) from Central China revealed that 8-year cycles of Hantaan virus outbreaks are driven by the confluence of cyclic dynamics of striped field mouse (Apodemus agrarius) populations and climate variability. Outbreaks occur only when climatic conditions are favorable for both rodent population growth and virus transmission.[2]
El Niño-Southern Oscillation (ENSO): In the Americas, El Niño-associated increased rainfall leads to increased vegetation, higher deer mouse densities, and more frequent Sin Nombre virus transmission. The 1997–1998 ENSO resulted in a 5-fold increase in HCPS caseload above baseline in the Four Corners states in 1998–1999.[16]
Northwestern Argentina: A significant association between HCPS incidence and lagged rainfall and temperature with a delay of 2 to 6 months has been demonstrated.[17]
Future projections: Spatiotemporal modelling of HFRS in China (2005–2098) under 27 climate scenarios predicts that annual HFRS cases will increase significantly in 62 of 356 cities in mainland China. Rattus norvegicus regions are predicted to be the most active, surpassing Apodemus and mixed regions. Eighty cities are identified as at severe risk level, including 22 new cities primarily located in East China after 2020.[18]
Underreporting and Surveillance Challenges
Unrecognised cases exceed reported cases for Puumala, Seoul, and Choclo viruses.[1] HFRS and HCPS are reportable diseases in most countries, but reports largely reflect hospital admissions. From serosurveillance studies in Finland, only around 15% of infected people are diagnosed and reported.[1] Seropositive individuals have been identified in areas without known pathogenic hantaviruses, meaning these individuals might have been infected during travel or by unrecognised local viruses.[1] The actual incidence of hantavirus infections in Africa is not well known due to limited availability of diagnostic tests and the potential for cross-reactive antibodies from other infections in the region.[19]
Demographics
Age
HCPS (global): The median age for people with HCPS is 34 years (range 0–86 years).[1]
United States (first 100 cases): The average age of case-patients was 34.9 years, and 8 were children or adolescents aged ≤16 years.[20]
California (1993–2020): Mean age was 41.5 years.[11]
Sex
HCPS: 70–80% of cases occur in men.[1]
HFRS: The male-to-female ratio is 2.6:1.[1]
United States (first 100 cases): 54% were male.[20]
California (1993–2020): 63% were male.[11]
PUUV infection: The male/female ratio is 1.67 in Finland and 1.52 in Sweden.[15]
Race
United States (first 100 cases): 63% were Caucasian, 35% were Native American, and 2% were African American.[20]
Of cases with known ethnicity, 19% of HPS cases have been reported among Hispanics (ethnicity considered separately from race).[10]
Ethnicity has been shown to affect the clinical course of ANDV and LANV infection, suggesting that human genetic composition can influence the severity of hantavirus infections.[1]
Setting
HCPS: Acquired in rural settings by residents (80%) or visitors (20%) of endemic areas.[1]
HFRS: Most cases occur in rural settings, in farmers, military troops, and other people who spend extended time outdoors.[1]
Seoul virus: In contrast to other HFRS-causing hantaviruses, SEOV cases are mainly seen in urban settings, where wild rats are prevalent.[1]
Geographic Distribution
Of total US HPS cases reported from 1993 to 2020, 94.9% occurred in states west of the Mississippi River.[4]
HPS cases have been reported in 30 states, including most of the western half of the country and some eastern states as well. Over half of the confirmed cases have been reported from areas outside the Four Corners area.[10]
About three-quarters of patients with HPS have been residents of rural areas.[10]
Pediatric Populations
The proportion of cases in children varies by region. For HFRS, children and adolescents represent 1.7% of the cases in China, 6.0% in Finland, 9.7% in Russia, and 6.9% in Germany. In 2019, the incidence in Europe was less than 0.5 cases per 100,000 in children aged 14 years or younger, representing 1.3% of all cases in Europe. For HCPS, 18.6% of the cases in Chile, 8% in the USA, 10% in Brazil, and 9% in Argentina occur in children younger than 16 years. 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. The gender distribution in children (1:1) is different than in adults (4:1 male:female). The prodromal and cardiopulmonary phases, and laboratory findings in children are similar to those in adults.[1]
Among 719 HPS patients in the United States (1993–2018), 22 (3.0%) were aged ≤12 years, 47 (6.5%) were 13 to 18 years old, and the remaining 650 (90.4%) were adults. Overall mortality was 35.4% and did not differ between age groups (P = .8). However, the time between symptom onset and death differed by age group, with children living a median of 2 days (interquartile range [IQR] 2 to 3), adolescents 4 days (IQR 3 to 5), and adults 5 days (IQR 4 to 8; P = .001). The mean highest hematocrit and median highest creatinine level were significantly associated with mortality in those 0 to 18 years old but not in adults.[8]
Risk Factors
Risk factors for hantavirus infection include:[1][5]
Forestry or agricultural work
Weeding, construction, and demolition activities
Cleaning previously unused homes, cellars, storage areas, or stables
Actions that raise dust in rodent-contaminated environments
Peridomestic rodent presence
Outdoor military training
Smoking (reported as a risk factor for contracting Puumala virus infection and for more severe disease)[1]
Condition of housing (whether there are holes allowing rodents to enter)[15]
Use of rodent traps instead of poison in rodent control[15]
Woodcutting and house warming with firewood[15]
Pet rat ownership or breeding (for Seoul virus)[13]
Residence in open developed areas and arid climates in the western United States[21]
Person-to-Person Transmission
Andes virus is the only hantavirus known to be transmitted from person to person.[1] In 2018–2019, a person-to-person transmission outbreak affected 34 patients in Argentina, 11 of whom died. A prospective study in Chile followed 476 household contacts of 76 confirmed ANDV cases for 5 weeks and found 16 additional patients, with a secondary attack rate of 3.4%.[1]
Genetic Susceptibility
Host human leukocyte antigen (HLA) type appears to influence the severity of hantavirus disease:
Puumala virus (PUUV): Individuals with HLA-B08 and HLA-DRB10301 alleles are likely to have a severe form of PUUV infection, whereas those with HLA-B27 are likely to have a benign clinical course. Other genetic factors related to the tumor necrosis factor (TNF) gene and the C4A component of the complement system may also be involved.[22]
Sin Nombre virus (SNV): Individuals with HLA-B3501 have an increased risk of developing severe HCPS. Significantly higher frequencies of SNV-specific CD8+ T cells (up to 44.2% of CD8+ T cells) were found in patients with severe HPS requiring mechanical ventilation compared with moderately ill patients (up to 9.8% of CD8+ T cells).[23]
Hantaan virus (HTNV) and Seoul virus (SEOV): In a Chinese Han population, HLA-DRB10401-0411, HLA-DRB11001, and DRB11305 alleles were more frequent in moderate HTNV-infected HFRS, whereas DRB11101-1105 was more frequently observed in severe HTNV-infected HFRS. The DRB50101-0201 allele may play a protective role in moderate HFRS caused by both HTNV and SEOV.[24]
A genetic predisposition related to HLA type is considered important for the severity of both HFRS and HCPS, although results across studies have been discordant, even involving the same species of hantavirus.[7]
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 Vial PA, Ferrés M, Vial C, Klingström J, Ahlm C, López R, Le Corre N, Mertz GJ (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 Tian H, Yu P, Cazelles B, Xu L, Wang H, Wallinga J, Stenseth NC (2017). "Interannual Cycles of Hantaan Virus Outbreaks at the Human-Animal Interface in Central China Are Controlled by Temperature and Rainfall". Proc Natl Acad Sci USA. 114 (30): 8041–8046. doi:10.1073/pnas.1701777114. PMID 28696305.
- ↑ 3.0 3.1 3.2 Tortosa F, Perre F, Tognetti C, Bianchi A, Figueiredo L, Padula P, Bellomo CM (2024). "Seroprevalence of Hantavirus Infection in Non-Epidemic Settings Over Four Decades: A Systematic Review and Meta-Analysis". BMC Public Health. 24 (1): 2553. doi:10.1186/s12889-024-20014-w. PMID 39300359 Check
|pmid=value (help). Vancouver style error: initials (help) - ↑ 4.0 4.1 4.2 4.3 4.4 Whitmer S, Whitesell A, Mobley M, Shoemaker T, Nichol ST, Spiropoulou CF, Montgomery JM, Klena JD (2024). "Human Orthohantavirus Disease Prevalence and Genotype Distribution in the U.S., 2008-2020: A Retrospective Observational Study". Lancet Reg Health Am. 37: 100836. doi:10.1016/j.lana.2024.100836. PMID 39100240 Check
|pmid=value (help). Vancouver style error: initials (help) - ↑ 5.0 5.1 5.2 Watson DC, Sargianou M, Papa A, Chra P, Starakis I, Panos G (2014). "Epidemiology of Hantavirus Infections in Humans: A Comprehensive, Global Overview". Crit Rev Microbiol. 40 (3): 261–72. doi:10.3109/1040841X.2013.783555. PMID 23607444.
- ↑ Sehgal A, Mehta S, Sahay K, Martynova E, Rizvanov A, Baranwal M, Chandy S, Khaiboullina S (2023). "Hemorrhagic Fever With Renal Syndrome in Asia: History, Pathogenesis, Diagnosis, Treatment, and Prevention". Viruses. 15 (2): 561. doi:10.3390/v15020561. PMID 36851775 Check
|pmid=value (help). - ↑ 7.0 7.1 Avšič-Županc T, Saksida A, Korva M (2019). "Hantavirus Infections". Clin Microbiol Infect. 21S: e6–e16. doi:10.1111/1469-0691.12291. PMID 24750436.
- ↑ 8.0 8.1 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). - ↑ 9.0 9.1 Lv CL, Tian Y, Qiu Y, Zhong XL, Sun Y, Yin JH, Bi P, Tong SL, Wang Q (2023). "Dual Seasonal Pattern for Hemorrhagic Fever With Renal Syndrome and Its Potential Determinants in China". Sci Total Environ. 859 (Pt 2): 160339. doi:10.1016/j.scitotenv.2022.160339. PMID 36427712 Check
|pmid=value (help). - ↑ 10.0 10.1 10.2 10.3 10.4 "Hantavirus Pulmonary Syndrome (HPS) Cases, by State of Exposure". Centers for Disease Control and Prevention.
- ↑ 11.0 11.1 11.2 Jackson BT, Kjemtrup AM, Novak MG, Padgett KA, Fritz CL (2025). "Epidemiologic and Environmental Investigations of Reported Hantavirus Cases Inform Exposure Risk in California, 1993-2020". Am J Trop Med Hyg: tpmd250270. doi:10.4269/ajtmh.25-0270. PMID 41115422 Check
|pmid=value (help). - ↑ Alonso DO, Iglesias A, Coelho R, Periolo N, Bruno A, Córdoba MT, Filomarino N, Quarleri J, Biondo E, Fortunato E, Bellomo CM, Martínez VP (2019). "Epidemiological Description, Case-Fatality Rate, and Trends of Hantavirus Pulmonary Syndrome: 9 Years of Surveillance in Argentina". J Med Virol. 91 (7): 1173–1181. doi:10.1002/jmv.25446.
- ↑ 13.0 13.1 Knust B, Brown S, de St Maurice A, Waltenburg MA, Tenover F, Kato C, Rollin PE, Nichol ST, Whitmer S, Klena JD (2020). "Seoul Virus Infection and Spread in United States Home-Based Ratteries: Rat and Human Testing Results From a Multistate Outbreak Investigation". J Infect Dis. 222 (8): 1311–1319. doi:10.1093/infdis/jiaa307. PMID 32484879 Check
|pmid=value (help). - ↑ 14.0 14.1 Riccò M, Peruzzi S, Ranzieri S, Magnavita N (2021). "Occupational Hantavirus Infections in Agricultural and Forestry Workers: A Systematic Review and Metanalysis". Viruses. 13 (11): 2150. doi:10.3390/v13112150. PMID 34834957 Check
|pmid=value (help). - ↑ 15.0 15.1 15.2 15.3 15.4 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 23280975.
- ↑ Carver S, Mills JN, Parmenter CA, Parmenter RR, Richardson KS, Harris RL, Douglass RJ, Kuenzi AJ, Luis AD (2015). "Toward a Mechanistic Understanding of Environmentally Forced Zoonotic Disease Emergence: Sin Nombre Hantavirus". Bioscience. 65 (7): 651–666. doi:10.1093/biosci/biv047. PMID 26955081.
- ↑ Ferro I, Bellomo CM, López W, Coelho R, Alonso D, Bruno A, Córdoba MT, Periolo N, Martínez VP (2020). "Hantavirus Pulmonary Syndrome Outbreaks Associated With Climate Variability in Northwestern Argentina, 1997-2017". PLoS Negl Trop Dis. 14 (11): e0008786. doi:10.1371/journal.pntd.0008786. PMID 33253144 Check
|pmid=value (help). - ↑ Wang Y, Zhang C, Gao J, Gao L, Luo Y, Lv H, Yan H, Ge S (2024). "Spatiotemporal Trends of Hemorrhagic Fever With Renal Syndrome (HFRS) in China Under Climate Variation". Proc Natl Acad Sci USA. 121 (4): e2312556121. doi:10.1073/pnas.2312556121. PMID 38227655 Check
|pmid=value (help). - ↑ 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.
- ↑ 20.0 20.1 20.2 Khan AS, Khabbaz RF, Armstrong LR, Holman RC, Bauer SP, Graber J, Strine T, Miller G, Reef S, Tappero J, Rollin PE, Nichol ST, Zaki SR, Bryan RT, Chapman LE, Peters CJ, Ksiazek TG (1996). "Hantavirus Pulmonary Syndrome: The First 100 US Cases". J Infect Dis. 173 (6): 1297–303. doi:10.1093/infdis/173.6.1297. PMID 8648200.
- ↑ Gorris ME, Whitesell A, Telford C, Shoemaker T, Bartlow AW (2025). "Hantavirus Is Associated With Open Developed Areas and Arid Climates, Highlighting Increased Risk in the Western United States". Transbound Emerg Dis. 2025: 7126411. doi:10.1155/tbed/7126411. PMID 41141578 Check
|pmid=value (help). - ↑ Vaheri A, Smura T, Vauhkonen H, Mäkelä S, Mustonen J (2023). "Puumala Hantavirus Infections Show Extensive Variation in Clinical Outcome". Viruses. 15 (3): 805. doi:10.3390/v15030805. PMID 36992513 Check
|pmid=value (help). - ↑ Kilpatrick ED, Terajima M, Koster FT, Nolte KB, Ennis FA, de St Groth BF, Gruener NH (2004). "Role of Specific CD8+ T Cells in the Severity of a Fulminant Zoonotic Viral Hemorrhagic Fever, Hantavirus Pulmonary Syndrome". J Immunol. 172 (5): 3297–304. doi:10.4049/jimmunol.172.5.3297. PMID 14978138.
- ↑ Zhu N, Luo F, Chen Q, Hu L, Yang Q (2015). "Influence of HLA-DRB Alleles on Haemorrhagic Fever With Renal Syndrome in a Chinese Han Population in Hubei Province, China". Eur J Clin Microbiol Infect Dis. 34 (1): 187–195. doi:10.1007/s10096-014-2213-9. PMID 25169964.