Andes virus: Infectious substances pathogen safety data sheet

For more information on Andes virus, see the following:

Section I – Infectious agent

Name

Andes virus

Agent type

Virus

Taxonomy

Family

Hantaviridae

Genus

Orthohantavirus

Species

Orthohantavirus andesenseFootnote 1Footnote 2

Synonym or cross-reference

Viruses within the species Orthohantavirus andesense cause a disease known as hantavirus pulmonary syndrome (HPS)Footnote 3Footnote 4 or hantavirus cardiopulmonary syndrome (HCPS)Footnote 5Footnote 6. Member viruses currently assigned to the species Orthohantavirus andesense include Andes virus (ANDV), Castelo dos Sonhos virus (CASV), Lechiguanas virus (LECV), and Orán virus (ORNV)Footnote 2Footnote 7Footnote 8Footnote 9Footnote 10Footnote 11.

Characteristics

Brief description

ANDV has a tripartite, single-stranded, negative-sense RNA genome, with the S, M, and L segments being 1.9kb, 3.7kb, and 6.6kb, respectivelyFootnote 3Footnote 12. The S segment encodes the nucleocapsid (N) protein as well as non-structural proteins, the M segment encodes the glycoproteins, and the L segment encodes the RNA-dependent RNA polymerase. ANDV is a lipid enveloped virus with helical nucleocapsidsFootnote 13, and with two surface glycoproteins, Gn and Gc, embedded within the envelopeFootnote 3Footnote 12. ANDV virions are predominantly round with an average diameter of 104 nm; however, tubular and irregular particles have also been observedFootnote 3Footnote 14Footnote 15.

Properties

ANDV non-structural proteins can antagonize the type 1 interferon induction pathway of the host's innate immune systemFootnote 16. The ANDV nucleocapsid protein is able to inhibit beta-interferon (IFN-β) induction and may contribute to virulence and spreadFootnote 17.

The receptors for pathogenic hantaviruses, including ANDV, are integrin β3 and a cadherin-superfamily protein, protocadherin-1Footnote 3Footnote 18Footnote 19 with viral glycoproteins Gc and Gn mediating cell attachmentFootnote 3. Hantaviruses primarily target endothelial cells and may also infect monocytes, macrophages, dendritic cells, and epithelial cells. Viral particles enter the host cells via receptor-mediated endocytosis, which is followed by low pH dependent fusion of the virus and endosomal membranesFootnote 3Footnote 18Footnote 19. This results in release of the viral ribonucleoprotein (RNP) cores into the cell cytoplasmFootnote 3. After virus replication and transportation to the Golgi apparatus, viral assembly and maturation occurs at the plasma membraneFootnote 3Footnote 19. After maturation, progeny virions are released via buddingFootnote 3.

Section II – Hazard identification

Pathogenicity and toxicity

Hantaviruses primarily infect endothelial cells, altering capillary permeability and leading to acute pulmonary edema and severe diseaseFootnote 15. Disease caused by ANDV is referred to as hantavirus pulmonary syndrome (HPS) or hantavirus cardiopulmonary syndrome (HCPS).

HPS is characterized by up to four stages including the febrile prodrome, cardiopulmonary stage, diuresis, and convalescenceFootnote 20. The prodromal phase is characterized by non-specific symptoms such as high fever, chills, myalgia, nausea, headache, vomiting, abdominal pain, and diarrhea, lasting around 3 to 6 daysFootnote 21. By the end of the prodromal phase, dyspnea (shortness of breath) and dry cough may appearFootnote 8. Approximately half of cases progress to the cardiopulmonary phaseFootnote 21, which typically lasts from 2 to 10 days with illness ranging from mild to severeFootnote 20. In mild cases, the cardiopulmonary phase is characterized by dyspnea and the need for supplemental oxygenFootnote 20Footnote 21. In severe cases, tachycardia, hypotension as a consequence of rapidly progressing pulmonary edema from capillary leakage, respiratory failure, lactic acidosis, and shock can occur. Cardiogenic shock is the main cause of death during the cardiopulmonary phase, and may occur within hoursFootnote 20Footnote 21. One report of encephalitis caused by ANDV infection has been describedFootnote 22. In survivors of the cardiopulmonary phase, diuresis occurs abruptly and is usually associated with rapid clinical improvementFootnote 20. During the convalescence phase, patients report persistent fatigue and limited tolerance for exercise for at least several monthsFootnote 20. Overall, the reported case fatality rate for ANDV-HPS ranges from 20-40%Footnote 6Footnote 8Footnote 20Footnote 21.

Epidemiology

Hantaviruses endemic to Eurasia are referred to as Old World hantaviruses, whereas hantaviruses endemic to the Americas are referred to as New World hantavirusesFootnote 14. Old World hantaviruses include pathogens that cause hemorrhagic fever with renal syndrome (HFRS). New World hantaviruses, including ANDV, cause HPS/HPCS. ANDV is the primary cause of HPS in Argentina and ChileFootnote 8Footnote 15Footnote 23. Other hantaviruses that cause HPS/HCPS include Sin Nombre virus (SNV) in North America, and Laguna Negra virus in Brazil, Paraguay, and BoliviaFootnote 23.

South American hantaviruses have been divided into 3 clades: Andes clade, Laguna Negra clade, and Rio Mamore cladeFootnote 15. The Andes clade comprises viruses that are found in 6 countries, including Argentina, Chile, Bolivia, Brazil, Paraguay, and Uruguay. Based on geographical location in South America, different lineages have been described, such as AND-Oran, AND-Lechiguanas, AND-Bermejo, AND-Buenos-Aires, AND-South, and AND-PlataFootnote 7Footnote 8Footnote 24Footnote 25.

Between March and April 1995, an outbreak of HPS/HCPS occurred in southwestern Argentina, in a rural area near El Bolson in the province of Rio NegroFootnote 26Footnote 27. Out of the three cases, two had fatal outcomes, and based on retrieved tissue samples, the causative virus was found to be novel and later named ANDVFootnote 26Footnote 27. In 1996, another 20 cases were identified in visitors and residents of El Bolsón, Bariloche, and Esquel with a CFR of 50%Footnote 27. Additionally, sporadic cases of HPS and possible cases of HFRS from as early as 1987, have been retrospectively identified in Argentina. Within Argentina, endemic areas include Northern (provinces of Salta and Jujuy), Central (provinces of Buenos Aires, Santa Fe, and Entre Ríos), Northeastern (Misiones) and Southern (Neuquén, Río Negro, and Chubut) regionsFootnote 28. Between 2009 and 2017, 533 laboratory-confirmed cases of HPS caused by ANDV were reported in Argentina for an average of 59 cases per yearFootnote 8. ANDV is also primarily responsible for HPS cases in ChileFootnote 15. Between 1995 and 2018, there were 1157 confirmed HPS cases in 11 administrative regions in ChileFootnote 29. An average of 67 cases were reported annually between 1995 and 2013Footnote 30.

On 2 May 2026, a cluster of severe cases of HPS linked to a cruise ship was reported to the World Health Organization (WHO)Footnote 31. The ship had embarked from Ushuaia in Argentina and traversed Antarctic waters en route to South Georgia, Nightingale Island, Tristan da Cunha, Saint Helena, Ascension Island, and Cabo VerdeFootnote 32. As of 8 May, a total of eight cases, including three deaths (two confirmed and one probable, case fatality ratio 38%), have been reportedFootnote 31. Six cases have been laboratory-confirmed as caused by ANDV.

Individuals at high risk of infection with hantaviruses are those working in agriculture, forestry, or animal husbandryFootnote 23.

Host range

Natural host(s)

Natural hosts for ANDV include humans and rodents, particularly the long-tailed pygmy rice rat (Oligoryzomys longicaudatus)Footnote 8Footnote 15Footnote 21.

Other host(s)

Hamsters and rhesus monkeys have been experimentally infected with ANDVFootnote 15Footnote 33Footnote 34.

Infectious dose

The infectious dose for ANDV is unknown. However, in experimental settings with the inoculation of hamsters, the LD50 was calculated to be 8 plaque-forming units (PFU)Footnote 33.

Incubation period

The incubation period for ANDV infection is 7 to 39 days (median 18 days); however, a longer period of up to 42 days has also been reportedFootnote 6Footnote 21Footnote 31.

Communicability

The preferred mode of transmission of ANDV in humans is inhalation of contaminated rodent excreta or secretaFootnote 6Footnote 15. Infection may also occur through consumption of food contaminated with rodent excreta or secretaFootnote 23. ANDV is regarded as the only orthohantavirus with documented human-to-human transmissionFootnote 6Footnote 31Footnote 35. Human-to-human transmission of ANDV is associated with prolonged, close contact with symptomatic individualsFootnote 36. Evidence consistent with the shedding of infectious virus in bodily fluids of human ANDV-HPS patients has been observed during the acute phase of illnessFootnote 6. Transmission from mother-to-child through breast milk has been suggestedFootnote 23.

Section III – Dissemination

Reservoir

The long-tailed pygmy rice rat, O. longicaudatus, is the primary reservoir of ANDVFootnote 6Footnote 8Footnote 15.

Zoonosis

ANDV is primarily transmitted to humans through the inhalation of excreta or secreta from infected rodentsFootnote 6Footnote 15.

Vectors

None.

Section IV – Stability and viability

Drug susceptibility/resistance

There are no drugs available for the treatment of ANDV. The antivirals ribavirin and favipiravir, as well as vandetanib, a tyrosine-kinase inhibitor of the vascular endothelial growth factor receptor 2 (VEGF2), have demonstrated efficacy against ANDV in animal modelsFootnote 18Footnote 37.

Susceptibility to disinfectants

ANDV was susceptible to two alcohol-based disinfectants, two aldehyde-based disinfectants, and one hydrogen-peroxide-based disinfectantFootnote 38. The alcohol-based disinfectants (100%), composed of 450 mg/g 1-propanol, 250 mg/g 2-propanol, 47 mg/g ethanol and 250 mg/g ethanol, 350 mg/g 2-propanol, respectively, inactivated ANDV after 30 seconds of exposure time. The aldehyde-based disinfectants (0.5%), containing 50 mg/g glutaraldehyde, 30 mg/g benzylalkyldimethylammonium chloride, 30 mg/g didecyldimethylammonium chloride, or 98 mg/g glutaraldehyde, 50 mg/g alkyldimethylbenzylammonium chloride, 50 mg/g didecyldimethylammonium chloride, inactivated ANDV after an exposure time of 5 minutes. The hydrogen peroxide-based disinfectant (100%) containing 15 mg/g hydrogen peroxide completely inactivated ANDV after 30 seconds of exposure time.

ANDV was also inactivated following 30 seconds of exposure to two hand-rub formulations at room temperatureFootnote 38. The first formulation contained 80% ethanol and a concentration of 40% was required for inactivation. The second formulation was 75% 2-propanol-based and a concentration of 30% fully reduced viral titres.

Physical inactivation

Similar to other enveloped viruses, hantaviruses are inactivated by heat treatment at 60°C for 30 minutes and through exposure to UV irradiationFootnote 39.

Survival outside host

Dried ANDV was found to remain stable for 8 hours on stainless steel discs stored in the dark at room temperature (∼21 °C)Footnote 38. After 24 hours, a significant decline of nearly 3 log10 focus-forming units/mL was observed. Detectable levels of infectious virus were still present after 5 days, which corresponds to a half-life of 23.61 hours.

Section V – First aid/medical

Surveillance

ANDV RNA may be detected in blood, respiratory secretions, gingivocrevicular fluid, saliva, and urine using reverse transcription-polymerase chain reaction (RT-PCR) or quantitative RT-PCRFootnote 5Footnote 6Footnote 7Footnote 15Footnote 21Footnote 40, while enzyme-linked immunosorbent assays (ELISA) can detect specific IgM or IgG antibodies in bloodFootnote 5Footnote 7Footnote 15.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook.

First aid/treatment

There is currently no specific treatment for HPSFootnote 6Footnote 8. Management of severe cases is based on supportive care, such as maintaining fluid and electrolyte balance as well as mechanical ventilation or extracorporeal membrane oxygenationFootnote 37.

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the Canadian Biosafety Handbook.

Immunization

There is no vaccine currently availableFootnote 6Footnote 18.

In 2020, a phase 1 clinical trial designed to assess the safety, reactogenicity, and immunogenicity of an ANDV DNA vaccine was completedFootnote 41Footnote 42. This first-in-human candidate HPS vaccine trial demonstrated that this vaccine was safe, and induced a robust, durable immune responseFootnote 42.

Note: More information on the medical surveillance program can be found in the Canadian Biosafety Handbook, and by consulting the Canadian Immunization Guide.

Prophylaxis

None.

Note: More information on prophylaxis as part of the medical surveillance program can be found in the Canadian Biosafety Handbook.

Section VI – Laboratory hazard

Laboratory-acquired infections

Two laboratory researchers at the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) were reported to be exposed to hantavirusesFootnote 43. One of the researchers had potential aerosol exposure to ANDV (mechanism unknown), while the other researcher was confirmed to be exposed to 7 ml of cell culture supernatant containing a high concentration of SNV. Both individuals remained asymptomatic and RT-PCR and IgM ELISA assays were negative.

Note: Please consult the Canadian Biosafety Standard and Canadian Biosafety Handbook for additional details on requirements for reporting exposure incidents.

Sources/specimens

Biological samples/specimens known to contain infectious material include salivaFootnote 5Footnote 6Footnote 15, urineFootnote 5Footnote 6Footnote 15, gingival crevicular fluidFootnote 6Footnote 15, nasopharyngeal secretionsFootnote 6, semenFootnote 5Footnote 21, and bloodFootnote 6Footnote 15.

Primary hazards

Inhalation of airborne or aerosolized infectious material is the primary hazard associated with exposure to ANDVFootnote 6Footnote 15. Bites or scratches of an infected animal as well as ingestion of infectious material are also hazards associated with the exposure to ANDVFootnote 23.

Special hazards

None.

Section VII – Exposure controls/personal protection

Risk group classification

Orthohantavirus andesense is a Risk Group 3 human pathogen, Risk Group 1 animal pathogen, and a Security Sensitive Biological Agent (SSBA)Footnote 2.

Containment requirements

Containment Level 3 facilities, equipment, and operational practices outlined in the Canadian Biosafety Standard for work involving infectious or potentially infectious materials, animals, or cultures.

Note that there are additional security requirements, such as obtaining a Human Pathogens and Toxins Act Security Clearance, for work involving SSBAs.

Protective clothing

The applicable Containment Level 3 requirements for personal protective equipment and clothing outlined in the Canadian Biosafety Standard are to be followed. At minimum, use of full body coverage dedicated protective clothing, dedicated protective footwear and/or additional protective footwear, gloves when handling infectious materials or animals, face protection when there is a known or potential risk of exposure to splashes or flying objects, respirators when there is a risk of exposure to infectious aerosols, and an additional layer of protective clothing prior to work with infectious materials or animals.

Note: A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone must be documented.

Other precautions

All activities involving open vessels of pathogens are to be performed in a certified biological safety cabinet (BSC) or other appropriate primary containment device. Centrifugation of regulated materials to be carried out in sealed safety cups or rotors that are unloaded in a BSC or other primary containment device using a mechanism that prevents their release. The use of needles, syringes, and other sharp objects are to be strictly limited. Additional precautions must be considered with work involving animals or large scale activities.

Section VIII – Handling and storage

Spills

Allow aerosols to settle. Wearing personal protective equipment, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time with the disinfectant before clean up (Canadian Biosafety Handbook).

Disposal

Regulated materials, as well as all items and waste to be decontaminated at the containment barrier prior to removal from the containment zone, animal room, animal cubicle, or post mortem room. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the infectious material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (Canadian Biosafety Handbook).

Storage

The applicable Containment Level 3 requirements for storage outlined in the Canadian Biosafety Standard are to be followed. Primary containers of regulated materials removed from the containment zone to be stored in a labelled, leak-proof, impact-resistant secondary container, and kept either in locked storage equipment or within an area with limited access.

Containers of SSBAs stored outside the containment zone must be labelled, leakproof, impact resistant, and kept in locked storage equipment that is fixed in place (i.e., non-movable) and within an area with limited access.

An inventory of RG3 and SSBA toxins in long-term storage, to be maintained and to include:

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with Orthohantavirus andesense require a Pathogen and Toxin licence issued by the Public Health Agency of Canada (PHAC).

Note that there are additional security requirements, such as obtaining a Human Pathogens and Toxins Act Security Clearance, for work involving SSBAs.

The following is a non-exhaustive list of applicable designations, regulations, or legislations:

Last file update

May, 2026

Prepared by

Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.

Persons in Canada are responsible for complying with the relevant laws, including regulations, guidelines and standards applicable to the import, transport, and use of pathogens in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.

Copyright © Public Health Agency of Canada, 2026, Canada

References

Footnote 1

International Committee on Taxonomy of Viruses. 2025. Orthohantavirus andesense Taxon Details | ICTV. Available at https://ictv.global/taxonomy/taxondetails?taxnode_id=202500022&taxon_name=Orthohantavirus%20andesense

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Footnote 2

Public Health Agency of Canada. 2026. The Registry of Human Pathogens and Toxins (ePATHogen - Database).

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Footnote 3

MacNeil A, Nichol ST, and Spiropoulou CF. 2011. Hantavirus pulmonary syndrome. Virus Research 162:138-147.

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Footnote 4

Martinez V, Bellomo C, San Juan J, Pinna D, Forlenza R, Elder M, and Padula P. 2005. Person-to-Person Transmission of Andes Virus. Emerging Infectious Disease journal 11:223-226.

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Footnote 5

Ferrés M, Vial P, Marco C, Yañez L, Godoy P, Castillo C, Hjelle B, Delgado I, Lee S-J, Mertz GJ, and Group AVHCS. 2007. Prospective Evaluation of Household Contacts of Persons with Hantavirus Cardiopulmonary Syndrome in Chile. The Journal of Infectious Diseases 195:1563-1571.

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Footnote 6

Ferrés M, Martínez-Valdebenito C, Henriquez C, Marco C, Angulo J, Barrera A, Palma C, Barriga Pinto G, Cuiza A, Ferreira L, Rioseco ML, Calvo M, Fritz R, Bravo S, Bruhn A, Graf J, Llancaqueo A, Rivera G, Cerda C, Tischler N, Valdivieso F, Vial P, Mertz G, Vial C, and Le Corre N. 2024. Viral shedding and viraemia of Andes virus during acute hantavirus infection: a prospective study. The Lancet Infectious Diseases 24:775-782.

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Footnote 7

Martinez VP, Bellomo CM, Cacace ML, Suarez P, Bogni L, and Padula PJ. 2010. Hantavirus pulmonary syndrome in Argentina, 1995-2008. Emerg Infect Dis 16:1853-1860.

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Footnote 8

Alonso Daniel O, Iglesias A, Coelho R, Periolo N, Bruno A, Córdoba Maria T, Filomarino N, Quipildor M, Biondo E, Fortunato E, Bellomo C, and Martínez Valeria P. 2019. Epidemiological description, case-fatality rate, and trends of Hantavirus Pulmonary Syndrome: 9 years of surveillance in Argentina. Journal of Medical Virology 91:1173-1181.

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Footnote 9

Padula PJ, Colavecchia SB, Martínez VP, Valle MOGD, Edelstein A, Miguel SDL, Russi J, Riquelme JM, Colucci N, Almirón M, and Rabinovich RD. 2000. Genetic Diversity, Distribution, and Serological Features of Hantavirus Infection in Five Countries in South America. Journal of Clinical Microbiology 38:3029-3035.

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Footnote 10

Levis S, Morzunov SP, Rowe JE, Enria D, Pini N, Calderon G, Sabattini M, and St Jeor SC. 1998. Genetic diversity and epidemiology of hantaviruses in Argentina. J Infect Dis 177:529-538.

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Footnote 11

Bradfute SB, Calisher CH, Klempa B, Klingström J, Kuhn JH, Laenen L, Tischler ND, and Maes P. 2024. ICTV Virus Taxonomy Profile: Hantaviridae 2024. Journal of General Virology 105.

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Footnote 12

Meissner JD, Rowe JE, Borucki MK, and St. Jeor SC. 2002. Complete nucleotide sequence of a Chilean hantavirus. Virus Research 89:131-143.

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Footnote 13

Vera-Otarola J, Castillo-Vargas E, Angulo J, Barriga FM, Batlle E, and Lopez-Lastra M. 2021. The viral nucleocapsid protein and the human RNA-binding protein Mex3A promote translation of the Andes orthohantavirus small mRNA. PLOS Pathogens 17.

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Footnote 14

Parvate A, Williams EP, Taylor MK, Chu Y-K, Lanman J, Saphire EO, and Jonsson CB. 2019. Diverse Morphology and Structural Features of Old and New World Hantaviruses. Viruses 11:862.

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Footnote 15

Figueiredo LTM, Souza WMd, Ferrés M, and Enria DA. 2014. Hantaviruses and cardiopulmonary syndrome in South America. Virus Research 187:43-54.

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Footnote 16

Vera-Otarola J, Solis L, Lowy F, Olguín V, Angulo J, Pino K, Tischler Nicole D, Otth C, Padula P, and López-Lastra M. 2020. The Andes Orthohantavirus NSs Protein Antagonizes the Type I Interferon Response by Inhibiting MAVS Signaling. Journal of Virology 94.

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Footnote 17

Simons MJ, Gorbunova EE, and Mackow ER. 2019. Unique Interferon Pathway Regulation by the Andes Virus Nucleocapsid Protein Is Conferred by Phosphorylation of Serine 386. Journal of Virology 93.

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Footnote 18

Jacob AT, Ziegler BM, Farha SM, Vivian LR, Zilinski CA, Armstrong AR, Burdette AJ, Beachboard DC, and Stobart CC. 2023. Sin Nombre Virus and the Emergence of Other Hantaviruses: A Review of the Biology, Ecology, and Disease of a Zoonotic Pathogen. Biology (Basel) 12.

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Footnote 19

Jonsson CB, Figueiredo LT, and Vapalahti O. 2010. A global perspective on hantavirus ecology, epidemiology, and disease. Clin Microbiol Rev 23:412-441.

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Footnote 20

Galeno H, Mora J, Villagra E, Fernandez J, Hernandez J, Mertz GJ, and Ramirez E. 2002. First human isolate of Hantavirus (Andes virus) in the Americas. Emerg Infect Dis 8:657-661.

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Footnote 21

Züst R, Ackermann-Gäumann R, Liechti N, Siegrist D, Ryter S, Portmann J, Lenz N, Beuret C, Koller R, Staehelin C, Kuenzli AB, Marschall J, Rothenberger S, and Engler O. 2023. Presence and Persistence of Andes Virus RNA in Human Semen. Viruses 15:2266.

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Footnote 22

Talamonti L, Padula PJ, Canteli MS, Posner F, Marczeski FP, and Weller C. 2011. Hantavirus pulmonary syndrome: encephalitis caused by virus Andes. J Neurovirol 17:189-192.

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Footnote 23

Chen R-X, Gong H-Y, Wang X, Sun M-H, Ji Y-F, Tan S-M, Chen J-M, Shao J-W, and Liao M. 2023. Zoonotic Hantaviridae with Global Public Health Significance. Viruses 15:1705.

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Footnote 24

Iglesias AA, Bellomo CM, and Martínez VP. 2016. Hantavirus pulmonary syndrome in Buenos Aires, 2009-2014. Medicina (B Aires) 76:1-9.

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Footnote 25

Medina RA, Torres-Perez F, Galeno H, Navarrete M, Vial PA, Palma RE, Ferres M, Cook JA, and Hjelle B. 2009. Ecology, genetic diversity, and phylogeographic structure of andes virus in humans and rodents in Chile. J Virol 83:2446-2459.

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Footnote 26

López N, Padula P, Rossi C, Lázaro ME, and Franze-Fernández MT. 1996. Genetic identification of a new hantavirus causing severe pulmonary syndrome in Argentina. Virology 220:223-226.

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Footnote 27

Wells RM, Sosa Estani S, Yadon ZE, Enria D, Padula P, Pini N, Mills JN, Peters CJ, and Segura EL. 1997. An unusual hantavirus outbreak in southern Argentina: person-to-person transmission? Hantavirus Pulmonary Syndrome Study Group for Patagonia. Emerg Infect Dis 3:171-174.

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Footnote 28

World Health Organization. 2019. Hantavirus Disease – Argentina. Available at https://www.who.int/emergencies/disease-outbreak-news/item/23-January-2019-hantavirus-argentina-en

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Footnote 29

Torres-Pérez F, Palma RE, Boric-Bargetto D, Vial C, Ferrés M, Vial PA, Martínez-Valdebenito C, Pavletic C, Parra A, Marquet PA, and Mertz GJ. 2019. A 19 Year Analysis of Small Mammals Associated with Human Hantavirus Cases in Chile. Viruses 11:848.

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Footnote 30

World Health Organization. 2013. Epidemiological Alert: Hantavirus Pulmonary Syndrome (HPS). WHO.

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Footnote 31

World Health Organization. 2026. Disease Outbreak News: Hantavirus cluster linked to cruise ship travel, Multi-country. Available at https://www.who.int/emergencies/disease-outbreak-news/item/2026-DON600.

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Footnote 32

Velavan TP, and Schmidt-Chanasit J. 2026. When Rare Zoonoses Travel: Andes virus, Hantavirus Cardiopulmonary Syndrome, and the Preparedness Gap. International Journal of Infectious Diseases doi available at https://doi.org/10.1016/j.ijid.2026.108778:108778.

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Footnote 33

Hooper JW, Larsen T, Custer DM, and Schmaljohn CS. 2001. A Lethal Disease Model for Hantavirus Pulmonary Syndrome. Virology 289:6-14.

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Footnote 34

Custer DM, Thompson E, Schmaljohn CS, Ksiazek TG, and Hooper JW. 2003. Active and Passive Vaccination against Hantavirus Pulmonary Syndrome with Andes Virus M Genome Segment-Based DNA Vaccine. Journal of Virology 77:9894-9905.

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Footnote 35

Markotić A. 2024. Presence of Andes orthohantavirus in human body fluids. The Lancet Infectious Diseases 24:674-676.

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Footnote 36

Martínez VP, Paola ND, Alonso DO, Pérez-Sautu U, Bellomo CM, Iglesias AA, Coelho RM, López B, Periolo N, Larson PA, Nagle ER, Chitty JA, Pratt CB, Díaz J, Cisterna D, Campos J, Sharma H, Dighero-Kemp B, Biondo E, Lewis L, Anselmo C, Olivera CP, Pontoriero F, Lavarra E, Kuhn JH, Strella T, Edelstein A, Burgos MI, Kaler M, Rubinstein A, Kugelman JR, Sanchez-Lockhart M, Perandones C, and Palacios G. 2020. "Super-Spreaders" and Person-to-Person Transmission of Andes Virus in Argentina. New England Journal of Medicine 383:2230-2241.

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Footnote 37

Dheerasekara K, Sumathipala S, and Muthugala R. 2020. Hantavirus Infections-Treatment and Prevention. Curr Treat Options Infect Dis 12:410-421.

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Footnote 38

Nilsson-Payant BE, Dafi RF, Krüger S, Rosenthal M, Todt D, Addo MM, Steinmann E, and Meister TL. 2025. Stability of Andes virus and its inactivation by WHO-recommended hand-rub formulations and surface disinfectants. Journal of Hospital Infection 166:5-11.

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Footnote 39

Avšič-Županc T, Saksida A, and Korva M. 2019. Hantavirus infections. Clinical Microbiology and Infection 21:e6-e16.

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Footnote 40

Chaparro J, Vega J, Terry W, Vera JL, Barra B, Meyer R, Peters CJ, Khan AS, and Ksiazek TG. 1998. Assessment of person-to-person transmission of hantavirus pulmonary syndrome in a Chilean hospital setting. J Hosp Infect 40:281-285.

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Footnote 41

National Library of Medicine ClinicalTrials.gov. 2022. Andes Virus DNA Vaccine for the Prevention of Hantavirus Pulmonary Syndrome Using the PharamaJet Stratis® Needle Free Injection Delivery Device.

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Footnote 42

Paulsen GC, Frenck R, Jr., Tomashek KM, Alarcon RM, Hensel E, Lowe A, Brocato RL, Kwilas SA, Josleyn MD, and Hooper JW. 2024. Safety and Immunogenicity of an Andes Virus DNA Vaccine by Needle-Free Injection: A Randomized, Controlled Phase 1 Study. J Infect Dis 229:30-38.

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Footnote 43

Rusnak J. 2011. Experience with Ribavirin for Treatment and Postexposure Prophylaxis of Hemorrhagic Fever Viruses: Crimean Congo Hemorrhagic Fever, Lassa Fever, and Hantaviruses. Applied Biosafety 16:67-87.

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2026-05-25