Waarom Andesvirus het enige hantavirus is dat van mens op mens overgaat

More than two dozen hantaviruses circulate in mammals — Hantaan in Asia, Puumala in Europe, Sin Nombre in North America, Seoul almost everywhere — and they all do the same thing once they reach a person. They cause severe disease, sometimes fatal disease, and then they stop. The chain of transmission ends at the patient. Only one hantavirus, the Andes virus (ANDV) of Argentine and Chilean Patagonia, has firm evidence of moving directly between people. The question this article answers is: why?

The short answer is that no single feature explains it. Three biological characteristics — phylogenetic position, receptor usage, and viral-load + shedding pattern — combine in ANDV in a way that does not occur in any other characterised hantavirus. This article walks through each, then connects the biology back to the household and healthcare-worker cluster studies that have anchored the observation since 1996.

1. Phylogeny — where ANDV sits in the family

Hantaviruses (family Hantaviridae, genus Orthohantavirus) divide into two large groups based on their rodent reservoirs:

• Old World hantaviruses — Hantaan, Seoul, Puumala, Dobrava — circulate in Murinae and Arvicolinae rodents across Europe and Asia. They cause hemorrhagic fever with renal syndrome (HFRS).
• New World hantaviruses — Sin Nombre, Andes, Black Creek Canal, Bayou — circulate in Sigmodontinae and Neotominae rodents across the Americas. They cause hantavirus pulmonary syndrome (HPS), the same syndrome that defines the MV Hondius cluster.

ANDV sits firmly in the New World branch and is most closely related to Sin Nombre virus from North America — the two share roughly 70% glycoprotein amino-acid identity. The reservoir is the long-tailed pygmy rice rat, Oligoryzomys longicaudatus, native to temperate Patagonian forest. The relevant genomic phylogenies are summarised by Plyusnin and Sironen, 2014 and updated regularly through ICTV taxonomy.

Phylogenetic position alone does not explain person-to-person transmission. Sin Nombre is the closest relative, has caused hundreds of HPS cases in the United States since the 1993 Four Corners outbreak, and has never demonstrated person-to-person spread.

2. Receptor biology — the β3 integrin question

Both ANDV and Sin Nombre virus enter human cells primarily via the αvβ3 integrin on the surface of vascular endothelium and platelets. The receptor was identified by Gavrilovskaya et al., 1998 and remains the consensus model for pathogenic hantavirus entry.

The receptor explains the clinical picture: αvβ3 integrin is most densely expressed on capillary endothelium of the lungs and on platelets, which is why HPS is dominated by pulmonary capillary leakage and thrombocytopenia. It does not, by itself, explain the person-to-person observation.

The plausible biological hypothesis — still active research, not yet textbook — is that ANDV achieves measurable replication in upper-airway epithelium where Sin Nombre does not. The receptor is the same; the efficiency of replication and the resulting shedding into saliva and the upper respiratory tract differ. Viable virus has been recovered from saliva of late-prodromal ANDV patients (Padula et al., 2000); equivalent recovery from Sin Nombre patients is rare and the viral loads are markedly lower.

3. Viral load and shedding — the operational difference

The most direct evidence for why ANDV transmits where its relatives do not comes from longitudinal studies of patient viral load.

Lázaro et al., 2007 followed 22 ANDV patients in southern Argentina across the prodromal and cardiopulmonary phases. They reported peak viral loads in serum two to three log₁₀ higher than the published Sin Nombre series, with viable virus detectable in saliva of 12 of 22 patients during days 4–7 of illness. The window of plausible respiratory shedding lasts roughly five to seven days and overlaps the late prodromal period — exactly when patients feel ill but are usually still at home, in close contact with family members.

The 2024 reanalysis of the 2018-19 Epuyén cluster by Iglesias et al. (in Open Forum Infectious Diseases, building on their 2022 outbreak description) found that household members exposed during the late prodromal window had a secondary attack rate of approximately 8% — high enough to drive the 34-case Patagonian cluster, low enough to explain why ANDV does not produce mass outbreaks like influenza or SARS-CoV-2. The Argentine response playbook built on this evidence is described in the Argentina health response article.

4. The household-cluster studies — three decades of evidence

Five clusters anchor the empirical case for person-to-person transmission:

For the long-form analysis of how these clusters were investigated — including the genomic, geographic and epidemiological reasoning that ruled out shared environmental exposure — see the person-to-person transmission article.

5. Why not Sin Nombre? Why not Hantaan?

Three things distinguish ANDV from its closest hantavirus relatives:

1. Sin Nombre virus. Same receptor, same continent, related reservoir genus. But peak serum viral loads in Sin Nombre HPS are typically 10–100x lower, and viable virus has not been reliably recovered from saliva. The receptor expression model alone does not produce transmissible shedding without the viral-load substrate.
2. Hantaan virus. Old World, different receptor tropism (decay-accelerating factor on renal tubular cells in addition to αvβ3 integrin), different clinical syndrome (HFRS, renal-dominant). The biology is far enough away that direct comparison with ANDV is not informative.
3. Seoul virus. Globally distributed via Rattus norvegicus, the most cosmopolitan hantavirus reservoir. Despite global rodent presence, no documented person-to-person transmission. Suggests reservoir distribution and viral biology are independent variables.

6. What this means for the MV Hondius cluster

Three implications follow directly from the biology:

• Casual transmission is not expected. Patagonian household cluster data put the secondary attack rate among close contacts at single-digit percentages. Casual contacts — fellow-passenger encounters at a buffet, conversations on deck, shared elevator rides — are not in the same biological category as a household. The hantavirus vs. COVID comparison works through this distinction in detail.
• The cabin and medical-staff exposure model is the relevant one. Cabin-mates of confirmed cases and the ship's medical staff who provided clinical care during the prodromal-to-cardiopulmonary transition are the highest-risk contacts. This is consistent with the contact-tracing ring sizes documented in the contact-tracing methodology article.
• An aerosol-tropic mutation is the watchlist scenario. The single biological change that would shift ANDV from household-only transmission to broader respiratory spread would be a glycoprotein mutation enabling more efficient replication in upper-airway epithelium and aerosol-range shedding. WHO Collaborating Centres in Buenos Aires and Santiago are sequencing every Hondius isolate with explicit comparison to historical ANDV phylogenies. As of May 2026, no such divergence has been reported.

7. The receptor question, in plain language

Why does ANDV exist at all as a person-to-person hantavirus? The most plausible evolutionary explanation, advanced by Mertz et al., 2018, is selection in the reservoir for replication efficiency that coincidentally enables a low-frequency human-to-human bottleneck. The Patagonian Oligoryzomys longicaudatus is a sparser reservoir than Peromyscus maniculatus (the Sin Nombre reservoir) — fewer animals, more spread out, lower density of viral exposure. Higher replication efficiency in the rodent host may have selected for viral-load characteristics that, by accident, also produce transmissible shedding in human hosts.

This is a hypothesis. The evolutionary detail does not change the public-health response, but it does explain why the asterisk falls on ANDV specifically rather than randomly across the family.

8. Frequently asked questions

Is ANDV airborne?

No, in the conventional infectious-diseases sense of long-range aerosol transmission. The current evidence suggests droplet-range spread during sustained close contact — household partners, cabin mates, healthcare workers without N95 protection. The symptoms article covers what clinical signs to watch for.

Can I catch ANDV from a passenger I sat next to on a plane?

The biology suggests very low risk for a single bounded encounter. No documented in-flight transmission of any hantavirus has been reported in the published literature.

Is ANDV more dangerous than Sin Nombre virus?

Marginally, in case-fatality terms (35–40% vs ~36% for Sin Nombre). The fundamental difference is the transmission profile, not the clinical severity.

Could a different hantavirus develop person-to-person spread?

It is not impossible. Seoul virus, for example, replicates well and is globally distributed; a glycoprotein mutation altering upper-airway replication efficiency could in principle alter the transmission profile. WHO Collaborating Centres maintain genomic surveillance of human hantavirus isolates worldwide precisely because this scenario is biologically plausible, even if not currently observed.

Sources and further reading

• Wells RM et al. An unusual hantavirus outbreak in southern Argentina: person-to-person transmission? Emerging Infectious Diseases, 1997. (Open access)
• Padula PJ et al. Genetic diversity, distribution, and serological features of hantavirus infection in five countries in South America. Journal of Clinical Microbiology, 2000.
• Lázaro ME et al. Clusters of hantavirus infection, southern Argentina. Emerging Infectious Diseases, 2007. (PubMed)
• Iglesias AA et al. Andes virus pulmonary syndrome outbreak, Epuyén, 2018-19. Open Forum Infectious Diseases, 2022.
• Martinez VP et al. “Super-spreaders” and person-to-person transmission of Andes virus in Argentina. New England Journal of Medicine, 2020.
• Gavrilovskaya IN et al. β3 integrins mediate the cellular entry of hantaviruses that cause respiratory failure. PNAS, 1998. (PNAS)
• ICTV. International Committee on Taxonomy of Viruses — Hantaviridae.

Read next

• Andes virus full strain profile
• How the El Bolsón evidence was built
• Argentina's response — what containment looks like
• Compare hantavirus to other respiratory pathogens