Hantavirus at Sea
A deadly outbreak on a cruise ship raises urgent questions about a neglected pathogen
In late April 2026, passengers and crew aboard the MV Hondius, a Dutch-flagged expedition cruise ship returning from Antarctica and remote South Atlantic islands, began to fall gravely ill. Fever, pneumonia, and acute respiratory distress syndrome progressed rapidly. Three people died. Further confirmed or suspected cases of hantavirus infection were identified, with the Andes strain confirmed by PCR.
The ship, carrying 147 people from 23 countries, found itself marooned: Cape Verde lacked the capacity to manage an evacuation, and the president of the Canary Islands refused to allow the vessel to dock, citing fears of a local outbreak and the scarring memory of COVID-19. Spain’s central government eventually overruled him.
The Hondius saga is now, simultaneously, a clinical story, a public health story, and a story about how disease and inequality are inseparable — even at sea.
The leading investigative hypothesis is that the index cases, a Dutch couple, were exposed to infected rodent material during a birdwatching excursion to a landfill in Ushuaia, southern Argentina, before the voyage departed on 1 April 2026.
What is hantavirus, and why does the Andes strain matter?
Hantaviruses are a genus of single-stranded RNA viruses with a particular tropism for vascular endothelium. They are carried principally by rodents, which act as lifelong reservoirs without themselves becoming ill. Human infection is almost always acquired by inhaling aerosolised particles from infected rodent excreta. Most hantaviruses cause dead-end infections in humans: an individual gets sick, but the chain of transmission stops there. There is no person-to-person transmission.
The Andes virus, found predominantly in southern South America and carried by the long-tailed colilargo mouse (Oligoryzomys longicaudatus), is the single known exception. It is the only hantavirus strain for which human-to-human transmission has been documented. Transmission requires close, prolonged contact - household members, intimate partners, healthcare workers without adequate protection - and appears most likely during the early prodromal phase of illness.
Two principal disease syndromes result from hantavirus infection. Hantavirus Pulmonary Syndrome (HPS), the dominant pattern in the Americas, causes massive capillary leak into the pulmonary vasculature, producing non-cardiogenic pulmonary oedema and cardiogenic shock, with case fatality rates of 35–50% for the Andes strain. Haemorrhagic Fever with Renal Syndrome (HFRS), more common in Europe and Asia and caused by strains such as Puumala and Hantaan, primarily targets the kidney and carries lower but still significant mortality.
The pathophysiology: an immune system that becomes the enemy
Hantavirus pathology is immunopathological in nature. The virus does not destroy the endothelial cells it infects. Instead, it replicates within them while suppressing the early interferon response, buying time for widespread vascular spread before adaptive immunity can respond. When the immune response does engage, it is excessive and poorly regulated. A dense infiltrate of CD8+ cytotoxic T lymphocytes accumulates in affected tissues; the vigour of this response correlates with disease severity.
The result is a dysregulated cytokine storm — high TNF-α, IL-6, and interferon-γ — which destabilises the vascular endothelium through VE-cadherin disassembly (loosening the grip between endothelial cells and threatening barrier continuity) and elevated Vascular Endothelial Growth Factor (VEGF) signalling (increases vascular permeability). Capillary leak follows, flooding the lungs in HPS and the renal interstitium in HFRS. As the subsequent pulmonary oedema is due to increased capillary permeability, attempts to treat using a diuretic will not provide any benefit and can only decrease an already compromised circulating fluid volume.
Thrombocytopenia is almost universal, driven by platelet consumption, immune-mediated destruction, and direct viral binding via β3 integrin receptors, the receptors that hantavirus binds to to gain cellular access, and the occupation of which by the virus enhances the VEGF effect and further forces capillary leaking. Compensated disseminated intravascular coagulation can also emerge, with petechiae, haematuria, and occasionally more serious haemorrhagic complications.
In HPS specifically, a distinctive haemodynamic profile with low cardiac output, high systemic vascular resistance and relative bradycardia reflects direct cytokine-mediated myocardial depression rather than distributive shock. This pattern can mislead clinicians unfamiliar with the syndrome.
Could this become the next pandemic?
The question has circulated widely since the Hondius outbreak broke in early May 2026. The WHO has assessed the global public health risk as low, and epidemiologists are not anticipating a COVID-like scenario.
SARS-CoV-2 achieved global reach because it spread efficiently in the presymptomatic and asymptomatic phases: infected individuals who felt entirely well were seeding communities for days before their illness was apparent. Hantavirus does not do this. Individuals are not infectious before symptoms appear, and symptoms are severe enough to incapacitate quickly. The virus’s lethality constrains its spread.
Even in the Hondius outbreak, a confined ship with over 150 people in sustained close contact, an almost ideal scenario for respiratory pathogen spread, transmission remained limited to individuals with the most direct exposure. The R value estimated during the 2018–2019 Epuyen outbreak in Argentina, the largest documented Andes outbreak, was 2.12 before control measures, falling to 0.96 after their implementation. These figures reflect superspreader-driven dynamics in a tightly clustered community context, not a baseline biological constant, and should not be extrapolated to general population settings.
Continued vigilance, however, is necessary because of gaps in knowledge. Hantaviruses have been comparatively under-studied compared to other viruses. The mechanism by which the Andes virus acquired human-to-human transmissibility is not fully understood. No approved vaccine exists for any Americas-affecting hantavirus strain. And rising rodent populations in endemic regions, potentially linked to climate-driven shifts in habitat and food availability, may increase the frequency of zoonotic spillover events that could, in theory, provide further opportunities for adaptive evolution - and for human-to-human transmission.
At present, there is no specific treatment for hantavirus infection though access to intensive care does improve outcomes.
Who bears the burden?
The Hondius outbreak occurred aboard a luxury expedition cruise ship carrying passengers from wealthy nations on a voyage to Antarctica, but hantavirus is fundamentally a disease of poverty and marginalisation.
In endemic regions of South America, hantavirus disproportionately affects agricultural workers, forestry workers, and those living in rural housing with inadequate rodent exclusion. In Argentina, where the Andes strain is most prevalent, cases cluster among low-income rural communities with limited access to healthcare, poor housing stock, and occupational exposures that cannot be easily avoided. The 25.7% case fatality rate recorded across the Americas in 2025 reflects, in part, the absence of ECMO infrastructure in communities where cases actually occur. Survival from severe HPS in a well-resourced intensive care unit is better than survival in a rural district hospital.
In the UK context, hantavirus remains rare but is present. The predominant strains are Seoul virus (carried by brown rats) and Puumala virus (carried by bank voles). Cases are most commonly associated with occupational exposure - agricultural workers, sewer workers, laboratory staff, and increasingly, pet rat owners and hobbyist rat breeders. The UKHSA monitors cases and issues guidance on safe handling of potentially contaminated environments. Critically, rodent infestation in substandard housing represents a structural exposure risk that no amount of individual health messaging can adequately address without improvement in housing conditions.
For healthcare workers, awareness of hantavirus is important because of the importance in avoiding diagnostic delay. The prodromal syndrome is non-specific - fever, myalgia, headache, nausea, abdominal pain, very much like a flu or Covid presentation - and in the UK context, a clinician who has not considered hantavirus may pursue an extensive differential workup before the diagnosis is made. Occupational and exposure history, including contact with rodents or rodent-contaminated environments, should be routine.
Clinical and public health takeaways
Consider the exposure history. In any febrile illness with rapid respiratory deterioration, ask about rodent contact, rural environments, or travel to South America.
Thrombocytopenia plus haemoconcentration is a useful early marker of capillary leak syndrome; combined with an appropriate exposure history, it should prompt hantavirus testing.
The haemodynamic profile of HPS - low output, high resistance, relative bradycardia - is distinct from septic shock and requires a different management approach.
ECMO capability. Referral to an ECMO-capable centre for severe HPS should be considered early.
Infection control in suspected cases should include respiratory precautions given the theoretical risk of aerosol transmission, particularly for the Andes strain.
Housing and occupational policy are hantavirus prevention. Individual advice is necessary but insufficient without structural intervention in the conditions that drive rodent exposure.
Key references
Superspreaders and person-to-person transmission of Andes virus in Argentina — NEJM (2020)
Person-to-person transmission of Andes virus — NCBI PMC