Hantavirus Pulmonary Syndrome (HPS): Phases, Risk, and Care

Hantavirus pulmonary syndrome — usually abbreviated HPS — is the respiratory form of hantavirus disease, and it is the form driving the 2026 MV Hondius cluster. Unlike the slower kidney-centred syndrome seen in Eurasia, HPS kills by flooding the lungs from the inside within hours of a turning point that is easy to miss. This guide explains what HPS is, how it progresses, why it is so lethal, and how clinicians on three continents are now treating it.

1. HPS defined

Hantavirus pulmonary syndrome is a viral hemorrhagic-fever–adjacent illness caused by New World hantaviruses, most importantly Sin Nombre virus (SNV) in North America and Andes virus (ANDV) in South America. The defining lesion is non-cardiogenic pulmonary edema: damaged pulmonary capillaries leak plasma into the alveoli, the lungs become stiff and waterlogged, and oxygen exchange collapses. Cardiac output falls in parallel as the same vascular leak depressurises the circulation.

HPS was first recognised in May 1993 in the Four Corners region of the southwestern United States, where a cluster of previously healthy young adults developed sudden respiratory failure. Within weeks, investigators traced the disease to a then-unknown hantavirus carried by the deer mouse (Peromyscus maniculatus), later named Sin Nombre virus. The story of that outbreak is covered in our Four Corners 1993 deep-dive. Since 1993, HPS has been documented in more than a dozen countries across the Americas, and Andes virus has become the most clinically important strain because it is the only hantavirus with confirmed person-to-person transmission.

HPS, HCPS, and naming

Some references use the term hantavirus cardiopulmonary syndrome (HCPS)to emphasise the cardiac involvement that accompanies the lung disease. HPS and HCPS describe the same clinical entity. The U.S. Centers for Disease Control and Prevention and most surveillance systems still report under “HPS,” and that is the term used here.

2. The three phases of HPS

Clinicians describe HPS in three phases. Recognising which phase a patient is in changes everything about triage and transport.

Phase 1 — Prodrome (days 1–7)

The illness opens with a febrile, flu-like prodrome:

• Fever above 38.5 °C (101 °F)
• Severe myalgia, particularly thighs, hips, lower back
• Headache, dizziness, profound fatigue
• Gastrointestinal symptoms in roughly half of patients — nausea, vomiting, abdominal pain, diarrhea
• Notably absent or minimal: cough, sneezing, sore throat, runny nose

Routine influenza and COVID-19 tests are negative. Chest imaging is usually clear or shows only minimal interstitial markings. A complete blood count, however, may already show a falling platelet count, hemoconcentration, and a left-shifted neutrophil response with characteristic immunoblasts — laboratory clues experienced clinicians use to flag possible HPS before the lungs fail. Detail on these markers is in our diagnosis guide.

Phase 2 — Cardiopulmonary phase (days 4–10)

The transition to phase 2 can take hours. A patient who seemed merely flu-ish in the morning can be in respiratory failure by evening. The hallmarks are:

• New shortness of breath at rest, even brief
• Tachypnea (more than 22 breaths per minute) and tachycardia
• Hypotension and orthostatic light-headedness
• Initially dry cough, sometimes progressing to pink, frothy sputum
• Cyanosis, confusion, somnolence
• Chest x-ray showing diffuse bilateral infiltrates consistent with non-cardiogenic pulmonary edema

Hemodynamically, patients develop a low-cardiac-output state with narrow pulse pressures. Lactate rises, hematocrit climbs as plasma leaks out of the circulation, and the platelet count typically bottoms below 100 ×10⁹/L. This is the phase that kills.

Phase 3 — Convalescent phase

Patients who survive phase 2 enter a diuretic, convalescent phase. Capillary integrity is restored, fluid that leaked into the lungs is mobilised, and oxygen requirements fall over 24–72 hours. Recovery from this point is usually steady, although patients may experience weeks to months of exertional dyspnea and exercise intolerance. Long-term pulmonary function returns to normal in the majority of reported series.

3. Why HPS is so dangerous

Across all reported HPS series, the case-fatality rate sits between 30% and 50%. For Andes virus specifically, published series from Argentina and Chile have reported CFR in the 38–50% range, with the MV Hondius cohort tracking inside that band so far. Three features explain the lethality:

• Speed.The window between “feels like flu” and “needs ventilation” is sometimes less than 24 hours. Patients who self-isolate at home miss this window.
• Low clinical suspicion. HPS is rare. Most emergency physicians outside endemic zones have never seen a case. The prodrome mimics influenza, sepsis, or appendicitis.
• No specific antiviral. Care is supportive. Survival depends on recognising the cardiopulmonary phase early and providing intensive support — high-flow oxygen, mechanical ventilation, vasopressors, and where available, veno-arterial ECMO.

4. HPS in the 2026 MV Hondius outbreak

The MV Hondius cluster is unusual in three respects, all of which sharpen the public-health response.

The strain is Andes virus. ANDV is the only hantavirus with documented human-to-human transmission, mostly between close household and intimate contacts. This is why passenger contact tracing has been so aggressive, and why healthcare workers caring for HPS patients now wear airborne-precaution PPE rather than droplet-only. Background on the strain is in our Andes virus primer.

The exposure was a shared confined space. A cruise-ship outbreak concentrates a large, mobile cohort with a narrow exposure window. That is good for epidemiology (the index period is bounded) but bad for containment, because passengers disperse to dozens of countries during incubation. The 45-day active surveillance window adopted by France and others reflects the longer end of the documented incubation range.

Several patients have required ECMO. Tertiary centres in Argentina, Chile, France, the Netherlands, and Türkiye have reported the use of veno-arterial extracorporeal membrane oxygenation in HPS patients in profound cardiogenic shock. Where it has been initiated early — before multi-organ failure sets in — ECMO has appeared to improve survival in case series, though randomised data do not exist for HPS.

5. Diagnosis and testing

Laboratory confirmation of HPS rests on two pillars:

• Serology. Hantavirus-specific IgM antibodies appear within the first week of symptoms in nearly all patients and are the workhorse test in most reference laboratories. IgG rises slightly later and persists for years.
• Molecular testing. Reverse-transcription PCR on whole blood or serum can detect hantavirus RNA during the prodrome and into the cardiopulmonary phase. Strain-typing PCR distinguishes ANDV from SNV and from other regional hantaviruses — important for both clinical and epidemiological reasons.

In a suspected HPS case, clinicians typically order both simultaneously, along with a chest x-ray, lung ultrasound, complete blood count, basic metabolic panel, lactate, and coagulation studies. A normal chest x-ray does not exclude HPS in the prodrome. Patients with the right exposure history and suggestive laboratory clues should be admitted for observation even if imaging is clear. A fuller workup is described in our guide to hantavirus diagnosis.

6. Treatment and supportive care

There is no licensed antiviral for hantavirus pulmonary syndrome. Ribavirin, which has modest activity against the kidney-syndrome hantaviruses, has not shown a survival benefit in HPS in controlled trials. Care is therefore aggressive supportive care, ideally in a centre with critical-care expertise.

Core principles in current guidance:

• Early ICU transfer. Any patient with confirmed or strongly suspected HPS and any phase-2 sign should be managed in an intensive-care setting, even if currently stable.
• Cautious fluid management. Capillary leak means that aggressive crystalloid resuscitation will worsen pulmonary edema. Vasopressors are usually preferred over large volumes for hypotension.
• Mechanical ventilation with lung-protective settings (low tidal volumes, judicious PEEP) when oxygenation fails.
• ECMO referral pathways in centres equipped for it, particularly for younger patients with refractory shock.
• No empiric antibiotics needed once HPS is confirmed, although bacterial co-infection is sometimes treated while awaiting cultures.

General principles of supportive treatment, including what patients and families can expect in the ICU, are covered in our hantavirus treatment article.

7. Prevention

Outside of the MV Hondius outbreak, the overwhelming majority of HPS cases follow inhalation of aerosolised rodent excreta — urine, droppings, or saliva — in poorly ventilated indoor spaces such as cabins, sheds, or barns. Standard prevention is:

• Seal rodent entry points; do not sleep in rodent-infested structures
• Ventilate enclosed spaces for at least 30 minutes before cleaning
• Wet-clean with disinfectant; never sweep or vacuum dry droppings
• Wear gloves and an N95-equivalent respirator when handling rodent waste

The MV Hondius incident added a maritime dimension to this playbook. Cruise-line trade associations are now revisiting integrated pest-management standards, and several flag states have opened consultations on mandatory rodent surveillance during provisioning calls in endemic ports. The detail is in our piece on cruise-ship rodent control.

8. HPS vs HFRS — a quick comparison

Hantaviruses cause two clinically distinct syndromes. Knowing which one a clinician is looking at changes both monitoring and prognosis.

A more detailed contrast, including overlapping early features, is in our HPS vs HFRS comparison.

9. When to seek emergency care

Go to an emergency department, or call your local emergency number, if any of these apply:

• You had possible MV Hondius exposure within the last 8 weeks and you develop a fever
• You had close contact with a confirmed Andes-virus case and any new febrile or respiratory symptom
• You have new shortness of breath at rest
• You feel light-headed when you stand up
• Your fingernails or lips look bluish
• You are unusually confused, drowsy, or unable to keep fluids down with a high fever

For symptom-by-symptom detail, see our symptoms guide. For non-emergency questions about exposure or follow-up, contact your national or regional public-health authority; surveillance hotlines are listed alongside the MV Hondius timeline.

10. Frequently asked questions

How fatal is hantavirus pulmonary syndrome?

Across reported series, HPS kills 30–50% of recognised cases. Andes-virus HPS sits at the higher end. Survival is strongly linked to how quickly patients reach an ICU after the cardiopulmonary phase begins.

Is HPS contagious between people?

Most hantaviruses are not. Andes virus is the documented exception — it has caused household and healthcare-associated transmission chains in Argentina and Chile, which is why current infection-control guidance for ANDV is stricter than for other hantaviruses.

Is there a vaccine?

No vaccine is approved in North America, South America, or Europe. Candidate vaccines are in development. The current state of play is summarised in our vaccine status article.

Can HPS be treated with antibiotics?

No. HPS is viral. Antibiotics do not change the course of hantavirus infection, although clinicians may use them empirically until bacterial pneumonia or sepsis has been excluded.

Can HPS recur?

Re-infection has not been documented in survivors. The IgG antibody response after natural infection is durable, although long-term studies are limited.

This article is not medical advice. It is intended as a plain-language summary of hantavirus pulmonary syndrome for patients, families, and clinicians outside endemic zones who may encounter the disease in the context of the 2026 MV Hondius outbreak. For individual clinical decisions, defer to local public-health authorities, treating physicians, and current WHO, CDC, and PAHO guidance.