Hantavirus kills fast while leaving survivors unscarred

Andes hantavirus – From a cruise ship outbreak on the MV Hondius to deep questions about how Andes virus harms blood vessels without attacking lung tissue, scientists are racing to explain why hantavirus pulmonary syndrome can turn deadly within hours—and why survivors often wal

For many respiratory viruses, the story is familiar: they invade lung cells, inflame the tissue, and damage is what lingers. With New World hantaviruses, including Andes virus, the timing and the damage pattern don’t match that script.

Andes virus infections can progress from infection to severe illness in a matter of days at most—and then fast. brutal decline when it begins. Scientists studying the strange mechanics behind hantavirus pulmonary syndrome say the virus grows slowly at first. yet can kill swiftly once symptoms begin. claiming the lives of up to half of the people it infects. Even stranger, survivors are left with no lasting damage from the illness.

That puzzle is now part of the emergency response to the recent outbreak of the Andes hantavirus on the cruise ship MV Hondius. More than 150 individuals worldwide are currently in quarantine, and three people have already died in the outbreak. Nine others are ill, some critically.

It has also become the driving question for treatment research: how a virus that doesn’t attack lung cells can still flood the lungs, trigger shock, and overwhelm patients so quickly—then appear to “switch off” and allow recovery.

When hantavirus takes a different route into the body

Respiratory viruses such as influenza, RSV and the coronavirus that causes COVID-19 infect and kill lung cells, while immune reactions further the damage.

New World hantaviruses cause a severe lung disease called hantavirus pulmonary syndrome, but they don’t attack lung cells. Instead, the virus infects cells lining blood vessels throughout the body. Clinical virologist Pablo Vial. who directs the hantavirus and zoonoses program at the German Clinic at the Universidad del Desarrollo in Santiago. Chile. says the main target is the tiny blood vessels called capillaries.

Jonas Klingström, a virologist and immunologist at Linköping University in Sweden, describes what happens to infected cells: “Infected cells may lose some function, but they don’t die. They are not killed.”

This focus on capillaries helps explain why hantavirus behaves differently from the lung-centered pattern people expect from respiratory illness. But scientists say there’s more to it than geography in the body.

Andes virus and other New World hantaviruses have only four proteins. By contrast, other respiratory viruses have more than twice as many. Two of the four proteins help the virus enter cells. One replicates viral RNA, and one forms the viral shell. Old World hantaviruses—known mainly from Europe and Asia and generally associated with kidney damage—have an additional protein.

With such a small toolkit, the virus appears to do its work with precision. Klingström says the viruses are “really sneaky.” They can both inhibit antiviral responses and avoid activating them.

A long incubation, then a sudden collapse

Scientists say it may take up to 45 days for an infected person to develop symptoms. Vial says most people with Andes virus infections become sick enough to need oxygen. but 40 percent recover without serious medical intervention. The remaining patients develop severe disease requiring intensive care.

The turning point comes when tight junctions—proteins that weld blood vessel cells to their neighbors—loosen. Blood plasma, the fluid part of blood, can then seep out while blood cells stay inside. Scientists don’t yet know what turns on the process that makes those junctions loosen.

Vial says it isn’t viral replication that drives the change. Whatever it is happens fast. Within hours, patients’ lungs fill with leaking fluid, disrupting breathing. Their hearts fail and their blood pressure drops, putting them into shock.

The gap between infection and symptoms helps explain why public health monitoring has to be so careful. Crew and passengers of the MV Hondius—and people exposed to a cruise passenger on later airline flights—are being monitored for six weeks after their last possible exposure.

The U.S. Centers for Disease Control and Prevention has asked that the 18 Americans being monitored at special quarantine facilities in Omaha. Neb. remain there at least until May 31. even though some passengers have requested to quarantine at home. The speed from symptom onset to serious illness is part of the reason for that caution.

Vial says his team has learned what the disease looks like early and how it progresses. He has helped treat many of the nearly 1,500 Andes hantavirus cases that have been diagnosed in Chile since 1995.

When patients die, it often happens quickly after admission. Vial and colleagues discovered this by reviewing 100 hantavirus cases treated at eight hospitals in Chile over about eight years. According to the unpublished data they reviewed, there were 21 deaths among those cases. Most patients who died did so either while being admitted to the hospital or within the first 24 hours after admission.

Once the fluids start leaking into lungs, the picture can look deceptive. Some people have mild cases with little fluid hazing X-ray images of their lungs. but in most cases the fluid floods the small airways. producing an appearance described as being stuffed with cotton. That degree of fluid build-up requires intensive care and perhaps support from a heart-lung machine to survive.

Ventilators may not be enough

That urgency is part of why Vial describes treatment timing in stark terms. When a ventilator isn’t enough, doctors turn to extracorporeal membrane oxygenation, or ECMO. Vial describes ECMO as a heart-lung machine that pumps blood out of the body. oxygenates the blood. and returns it to the body so the ailing lungs and heart get a rest.

He says the clinical pace can be shockingly rapid: “I’ve been talking to patients at noon and at two in the afternoon, they’re already connected to mechanical ventilation, and at three, they are already on ECMO. So this is very, very fast development.”

Then comes the reversal that researchers say is almost unlike other respiratory diseases. The spigots can dry up, and patients can recover. Vial says it takes 48 to 72 hours for this biological effect to reverse and become completely normal.

That kind of recovery speed is “unheard of” among respiratory diseases. Often, people spend weeks in intensive care for severe flu or COVID-19 and are left with damaged, scarred lungs that may never fully recover.

The mechanism behind that apparent reset is still unclear. Vial says antibodies developed over the course of infection may have something to do with getting the virus in check, but the immune system doesn’t cull infected cells. How hantaviruses protect host cells remains a mystery.

What’s missing in treatment—and what might be possible next

Current medical care can provide supportive treatment for symptoms, but it can’t stop the virus. There are currently no specific treatments or vaccines for hantaviruses.

Vial and colleagues have tried several ways to keep patients off life support. An antiviral drug that stops hantavirus growth in lab dishes didn’t work in patients who were developing severe symptoms. Steroid treatment with methylprednisolone—used in other respiratory illnesses such as COVID-19—also didn’t work.

Plasma from patients who have recovered from a hantavirus infection can help when people are just developing symptoms. Vial says antibodies in recovered people’s blood may keep the virus from entering blood vessel cells.

Other ideas depend on older immunity. Mattias Forsell, an immunologist at Umeå University in Sweden, says antibodies developed over the course of infection with Puumala virus—an Old World hantavirus carried by bank voles—could also fight Andes virus.

Puumala virus is carried by bank voles and caused. on average. about 3. 100 cases annually in Europe from 2010 through 2020. particularly in Finland. Sweden and Germany. Forsell and colleagues have tracked hantavirus antibody levels in blood from about 150. 000 participants in the Northern Sweden Health and Disease Study. In areas where Puumala virus is endemic, about 11 to 12 percent of participants have antibodies against the virus. Those antibodies persist for at least 22 years, the team found.

Forsell says: “These infections may actually provide immunity for life.” In unpublished studies, his team has found that some of those antibodies can latch onto other hantaviruses, including Andes virus. He suggests those antibodies may become the basis for future therapies.

For the capillary leaks themselves, researchers are looking at immune signals that might pry open the connections between blood vessels. Klingström and other researchers have found elevated levels of certain immune system proteins called cytokines in people with severe hantavirus disease. Among the cytokines suspected of prying open the connections are interleukin-6 (IL-6) and bradykinin.

Klingström and colleagues report that blood vessel cells infected with hantaviruses also make IL-6. In the case of Andes virus, increased levels of IL-6 in the blood were associated with more severe disease; they reported this in 2019 in the Journal of Infectious Diseases.

IL-6 is a messenger molecule that signals immune cells to fight viruses, but it can also trigger damaging inflammation. Which pathway IL-6 uses determines whether capillaries leak, Klingström and colleagues reported in 2025 in PLOS Pathogens. Klingström says some drugs already in clinical trials may block a harmful delivery pathway, potentially stopping capillary leaks.

There’s also bradykinin. Vial and colleagues have experimented with a drug called icatibant that blocks bradykinin. The drug is already approved to treat a rare genetic condition called hereditary angioedema. in which people develop spontaneous swelling in the face. hands and other parts of the body. Vial says it has helped a woman with severe Puumala virus infection recover quickly. but large clinical trials are needed to establish whether the drug is an effective treatment.

The fastest-moving question may be how to stop the drowning without waiting for the biology to reverse on its own. Klingström says combinations of drugs may keep people from drowning in their own fluids.

No one expects new treatments to appear quickly enough for the current cruise ship outbreak. but researchers say the urgency could still accelerate progress. Klingström says it should be possible to design treatments that could quickly reverse the disease mechanics and save patients from this life-threatening condition.

The human stakes are immediate on the MV Hondius. Three deaths and nine seriously ill people are already known from the outbreak response. But behind them is a scientific problem that may be solved only once: how a virus can be both deadly and oddly self-limited—killing swiftly. yet leaving survivors with no lasting damage—while it spreads its effects through capillaries. not lung cells. and turns shock on and off on a timeline measured in hours.

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