Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne viral disease caused by Dabie bandavirus, first identified in central China around 2009 and now reported across East and Southeast Asia with growing concern about its potential to appear elsewhere. The disease gets its name from its two hallmark features: high fever and a dangerous drop in platelet count. Case fatality rates vary by region and patient population but can run well above 10 percent, making SFTS one of the more lethal tick-borne infections currently on the radar of global public health agencies.
The Virus Behind the Disease
SFTS is caused by Dabie bandavirus (sometimes still referred to as SFTSV in older literature), a member of the genus Bandavirus in the family Phenuiviridae.1PubMed Central. Genetic variants of Dabie bandavirus: classification and biological/clinical implications It belongs to the same broad order of viruses (Bunyavirales) that includes Crimean-Congo hemorrhagic fever virus and Rift Valley fever virus, though Dabie bandavirus is a distinct pathogen with its own biology. The virus carries a segmented RNA genome, meaning its genetic material is split across three separate pieces, which gives it some capacity to diversify through genetic reassortment. One key protein, the nonstructural protein known as NSs, acts as a kind of saboteur against the human immune system. Research has shown that NSs physically traps critical signaling molecules (STAT1 and STAT2) inside viral structures within infected cells, effectively blocking the body’s interferon response, the frontline antiviral defense system.2PubMed Central. Disruption of type I interferon signaling by the nonstructural protein of severe fever with thrombocytopenia syndrome virus via the hijacking of STAT2 and STAT1 into inclusion bodies Researchers have described these viral structures as a kind of “jail” for host immune proteins, which helps explain why the virus can replicate so aggressively in the early stages of infection.
How SFTS Spreads
The primary route of transmission is the bite of an infected tick, particularly the Asian longhorned tick, Haemaphysalis longicornis. This tick species has been shown to maintain the virus across its entire life cycle, from larva to nymph to adult, and can pass it to offspring through eggs, a process called transovarial transmission.3PubMed Central. Transmission of Severe Fever with Thrombocytopenia Syndrome Virus by Haemaphysalis longicornis Ticks, China The tick also passes the virus between its own developmental stages, so a larva that picks up the virus during a blood meal can carry it through to the nymph and adult stages and transmit it to new hosts at each feeding. This dual ability to transmit the virus both vertically (parent to offspring) and across life stages means the tick population itself acts as a long-term reservoir, keeping the virus circulating even when mammalian hosts are scarce.4PubMed Central. Haemaphysalis longicornis Ticks as Reservoir and Vector of Severe Fever with Thrombocytopenia Syndrome Virus in China
But ticks are not the whole story. A wide range of animals carry antibodies against the virus, suggesting widespread exposure. A systematic review and meta-analysis found pooled antibody rates of roughly 46 percent in goats and sheep, 37 percent in cattle, and 30 percent in dogs, with lower rates in chickens, rodents, and pigs.5International Journal of Infectious Diseases. Animals as amplification hosts in the spread of severe fever with thrombocytopenia syndrome virus: A systematic review and meta-analysis Animals with active viral RNA have also been detected across multiple species, and phylogenetic analysis has confirmed that these animal-derived viral sequences cluster with human strains, reinforcing the idea that they share a common transmission cycle.6PubMed Central. Prevalence of severe fever with thrombocytopenia syndrome virus in animals in Henan Province, China Free-ranging livestock, as opposed to confined animals, show significantly higher antibody rates, which makes sense given their greater exposure to tick habitats.
Transmission from Animals and People
Direct animal-to-human transmission is no longer theoretical. Case reports have documented pet owners and veterinarians acquiring SFTS through close contact with infected cats and dogs, likely through exposure to the animals’ bodily fluids such as vomit or blood. One household cluster demonstrated multi-directional transmission from an infected dog to both humans and a cat living in the same home.7One Health. Transmission of severe fever with thrombocytopenia syndrome virus from a dog to humans and a cat in a household cluster This means that people caring for sick pets in areas where SFTS circulates face a real infection risk, not just from tick bites but from the animals themselves.
Human-to-human transmission has also been confirmed, primarily through direct contact with an infected person’s blood. A retrospective study of one cluster found that among 12 people who had direct blood contact with the initial patient, seven became infected, an attack rate of about 58 percent. None of the 11 people who avoided direct blood contact became ill.8PubMed Central. A cluster of severe fever with thrombocytopenia syndrome with household and nosocomial transmission in Zhejiang Province, China, 2023 Hospital-based (nosocomial) transmission has been documented as well, with whole-genome sequencing confirming that secondary cases in healthcare workers were genetically linked to index patients.9PubMed. Evidence of nosocomial human-to-human transmission of Dabie bandavirus: a clinical, epidemiological, and virological investigation Even seemingly protective measures can fall short: one family cluster involved five secondary patients who had all worn gloves and masks while caring for the index patient, but none wore eye protection. The ocular route was identified as the most likely mode of transmission in that outbreak.10PubMed. Human-to-human transmission of severe fever with thrombocytopenia syndrome virus through potential ocular exposure to infectious blood
What the Disease Looks Like
SFTS typically unfolds in stages over roughly two to three weeks. Researchers analyzing clinical symptoms and lab results over the disease course have categorized SFTS progression into five stages: an initial phase (roughly days 1 through 4), a progressive phase (days 5 through 7), a multi-organ dysfunction phase (days 8 through 10), remission (days 11 through 14), and convalescence (days 15 through 20).11PLoS Neglected Tropical Diseases. Precise staging of severe fever with thrombocytopenia syndrome: Integrating the extent of organ damage for prognostic and therapeutic applications The initial phase brings fever, fatigue, and muscle aches, symptoms that overlap with many other febrile illnesses and make early diagnosis tricky. Platelet counts and white blood cell counts begin dropping early and continue to fall through the progressive phase.
The most dangerous window is the critical phase spanning roughly the first two weeks. In the staging study described above, about 86 percent of patients who died did so within this two-week window, with nearly half of all deaths concentrated in the multi-organ dysfunction stage around days 8 through 10.12PLoS Neglected Tropical Diseases. Precise staging of severe fever with thrombocytopenia syndrome: Integrating the extent of organ damage for prognostic and therapeutic applications – Section: Abstract Patients who survive this window generally enter remission, with platelet counts recovering and organ function stabilizing over the following week.
Neurological Complications
Brain involvement is one of the most concerning complications. About one in four patients develops neurological symptoms, which can range from tremors and confusion to seizures and coma. One study found neurological symptoms in roughly 28 percent of patients, and those patients had significantly higher mortality at 28 days. Neurological involvement was independently linked to death even after accounting for other risk factors, roughly doubling the hazard of dying.13PubMed Central. Neurological Manifestations and High Viral Load as Independent Predictors of Mortality in Severe Fever With Thrombocytopenia Syndrome In a separate analysis specifically of SFTS-associated encephalopathy, the prevalence was around 23 percent, and patients with brain involvement had an in-hospital mortality rate of about 45 percent. The silver lining: survivors of encephalopathy largely returned to a normal quality of life after discharge.14PubMed. Analysis of the risk factors and prognosis for severe fever with thrombocytopenia syndrome associated encephalopathy One case report documented a 69-year-old woman who initially presented with involuntary shaking of the mouth and limbs before developing a full cytokine storm and multi-organ failure. After aggressive treatment including antivirals, steroids, and immunoglobulin, she recovered with a good outcome.15PubMed Central. Severe fever with thrombocytopenia syndrome with central nervous system symptom onset: a case report and literature review
Why the Platelet Count Drops
The dramatic fall in platelets, which defines the syndrome, involves at least two mechanisms. In mouse models, researchers found that the virus physically attaches to platelets, and these virus-coated platelets are then gobbled up by macrophages (immune cells that engulf foreign material) in the spleen. The spleen essentially acts as a clearance station, removing virus-tagged platelets from circulation faster than the body can replace them.16PubMed Central. Pathogenesis of emerging severe fever with thrombocytopenia syndrome virus in C57/BL6 mouse model A second pathway involves direct viral damage to the platelets themselves: the virus triggers production of reactive oxygen species inside platelets, leading to mitochondrial dysfunction and platelet self-destruction through a process called apoptosis.17PubMed Central. Severe fever with thrombocytopenia syndrome virus induces platelet activation and apoptosis via a reactive oxygen species-dependent pathway The combined effect of accelerated clearance and direct platelet death explains why platelet counts can crater so rapidly.
Layered on top of this is a broader immune overreaction. Extensive viral replication drives immune cells into dysfunction, triggering a massive release of inflammatory signaling molecules. This cytokine storm is now considered one of the core drivers of disease worsening. It damages blood vessel walls, promotes abnormal clotting within small vessels, and ultimately leads to multi-organ failure in severe cases.18PubMed Central. Immunopathogenesis of Severe Fever with Thrombocytopenia Syndrome: Core Driving Role of Cytokine Storm This pattern of initial viral assault followed by immune system self-destruction is a recurring theme in severe viral hemorrhagic fevers.
Who Is Most at Risk of Dying
Several factors predict a worse outcome. Advanced age is consistently identified as a risk factor, with fatal cases clustering among patients in their late 60s and 70s.19Scientific Reports. A nomogram to predict mortality in patients with severe fever with thrombocytopenia syndrome Beyond age, the development of multi-organ dysfunction, prolonged clotting times, and elevated markers of blood clot breakdown are independently associated with death. High viral load is another strong predictor: each tenfold increase in viral RNA roughly doubled the hazard of dying in one study, and patients with neurological symptoms carried about 2.5 times the mortality risk compared to those without.13PubMed Central. Neurological Manifestations and High Viral Load as Independent Predictors of Mortality in Severe Fever With Thrombocytopenia Syndrome What ties these risk factors together is that they all reflect how far the disease has progressed before the body (or medical intervention) can catch up. A person with a lower initial viral load, younger age, and intact organ function at presentation has a meaningfully better chance of surviving.
How SFTS Is Diagnosed
Diagnosis in the early stages relies on detecting the virus’s genetic material through molecular testing. In surveillance data from endemic areas of China, about half of suspected cases tested positive for viral RNA, with detection rates peaking in samples collected within the first week of illness and declining afterward as the immune response kicks in.20PubMed Central. Detection of SFTS virus RNA and antibodies in severe fever with thrombocytopenia syndrome surveillance cases in endemic areas of China Antibody testing becomes more useful later: IgM antibodies peaked in the second week after symptom onset, while IgG antibody rates climbed over time. Neither test alone catches every case. About 23 percent of patients whose viral RNA tests came back negative were actually IgM antibody-positive, meaning they would have been missed by molecular testing alone. Conversely, nearly 9 percent of IgM-negative patients tested positive for viral RNA.20PubMed Central. Detection of SFTS virus RNA and antibodies in severe fever with thrombocytopenia syndrome surveillance cases in endemic areas of China The practical takeaway is that combining molecular and antibody testing, timed to the stage of illness, gives the most reliable picture.
Treatment Options
There is no approved antiviral specifically for SFTS, and treatment remains largely supportive: fluids, blood product transfusions when platelet counts are critically low, and management of organ failure. The most studied drug candidate is favipiravir, an antiviral originally developed for influenza that works by jamming the virus’s ability to copy its RNA genome.
A large integrated analysis pooling data from a single-arm study, a surveillance cohort, and a randomized controlled trial matched 780 patients and found that favipiravir cut the case fatality rate from 20 percent to 9 percent. However, the benefit was not universal. It was significant only among patients aged 70 or younger, those admitted within five days of symptom onset, those treated for at least five days, and those whose initial viral load was below a million copies per milliliter.21PubMed Central. Clinical efficacy and safety evaluation of favipiravir in treating patients with severe fever with thrombocytopenia syndrome A separate interventional study using a historical control group found that favipiravir halved the fatality risk and was associated with reduced markers of the immune overreaction (specifically ferritin, a proxy for the severity of macrophage activation) during the treatment window.22PubMed Central. Efficacy of favipiravir treatment for patients with severe fever with thrombocytopenia syndrome assessed with a historical control A smaller Japanese trial of 23 patients reported a 28-day mortality rate of about 17 percent, lower than historical rates, with surviving patients clearing detectable viral RNA within a median of eight days. Liver function abnormalities turned up in about a fifth of patients, though SFTS itself also commonly causes liver damage, making it hard to pin the blame on the drug.23PLoS Neglected Tropical Diseases. A multicenter non-randomized, uncontrolled single arm trial for evaluation of the efficacy and the safety of the treatment with favipiravir for patients with severe fever with thrombocytopenia syndrome
The overall signal from multiple studies is that favipiravir helps, especially when given early, but it is not a cure-all, and patients who are already elderly with high viral loads and organ failure do not appear to benefit as much. Larger randomized controlled trials are still needed to confirm these findings and pin down exactly who benefits most.
Where SFTS Is Found and Where It Might Spread
SFTS has been primarily an East Asian disease. China has reported the most cases by far, with incidence rates reaching over 100 cases per 100,000 population in some highly endemic pockets, though most areas see far fewer. South Korea has the highest overall notification rate relative to population, with about 48 cases per ten million people, while Japan’s rate sits much lower at roughly 2.5 per ten million.24The Lancet Regional Health – Western Pacific. Global epidemiology of severe fever with thrombocytopenia syndrome virus in human and animals: a systematic review and meta-analysis Vietnam confirmed its first cases in 2017, and the disease’s geographic footprint in Asia continues to expand.25PubMed Central. Epidemiological Characteristics of Severe Fever with Thrombocytopenia Syndrome Most cases cluster between April and September, coinciding with peak tick activity in temperate zones.
What makes public health officials uneasy is the tick vector’s expanding range. Haemaphysalis longicornis has been established in parts of East Asia and Oceania for a long time, but it has now been found rapidly spreading in the eastern United States.26PubMed Central. Importance of Considering Seasonality in Tick Activity When Assessing Spatial Expansion Potential: A Case Study on Haemaphysalis longicornis Climate modeling suggests that environmentally suitable habitat for this tick extends across broad areas of the U.S. coastal states, the eastern and central interior, southern Canada, and parts of the Gulf of Mexico coastline.27Scientific Reports. Climate change influences on the potential geographic distribution of the invasive Asian longhorned tick, Haemaphysalis longicornis No autochthonous SFTS case has been confirmed in North America, but a related virus called Heartland virus already circulates in the U.S., carried by the lone star tick. Heartland virus belongs to the same genus as Dabie bandavirus and causes a clinically similar illness. Intriguingly, lab studies show that some antibodies against one virus partially neutralize the other, though cross-protection is not complete.28PubMed. Characterization of pseudotyped vesicular stomatitis virus bearing the heartland virus envelope glycoprotein Mouse studies found that immunity to Heartland virus protected against subsequent SFTS virus challenge, though whether this translates to humans remains unknown.29PubMed. Reverse genetics and comparative pathogenesis of Lone Star virus
Vaccines in the Pipeline
No vaccine for SFTS is available for human use yet, but candidates are moving through preclinical testing. One mRNA vaccine candidate, called VER-001, targets the two main surface proteins (Gn and Gc) that the virus uses to attach to and enter host cells. In mouse experiments, all vaccinated animals survived a lethal viral challenge, while all unvaccinated controls died within a week. The vaccine produced strong neutralizing antibody responses in a dose-dependent manner and activated cellular immune defenses as well. Viral RNA was undetectable in the blood and liver of vaccinated mice within days of challenge.30PLOS Neglected Tropical Diseases. The immunogenicity and protection efficacy evaluation of mRNA vaccine candidate for severe fever with thrombocytopenia syndrome in mice These are early-stage results in animals, and the gap between a successful mouse study and a licensed human vaccine is wide, but the 100 percent survival in vaccinated mice is a strong signal that the approach warrants further development.
Practical Prevention
For people living in or traveling to endemic areas, prevention still comes down to avoiding tick bites. Wearing long sleeves and pants, using tick repellents, checking your body after spending time outdoors, and promptly removing attached ticks are the standard recommendations. Because most cases occur from spring through fall, outdoor activity during these months in endemic regions carries the highest risk.
But tick avoidance alone is not sufficient from a public health perspective. Researchers increasingly argue for a One Health approach, recognizing that SFTS circulates among ticks, wildlife, livestock, companion animals, and humans as an interconnected system.31One Health. Coinfection patterns and associations of tick-borne pathogens in natural foci of severe fever with thrombocytopenia syndrome: A One Health approach Surveillance efforts that integrate data from human cases, animal seroprevalence, and tick ecology give a much clearer picture of local risk than any one data stream alone.32PubMed Central. One Health–based Joint Epidemiological Investigation of a Severe Fever with Thrombocytopenia Syndrome Case in the Republic of Korea, 2025 For veterinarians and pet owners, the documented animal-to-human cases underscore the importance of using gloves and eye protection when handling sick animals, particularly cats and dogs showing unexplained fever and bleeding in areas where SFTS is present. The disease’s potential to spread through blood contact also makes standard precautions in healthcare settings, including goggles or face shields during procedures involving blood, especially relevant when treating confirmed or suspected SFTS patients.
Long-Term Tick Surveillance and Emerging Risks
Understanding how tick populations shift over time is critical to predicting where SFTS might appear next. Multi-year ecological surveillance in South Korea, tracking tick density, species composition, and viral prevalence from 2018 through 2024, has shown that combining climate data, ecological monitoring, and human case mapping improves risk assessment even in areas with relatively low virus detection rates in ticks.33PubMed Central. Long-term ecological surveillance of hard ticks (Acari: Ixodidae) and SFTSV in Dangjin, South Korea (2018-2024) The fact that H. longicornis ticks are now established and expanding in the eastern United States, with climate projections suggesting large additional suitable zones, means that even regions without any current SFTS cases may need to build the surveillance infrastructure to detect the virus if and when it arrives. Whether Dabie bandavirus itself will follow its tick vector across the Pacific remains one of the open questions in emerging infectious disease research, and the answer depends partly on whether North American wildlife can sustain the virus in the same way Asian livestock and small mammals do.