Lassa Fever Virus Explained

Lassa fever virus infects an estimated 100,000 to 300,000 people a year in West Africa, according to long-cited CDC estimates, yet most of those people never learn they were infected. About four in five infections cause mild symptoms or none. In the rest, the virus can trigger bleeding, shock, and organ failure, and the CDC says about one in three cases involves some level of deafness. This article explains how a rat-borne virus named for a Nigerian village spreads, what it does inside the body, and why the evidence behind its standard treatment is thinner than most people assume.

Educational content, not medical advice. This article summarizes published research and public-health guidance. It cannot diagnose or treat anyone. Anyone with a fever after travel to West Africa, or any health concern, should speak with a doctor or local health authority.

Discovery: a village, two nurses, and a laboratory accident

The virus takes its name from Lassa, a village in Nigeria. In January 1969, an American missionary nurse from that village was flown about 400 miles to Bingham Hospital in Jos with a fever and an unexplained hemorrhagic illness. She died about 24 hours later. A week later another nurse at the hospital fell ill with the same disease and died. A third nurse, Penny Pinneo, who had cared for both, became ill with a temperature of 107°F (about 41.7°C) (ASTMH).

Pinneo was evacuated to New York and admitted to Columbia-Presbyterian Hospital. She recovered after a stay of about nine weeks. Her blood went to a laboratory at Yale, where the virologist Jordi Casals isolated the new virus and named it for the village.

The discovery came at a price. According to the American Society of Tropical Medicine and Hygiene, Casals and a research technician, Juan Roman, were both infected in the laboratory. Roman died. Casals survived, which the same account largely attributes to convalescent serum (blood plasma containing antibodies) donated by Pinneo. Yale halted the work and sent the samples to the CDC in Atlanta (ASTMH). The episode was an early warning that hemorrhagic fever viruses demand specialized containment, a theme that runs through the history of Ebola and Marburg as well.

What kind of virus is Lassa?

Lassa virus belongs to the arenaviruses, a family whose name comes from the Latin word for sand, because the particles contain host ribosomes that look like grains under an electron microscope. Its genome is made of RNA split across two pieces, called the S (small) and L (large) segments. Each segment carries two genes in an arrangement called ambisense, meaning genes are read in both directions along the same strand (Lukashevich and Salvato, Current Genomics).

The two segments divide the labor roughly like a toolbox and a blueprint case:

Segment	Approximate size	What it encodes	Role
S (small)	about 3.4 kilobases	Nucleoprotein (NP) and glycoprotein precursor (GPC)	NP wraps the RNA; GPC is cut into GP1 and GP2, the spikes used to enter cells
L (large)	about 7.2 kilobases	Polymerase (L) and the Z protein	The polymerase copies the genome; Z, a small matrix protein, helps assemble new particles

Sizes and functions as summarized in the literature on arenavirus genomes (Current Genomics review).

How the virus gets into a cell: a keycard, then a side door

Entry works in two steps, a bit like a building that needs a keycard at the front door and a different pass for an inner room. The GP1 spike first binds a surface molecule called alpha-dystroglycan, which is found on many cell types. After the cell swallows the particle into a bubble called an endosome, the falling acidity inside that bubble pushes the virus off alpha-dystroglycan and onto a second receptor, LAMP1. GP2 then drives fusion of the viral envelope with the endosome membrane, releasing the genome into the cell (study of Lassa virus entry, PMC).

A later study found that LAMP1 helps fusion occur at a less acidic pH, which may let particles escape the endosome before its increasingly harsh interior inactivates them. LAMP1 is not strictly required, since cells lacking it still support low levels of infection (PMC5750398). Because both receptors are widespread, the virus can reach many organs, which fits the multi-system nature of severe disease. For a broader look at what happens after entry, see how viruses work from infection to replication.

The reservoir: how a household rat carries it

The natural host is the multimammate rat, Mastomys natalensis, a rodent that breeds frequently and produces large litters. The CDC describes it as numerous in the savannas and forests of West, Central, and East Africa and as the main source of human infection (CDC; CDC Stacks). Rodents shed the virus in urine and droppings, and because these rats live in and around homes and scavenge food scraps, household exposure is common.

The rats are the virus's long-term home, a bit like a river is the home of a fish. The animals carry the virus without the severe disease humans get, and humans are an accidental stop. That is why the ecology of the rodent, not the behavior of infected people, drives most of the epidemiology. The pattern is a textbook case of animal-to-human spillover, explored more broadly in how viruses jump from animals to humans.

Is every outbreak spread from person to person?

Genomic evidence says no. When Nigeria saw an unusual surge of cases in 2018, researchers sequenced 220 Lassa virus genomes from patients, 129 of them from the 2017 to 2018 season. The 2018 genomes came from many lineages already circulating in Nigeria rather than from one dominant strain, and the data fit many independent rodent-to-human transmissions better than chains of human-to-human spread. The authors could not say why cases rose, and noted possible roles for changes in rodent populations or for better surveillance (Siddle et al., New England Journal of Medicine, 2018).

How people get infected, and why it is not Ebola

According to the CDC, people mostly become infected by contact with rodent urine or droppings, including by breathing contaminated air or eating contaminated food. Lassa fever can also pass between people through contact with an infected person's body fluids, and it can spread in healthcare settings without proper protective equipment. It does not spread through casual contact such as hugging or shaking hands (CDC). The WHO adds that person-to-person spread occurs mostly in healthcare settings and that it found no epidemiological evidence of airborne spread (WHO).

That distinction separates Lassa from Ebola, which spreads through direct contact with the blood or body fluids of a sick or deceased person, including in funeral ceremonies. The WHO also notes that Ebola patients are not infectious before symptoms appear (WHO Ebola fact sheet).

Feature	Lassa fever	Ebola disease
Natural host	Multimammate rat (Mastomys natalensis)	Fruit bats thought to be the natural hosts
Main route to humans	Rodent urine and droppings, contaminated food and surfaces	Contact with blood, secretions, or organs of infected animals
Spread between people	Mostly in healthcare settings	Direct contact with blood or body fluids of a sick or deceased person
Case fatality	About 1% across all infections; 15% or more in hospitalized severe cases	Average about 50%; past outbreaks 25% to 90%
Licensed vaccine	None	Ervebo, plus Zabdeno and Mvabea

Sources: WHO Lassa fever fact sheet, WHO Ebola fact sheet. The case fatality figures are not directly comparable: the Lassa figure includes the many mild infections that never reach a hospital, while the Ebola figure describes confirmed disease.

Where it occurs: a snapshot from Nigeria

The WHO lists Benin, Ghana, Guinea, Liberia, Mali, Nigeria, and Sierra Leone as countries where the disease is endemic, and says the virus probably circulates in other West African countries too (WHO). Nigeria's national public-health agency, the Nigeria Centre for Disease Control and Prevention (NCDC), publishes weekly Lassa fever situation reports, which makes the country's numbers unusually visible.

The NCDC report for epidemiological week 7 of 2026 (February 9 to 15) gives a feel for the scale:

Measure	2026, weeks 1 to 7	2025, weeks 1 to 7
Suspected cases	1,538	2,178
Confirmed cases	326	451
Deaths among confirmed cases	75	89
Case fatality rate (confirmed)	23.0%	19.7%
States with a confirmed case	16 (58 local government areas)	12 (66 local government areas)

Source: NCDC Lassa Fever Situation Report, Epi Week 7, 2026. In the same report, 84 percent of confirmed cases came from four states (Bauchi, Ondo, Taraba, and Edo), the median age was 30 years, and five new healthcare workers were affected that week.

Two things stand out. First, the case fatality rate among confirmed cases (23 percent) is far above the WHO's 1 percent figure for all infections. That is not a contradiction: confirmed cases are the sick people who got tested, while the 1 percent figure counts the many who never showed up in any statistics. Second, a few hundred confirmed cases in seven weeks is tiny next to the CDC's estimate of 100,000 to 300,000 infections per year, which shows how much of the disease burden is never captured.

The iceberg: why estimates are so uncertain

The CDC's annual estimate of 100,000 to 300,000 infections and about 5,000 deaths comes with a frank caveat from the agency itself: "such estimates are crude, because surveillance for cases of the disease is not uniformly performed" (CDC Stacks). A 2018 review on Lassa-related hearing loss cited a higher figure of 500,000 cases a year with 5,000 deaths (Mateer et al., PMC). The range reflects how hard it is to count a disease that looks like malaria.

Think of the disease as an iceberg. The visible tip is the small number of patients who reach a hospital with severe symptoms and get a laboratory test. Below the waterline sit the roughly 80 percent of infections that are mild or silent, plus severe cases in places with no test, no clinic, or no record. The WHO notes that Lassa is clinically hard to distinguish from malaria and other fevers, and that confirmation requires RT-PCR, ELISA, antigen detection, or virus isolation in cell culture (WHO). Where those tests are scarce, the iceberg stays hidden.

Lassa fever's case fatality rate depends entirely on who is counted: about 1 percent of all infections, 15 percent or more of hospitalized severe cases (WHO), and 23.0 percent of confirmed cases in Nigeria's first seven weeks of 2026 (NCDC).

The clinical course: from vague fever to shock

The CDC says symptoms typically appear one to three weeks after infection. The WHO gives an incubation period of 2 to 21 days. Most people have mild symptoms such as slight fever, fatigue, and headache. In some, the illness becomes serious, with bleeding, difficulty breathing, shock, and facial swelling (CDC). About one in five infections becomes severe (WHO).

Clinicians have long tried to spot which patients are headed for trouble. A raised level of the liver enzyme AST (aspartate aminotransferase) is also used as a severity marker: the 2022 review discussed below analyzed patients split at 150 international units per liter, a cutoff commonly treated as a warning sign (Cheng et al., 2022).

Hearing loss: the virus's signature aftermath

The most distinctive long-term complication is sudden sensorineural hearing loss, damage to the inner ear or the nerve behind it. The figures vary by study, which is typical for a condition studied in hospitals with limited resources:

• WHO: sudden hearing loss affects up to 25 percent of recovered patients, usually permanently (WHO).
• CDC: about one in three cases involves some level of deafness, in mild and severe cases alike, and it is often permanent (CDC).
• Pooled literature: a 2018 review averaged five studies to 33.2 percent, with a range from 4 percent to 75 percent (Mateer et al.).

The landmark study came from Sierra Leone. Cummins and colleagues tested hospitalized febrile patients and found a sensorineural hearing deficit in 14 of 49 (29 percent) with confirmed Lassa fever, and in none of 20 febrile controls (Cummins et al., JAMA, 1990). The deafness began 5 to 12 days after the fever subsided, during convalescence.

What causes the deafness?

The answer is not settled, but the evidence leans toward the immune system rather than the virus itself. In the Sierra Leone work, deafness did not track with viral load, liver enzymes, disease severity, or ribavirin use, which led the authors to propose an immune-mediated mechanism. The idea resembles friendly fire: the body's defenses, ramping up to clear the infection, may injure the delicate cochlea as collateral damage. A mouse model supports this. Stat1-deficient mice developed hearing loss 16 to 45 days after infection, with an estimated 85 percent prevalence among survivors. Their inner ears showed nerve damage and infiltration by T cells, while mice lacking the interferon receptor had higher viral loads but did not develop hearing loss. The reviewers conclude that immune-mediated injury is favored but direct viral damage cannot be ruled out (Mateer et al.). To understand the structure involved, see how hearing works.

There is no proven treatment for the hearing loss either. In a Nigerian study of early-onset cases, patients received steroids, hyperbaric oxygen, vasodilators, vitamins, and hearing aids, and no improvement was reported. The same review estimated the hearing-loss burden at roughly $43 million per year in Nigeria, where about 1 percent of affected people have access to hearing aids.

Pregnancy: the highest-risk setting

The WHO states that in the third trimester of pregnancy, fetal death rates can exceed 80 percent and maternal death rates can exceed 30 percent (WHO). The CDC page gives a starker number, saying about 95 percent of fetuses do not survive when a pregnant woman is infected (CDC). The two agencies' figures differ because they draw on different, small case series, so treat them as a description of very high risk rather than a precise rate.

Treatment: what ribavirin can and cannot claim

Ribavirin, an antiviral that interferes with viral RNA copying, is the drug most often associated with Lassa fever. The CDC says it has been used successfully and works best when given soon after symptoms begin, alongside supportive care such as hydration (CDC). The WHO takes a more cautious line: ribavirin's efficacy is uncertain, as is the best dose, and patients should ideally be enrolled in randomized clinical trials (WHO).

Why the disagreement? Most of the support traces to one 1986 study by McCormick and colleagues, which reported that intravenous ribavirin started within six days of illness cut mortality in severe cases from 55 percent to 5 percent. Cheng and colleagues, writing in Emerging Infectious Diseases in 2022, classified that study as an observational cohort, not a randomized trial, because patients were not randomly assigned to treatment (Cheng et al., 2022).

Their review pooled 13 studies comparing ribavirin with no ribavirin, including unpublished Sierra Leone data obtained through a US Freedom of Information Act request. Nearly all results were rated at critical risk of bias, mostly from poor control of confounders, immortal time bias (a statistical trap where patients must survive long enough to receive the drug, flattering the treated group), and missing data. Most studies showed lower mortality with ribavirin, but the unadjusted original data showed higher overall mortality in the treated group, and results split by AST level pointed in opposite directions. The authors concluded: "it is uncertain based on the available literature whether ribavirin reduces mortality rates in Lassa fever patients" (Cheng et al., 2022).

That is not the same as saying ribavirin does not work. It says the evidence cannot yet separate a real benefit from the biases in old data. Until trials are done, the honest summary is that ribavirin is the standard drug by habit and limited evidence, not by proof.

What is being tested now?

A multinational randomized platform trial called INTEGRATE, registered as NCT06212336, is comparing favipiravir against intravenous ribavirin (ClinicalTrials.gov NCT06212336). No results had been published as of this writing. Until results appear, any claim that a specific drug is better should be treated as unproven.

Vaccines: a candidate in phase 2

No licensed vaccine exists (WHO). The most advanced candidate, according to IAVI (the International AIDS Vaccine Initiative, a nonprofit vaccine developer), is rVSVΔG-LASV-GPC, which uses a harmless vesicular stomatitis virus as a carrier for the Lassa glycoprotein. The phase 1 results were published on November 6, 2025 in the New England Journal of Medicine. The trial enrolled 114 volunteers, randomized to one of four dose levels or a placebo, at sites in Liberia and the United States.

Both antibody and cellular immune responses were detected at all dose levels up to 12 months, and the antibodies cross-reacted with other Lassa lineages circulating in West Africa. No vaccine-related serious adverse events and no hearing loss were reported. An IAVI-sponsored phase 2a trial supported by the Coalition for Epidemic Preparedness Innovations (CEPI) is ongoing in West Africa (IAVI). A phase 1 trial tests safety and immune response in small groups; efficacy in preventing disease has not been shown. For how vaccines train the immune system in general, see how vaccines work.

The WHO lists Lassa fever among the priority diseases in its R&D Blueprint, which focuses limited research resources on diseases with epidemic potential and no effective countermeasures. Lassa fever has been on that list since at least the February 2018 review, and the blueprint also names Ebola, Marburg, MERS, Nipah, Zika, and a placeholder "Disease X" (WHO).

When Lassa leaves West Africa

Travel-related cases are rare but real. In February 2022 the UK Health Security Agency confirmed three Lassa fever cases in one family in the East of England, all linked to recent travel to West Africa, and one patient died. Contact monitoring finished by March 4, 2022 with no further cases found, and the agency said the risk to the general public remained "very low." Before that cluster, eight Lassa cases had been imported into the UK since 1980, the most recent in 2009 (UK Government).

The pattern follows from the biology. The rat reservoir does not live outside Africa, and the virus does not spread easily between people outside healthcare settings, so imported cases tend to be dead ends if infection control is sound. A related rodent-borne virus on another continent, covered in hantavirus explained, shows a similar logic of animal reservoirs and rare human chains.

What people get wrong about Lassa fever

"It is basically Ebola." The two are both hemorrhagic fevers and both zoonoses (diseases that jump from animals to people), but the reservoir, the spread, and the case fatality differ, as the table above shows. Most Lassa infections are mild, and sustained community spread between people has not been the pattern.

"A 20 percent death rate means one in five infected people die." That number comes from confirmed or hospitalized patients. The WHO's overall figure is about 1 percent, and the gap is mostly a counting artifact, not a contradiction.

"There is a proven cure." There is a widely used antiviral with limited and contested evidence, plus supportive care. The trial that would settle the question has not yet reported results.

"Hearing loss only follows severe disease." The CDC states that deafness can occur in both mild and severe cases, which is why survivors of seemingly easy infections can still be affected.

For readers comparing Lassa with other dangerous viruses, the deadliest viruses on the planet puts several of them side by side.

Frequently Asked Questions

Q: How do people catch Lassa fever? A: Mostly through contact with the urine or droppings of infected multimammate rats, including by eating contaminated food or breathing contaminated air. The CDC also says it can spread between people through body fluids, particularly in healthcare settings without proper protective equipment. It does not spread by casual contact such as hugging or shaking hands.

Q: Can Lassa fever spread between people like Ebola? A: Not in the same way. The WHO says person-to-person spread occurs mostly in healthcare settings and that there is no epidemiological evidence of airborne spread. Ebola spreads through direct contact with the blood or body fluids of sick or deceased people, including during funerals, and has produced much larger outbreaks.

Q: What is the real death rate of Lassa fever? A: It depends on who is counted. The WHO puts the overall figure at about 1 percent of infections and 15 percent or more among hospitalized patients with severe disease. Among confirmed cases in Nigeria in the first seven weeks of 2026, the NCDC reported a fatality rate of 23.0 percent.

Q: Does ribavirin cure Lassa fever? A: That has not been shown. Ribavirin is widely used and the CDC says it works best early, but a 2022 systematic review found that nearly all supporting studies were at critical risk of bias and concluded it is uncertain whether ribavirin reduces mortality. The WHO calls its efficacy uncertain and recommends trials.

Q: Why do some survivors lose their hearing? A: The best-supported explanation is immune-mediated injury to the inner ear during convalescence, though direct viral damage is not ruled out. Studies report hearing loss in roughly 25 to 33 percent of survivors, with a very wide range between studies, and in mild as well as severe cases.

Q: Is there a vaccine for Lassa fever? A: No vaccine is licensed. The leading candidate from IAVI completed a phase 1 trial published in the New England Journal of Medicine in November 2025, showing immune responses and no vaccine-related serious adverse events, and a phase 2a trial is ongoing in West Africa. Efficacy in preventing disease has not yet been demonstrated.

Q: Is Lassa fever a risk outside West Africa? A: Rarely. Imported cases occur through travel, such as three linked cases in the UK in February 2022, but the rodent host is not found outside Africa and the UK Health Security Agency found no onward spread, assessing the public risk as very low.

The takeaway

Lassa fever is a story of counting problems as much as virology. A common household rat, a virus that most people clear without noticing, and a diagnostic gap together hide an epidemic whose true size can only be guessed, from 100,000 to a few hundred thousand infections a year. The headline fatality rate shifts from 1 percent to over 20 percent depending on whether the denominator is every infection or only the sick people who reach a laboratory. The same uncertainty shadows treatment: the standard drug rests on observational data that a 2022 review found too biased to prove benefit, and the trial to settle it has not yet reported. What is solid is the biology of spillover from rodents, the immune-linked deafness that follows many infections, and a vaccine candidate that has cleared its first human safety test.

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• BK Virus, JC Virus & Polyomaviruses Explained
• Chikungunya Virus Explained

Sources

• WHO — Lassa fever fact sheet (December 5, 2024)
• CDC — About Lassa fever
• CDC Stacks — Lassa fever document with annual infection estimate and surveillance caveat
• WHO — Ebola disease fact sheet
• WHO — Prioritizing diseases for research and development in emergency contexts
• NCDC — Lassa Fever Situation Report, Epi Week 7, 2026
• Cheng et al. (2022), Lack of evidence for ribavirin treatment of Lassa fever, Emerging Infectious Diseases
• Mateer et al. (2018), Lassa fever-induced sensorineural hearing loss, PMC
• Cummins et al. (1990), Acute sensorineural deafness in Lassa fever, JAMA
• Siddle et al. (2018), Genomic analysis of Lassa virus during an increase in cases in Nigeria, NEJM
• Lukashevich and Salvato, arenavirus genomics, Current Genomics
• LAMP1 and Lassa virus entry, PMC
• IAVI — Lassa vaccine phase 1 results and phase 2a status (November 2025)
• ClinicalTrials.gov — INTEGRATE trial, NCT06212336
• UK Government — Lassa fever cases identified in England following travel to West Africa (2022)
• ASTMH — Remembering Penny Pinneo