The Village at the Edge of the World
Brevig Mission sits on the southern shore of the Seward Peninsula in western Alaska, roughly forty miles northeast of Nome, fronting the Bering Strait. In 1918 it was known as Teller Mission, named for U.S. Senator Henry Teller. The village had been established in the 1890s around a Lutheran mission and a reindeer herding program. Its population was Inupiat, the indigenous people of coastal Alaska and the Bering Strait region, who had lived along this coast for thousands of years. In November 1918, about eighty people called it home.
The nearest significant settlement was Nome, some forty miles by sea. Nome had grown explosively during the gold rush that began in 1899, and by 1918 it was still a busy supply hub with steamship connections to the outside world. Teller Mission depended on Nome for trade goods and mail. What Nome had in November 1918, Teller Mission would have within days of the next boat arriving.
The Reverend Tollef Larson Brevig, the Norwegian Lutheran missionary after whom the village would eventually be renamed, had arrived in 1894. He and his wife Julia stayed for years, learning the Inupiat language and documenting village life. By 1918, Brevig himself had long since returned to the United States. The mission continued under new leadership. The village was quiet. The world war was ending. And somewhere in the shipping chain connecting Nome to the outside world, the influenza was moving.
The Flu That Arrived by Mail Boat
The 1918 influenza pandemic is often called the Spanish flu, a misnomer born from wartime censorship. Spain, neutral in the war, had a free press that reported freely on the outbreak. The warring nations did not. The name stuck, but the virus originated elsewhere and spread through military troop movements across three continents before reaching the general population in devastating waves.
By November 1918, the pandemic's second wave had already killed hundreds of thousands in Europe and the continental United States. It was unlike any flu the world had seen. The 1918 virus killed not just the elderly and very young, as seasonal influenza typically does, but overwhelmingly attacked healthy adults between twenty and forty years old. In some cases patients died within hours of their first symptoms. In others, the lungs filled with fluid over two to five days, followed by cyanosis and suffocation. The immune system's own response, a cytokine storm, was often what killed young, strong bodies.
In mid-November, a mail boat arrived in Teller Mission from Nome. The precise cargo of the flu's arrival is not recorded. Whether it came through handling a parcel, a handshake with a crew member, or contact with a package from the outside world, no one documented. What is documented is what happened afterward. Within five days, 72 of the village's 80 residents were dead. Eight people survived, most of them children.
| Detail | Figure |
|---|---|
| Village population | ~80 people |
| Deaths in 5 days | 72 |
| Mortality rate | ~90% |
| Survivors | 8 (mostly children) |
| Global 1918 flu deaths | Estimated 50–100 million |
| U.S. death toll | ~675,000 |
| Alaska Native death rate | Estimated 40x higher than non-Native Alaskans |
Ninety percent. In the broader context of the 1918 pandemic, which killed roughly two to three percent of those it infected globally, Teller Mission's mortality rate was catastrophic even by the standards of the worst-hit communities. Gold miners from Nome were reportedly among those who came to dig the mass grave. The bodies were interred in the permafrost. White wooden crosses were placed to mark them. The village, in effect, ceased to exist as a functioning community. It was rebuilt afterward by the few survivors and by Inupiat people who resettled from surrounding areas.
Why Alaska Was So Devastated
Alaska Native communities throughout the territory suffered mortality rates dramatically higher than the non-Native population during the 1918 pandemic. Estimates suggest Alaska Natives died at roughly forty times the rate of non-Native Alaskans. The reasons were biological, geographic, and structural simultaneously.
Geographic isolation meant the virus arrived all at once to populations with no warning and no time to build even partial immunity within the community. In dense urban populations, the flu moved through in waves over weeks or months. Some people recovered while others were still falling ill, and the community's capacity to care for the sick was never entirely overwhelmed at once. In an isolated village like Teller Mission, the virus hit everyone at the same time. There was no one well enough to bring water to the sick. There were no medical supplies and no physician within forty miles.
There is also evidence that Alaska Native populations had less prior exposure to influenza variants than populations in frequent contact with global shipping networks. Immunological memory builds through repeated low-level exposures over generations. Communities with centuries of uninterrupted contact with European and Asian trade routes had developed some residual protection against influenza strains. Inupiat communities in remote western Alaska had not.
The combination was lethal. And in the permafrost below the crosses at Teller Mission, the bodies of seventy-two people lay frozen. They would remain there, intact and preserved, for decades.
The First Expedition: Johan Hultin, 1951
Johan Hultin was born in Sweden in 1925 and came to the United States to study at the University of Iowa. In 1951, while a graduate student in microbiology, he became focused on a question that few researchers were then taking seriously: could the 1918 virus be recovered from the permafrost graves of its victims? If the bodies were sufficiently frozen, the virus might still be viable. If it were viable, it could be cultured and studied, and potentially a vaccine could be developed.
Hultin knew about the Teller Mission graves. He contacted the village council, received permission, and traveled to Alaska with a small team. They excavated the mass grave and found four bodies in acceptable condition. Hultin took tissue samples from the lungs and brought them back to Iowa, packed in dry ice. There, he attempted to culture the virus, infecting fertilized eggs with the tissue samples. The cultures failed. The virus could not be revived. The techniques available in 1951 were not equal to the problem.
Hultin published his results, noted that viable virus recovery had been unsuccessful, and moved on to a career in pathology in San Francisco. For the next forty-six years, he did not return to the grave site. The question of the 1918 virus's identity remained unanswered.
The Paper That Changed Everything
In 1997, Johan Hultin was seventy-two years old and retired. He was reading the journal Science when he came across a paper by Jeffery Taubenberger, a molecular pathologist at the Armed Forces Institute of Pathology in Washington, D.C. Taubenberger and his colleagues had done something remarkable. Working not with fresh tissue but with formalin-fixed, paraffin-embedded lung samples from U.S. Army soldiers who had died of influenza in 1918, they had successfully extracted fragments of the viral genome. They had begun to sequence the 1918 virus from archive material that had been sitting in storage for nearly eighty years.
The fragments were incomplete. The Army archive samples were degraded by decades of chemical fixation. Taubenberger's team had sequences, but not enough to reconstruct the full genome. They needed better-preserved tissue.
Hultin read the paper, set it down, and wrote Taubenberger a letter. He explained who he was. He explained what he had done in 1951. He asked whether Taubenberger would want him to try again. Taubenberger wrote back within days: yes.
"I thought, here is my chance to make good on what I started in 1951."
-- Johan Hultin, interview with Science, 1997
The Return: Garden Shears and Permafrost
Hultin did not apply for a grant. He did not assemble a team. He paid his own way, roughly three thousand dollars in airfare and supplies. He contacted the Brevig Mission village council, explained what he was doing and why, and received permission again. He flew to Alaska carrying garden shears and the equipment he needed to preserve tissue.
He dug alone. The permafrost was hard work even with proper tools, and the grave held the remains of seventy-two people. Hultin worked through the site carefully. Most of the bodies were too decomposed to yield usable tissue. Then he found her.
She was a woman in her thirties, obese. Her body fat had insulated her lungs from the freeze-thaw cycles that had degraded the other remains. Her lungs were dark red, preserved. Hultin cut four small pieces of lung tissue, each roughly the size of a thimble. He placed them in a preservative solution and packed them for transport. He sent them to Taubenberger's laboratory at the Armed Forces Institute of Pathology via FedEx, packed in dry ice.
He reburied everyone. He placed a small cross at the grave. He flew home.
Sequencing the Virus
Taubenberger's team received Hultin's samples and found exactly what they had hoped for. The lung tissue was intact enough to yield complete viral RNA. Combined with the fragments they had already extracted from the Army archive slides, Taubenberger's laboratory was able to piece together the full genome of the 1918 influenza virus. The work proceeded over several years. In 2005, the complete sequence was published simultaneously in the journals Nature and Science.
What the sequence revealed was striking. The 1918 virus was not, as some had theorized, a human influenza strain that had mutated gradually into a killer. It was a novel hybrid. The virus appeared to have jumped from birds to humans, acquiring mutations that allowed it to replicate efficiently in the human respiratory tract. This avian origin explained the lack of any prior immunity in human populations. No one had ever encountered anything like it. The immune systems of healthy adults, encountering a completely foreign pathogen and mounting a maximal response, were often what caused the fatal lung damage, not the virus alone.
In October 2005, scientists at the CDC reconstructed a live copy of the 1918 virus from the sequenced genome. The work was done in a Biosafety Level 4 facility, the highest containment level available. Experiments with the reconstructed virus confirmed what the genome sequence had suggested: it was extraordinarily lethal in animal models, killing mice with a speed and efficiency that modern flu strains could not match. It replicated rapidly in lung tissue and triggered an inflammatory response unlike anything seen in seasonal influenza.
The Ethics of Reconstruction
The reconstruction of the 1918 virus was not universally welcomed. The decision to synthesize a live copy of the most lethal pandemic pathogen in modern history, even under maximum biosecurity conditions, drew serious criticism from scientists, biosecurity experts, and ethicists.
The arguments in favor were straightforward: understanding the virus is essential for pandemic preparedness. The 1918 flu killed more people in a year than the Black Death killed in a decade. If a similar virus emerged again, whether through natural mutation or deliberate engineering, the ability to recognize it and respond quickly could save millions of lives. The reconstructed genome allows researchers to test antiviral drugs, develop vaccines, and study the specific molecular features that made the 1918 strain so lethal.
The arguments against were also serious. A Biosafety Level 4 facility has never had a containment failure that released a pathogen into the broader environment, but the history of biosafety incidents at even the most secure laboratories includes near-misses. In 2014, the CDC itself discovered forgotten vials of smallpox in an unsecured storage room. The argument was made that reconstructing a pathogen of this lethality from a published genome sequence also lowers the barrier for bad actors. Once the sequence is public, reconstruction is theoretically possible for any laboratory with sufficient resources.
The virus remains in a CDC freezer in Atlanta, behind locked doors, under constant monitoring. Taubenberger's work continues. Hultin's four thimble-sized tissue samples made it all possible.
What Brevig Mission Carries Now
The village was renamed Brevig Mission in honor of Tollef Brevig in 1963. It remains a small Inupiat community today, home to roughly three hundred people. The mass grave is still there, marked by crosses. The village has a school, a post office, an airstrip. Subsistence hunting and fishing remain central to daily life. The Bering Strait is visible from the shore.
The 1918 deaths are remembered. The village council that gave Johan Hultin permission to dig in both 1951 and 1997 understood what was at stake. A member of that council, quoted in a 1997 newspaper account, described the decision simply: the community wanted the world to understand what had happened to them, and if the research helped prevent future deaths, then disturbing the rest of the ancestors was worth it.
Johan Hultin returned to Brevig Mission one more time after 1997, to pay his respects. He made a wreath and placed it at the grave site. He was not a young man making a scientific expedition. He was someone who had spent forty-six years thinking about seventy-two people he had never met, and what their deaths might still teach the living.
The virus he recovered is locked away in Atlanta. The grave is quiet again. The permafrost that preserved the evidence of the worst mortality event of the twentieth century still lies beneath the tundra of the Seward Peninsula, a few feet underground, cold and intact. What else it holds, no one has gone to find out.