In January 2025, Linda-Gail Bekker stood inside a vaccine manufacturing plant and allowed herself to believe that the first HIV vaccine candidate conceived through African science and led by Africans might finally become a reality.

The vaccine would be built on mRNA technology, the same platform that had helped tame the Covid-19 pandemic. Bekker hoped it might finally crack the puzzle that had frustrated HIV researchers for more than four decades.

No virus has proved more evasive. Hundreds of HIV vaccines have entered testing; none has succeeded at providing durable protection against infection. And the need remains vast: In 2025, roughly 1.2 million new HIV infections were reported; anti-retroviral treatments have turned it into more of a survivable disease, but more than half a million people died from AIDS-related causes the same year. There is still no known cure.

So researchers like Bekker, an infectious disease specialist at the University of Cape Town, have more hope now, in part because there is finally a clearer idea of what an effective vaccine needs to do. It must coax the immune system into producing a particular type of protective antibody, a rare class of defender, capable of recognizing and disabling HIV despite the virus’s extraordinary diversity and rapid ability to mutate.

No one yet knows how to reliably do that. But mRNA is uniquely suited to the task of finding out, vaccinologists say. Thanks to the platform’s speed and flexibility, researchers can iterate rapidly through the otherwise laborious process of designing, testing, and refining the series of vaccine components needed to guide the body toward making those essential antibodies.

At the start of last year, Bekker and her colleagues were ready to put that strategy to the test. The clinical trial for their new mRNA-based HIV vaccine was just on the verge of enrolling its first participants. But the project depended on the same backing that had sustained HIV vaccine research for decades: US government funding. Washington had long supplied roughly 90 percent of the world’s investment in the field. Then President Donald Trump returned to office.

Within hours of his inauguration, Trump signed an executive order freezing foreign aid. The $45 million contract from the US Agency for International Development (USAID) that was supposed to fund clinical trials like Bekker’s disappeared, as did a web of other funds, many routed through the National Institutes of Health (NIH), that had helped fuel the field’s progress for years.

The timing could hardly be more cruel. After 40-odd years of chasing a shape-shifting foe, scientists believe they now know what kind of immune response an HIV vaccine must generate — and have in mRNA a powerful new tool for pursuing it. But just as many researchers have finally glimpsed a path to victory, the United States and much of the funding has pulled away from the fight. 

Pushing the envelope

From the outset, the target for preventing HIV was clear. Within a year of identifying the virus as the cause of AIDS in 1983, researchers had zeroed in on its envelope protein as the most promising point of attack for a vaccine.

Protruding from the virus’s surface in knobby clusters, the envelope protein acts like a molecular grappling hook, latching onto immune cells before pulling the virus itself inside. Without this feature, HIV cannot infect a cell.

Much as the coronavirus spike protein would later become the basis for Covid vaccines, this protein on the surface of HIV seemed an obvious bullseye. But identifying the target didn’t mean researchers could hit it. Most of what the immune system sees of the envelope protein is actually just a decoy. The parts that stick out and draw the strongest immune response are also its most changeable, differing from one strain to the next and mutating freely whenever antibodies close in, leaving the body to waste its firepower on a target that keeps slipping away.

Candidate vaccines kept making the same mistake. They would elicit plenty of antibodies, but not the kind that could keep up with the virus. Time and again, promising candidate vaccines generated excitement in the laboratory, only to come up empty when it mattered most in large-scale clinical testing.

The field’s fortunes started to change in the late 2000s when researchers began studying the small fraction of people living with HIV who developed antibodies capable of recognizing the virus’s concealed, conserved features. Though these hard-won antibodies came too late to protect their makers, they gave scientists a molecular blueprint for the defenses a vaccine would need to build.

As the field came to learn, these “broadly neutralizing antibodies” do not appear overnight but rather after years of battle with the virus. 

The challenge, then, was to design a vaccine that would not just trigger an immune response but guide a person’s immune system through the same evolutionary journey. This would require a succession of vaccine components to prompt a carefully choreographed process within the body, rather than the single, fixed target that suffices for shots against measles or hepatitis B.

It was a strategy rooted in rational design but dependent on trial and error. Progress would come through a steady stream of small proof-of-concept studies, each informing the next generation of vaccine candidates. Ordinarily, it would take at least a year — often longer — to manufacture and prepare each vaccine iteration before it could be tested in people. 

But then the Covid pandemic rocketed mRNA into the spotlight.

The mRNA advantage

mRNA technology upends the old recipe of vaccine development. Conventional shots work by showing the immune system a mugshot of the enemy: a killed or weakened germ, or one of its proteins, grown batch by batch in vats of cells or eggs. An mRNA vaccine takes a different route. Rather than supplying the mugshot, it supplies the instructions to draw one: a short, lab-printed strip of messenger RNA, the molecule cells normally use to ferry genetic directions from DNA to their protein-making machinery.

Inject the right sequence, and it will program the body’s own cells to become tiny factories, producing the target protein and presenting it to the immune system as if it were the real intruder. Because it is all just code, refining a design means editing text, not rebuilding a factory — the work of days, not months.

“We’ve been able to design vaccines in real time,” said University of Pennsylvania Perelman School of Medicine assistant professor Ted Kreider, who is a specialist in infectious diseases.

To HIV researchers, the appeal was obvious. HIV’s greatest weapon was its ability to shift and adapt. Now, at last, a vaccine could, too. 

The timing was ideal. Just as researchers were beginning to map the path to an effective vaccine, mRNA offered a way to move down that path at speed. With vaccine designs no longer bottlenecked by design and manufacturing, what once might have taken decades of stepwise vaccine development could, thanks to mRNA, be compressed into years.

Across a growing number of clinical trials, researchers are now testing different vaccine components, different sequences, and different delivery platforms, searching for the combination that most effectively nudges the immune system toward a truly HIV-thwarting response.

A paper published last month in Nature offered one such path forward, showing in monkeys that a painstaking sequence of eight shots could coax the immune system into producing potent antibodies capable of neutralizing a broad range of HIV strains. But even the study’s authors see a catch. “It’s still too many [shots] to be practical in humans,” said Dennis Burton, a professor of immunology and microbiology at Scripps Research who worked on the project.

Whether mRNA ultimately becomes the vaccine itself — or simply the tool that helps researchers discover it — remains an open question.

The fundamental challenge for now, after all, is vaccine design, notes Mark Feinberg, president and CEO of IAVI, a nonprofit research organization focused on developing vaccines against HIV. And for that task, he says, “the most obvious advantage of mRNA is simply the speed of getting an idea from the laboratory to the clinic.”

But if the technology reaches the finish line, researchers say it could offer other advantages as well. Because the protein is made inside the body’s own cells rather than in a lab, it folds and displays itself much as it would on the real virus, giving the immune system a more faithful target to train against. That way, when the real virus arrives, the body already knows its true face.

It also gives vaccine designers an unusual number of knobs to turn, notes Kristie Bloom, an mRNA vaccine researcher and molecular biologist at the University of Witwatersrand in South Africa. By altering the vaccine’s formulation, dose, or genetic design, researchers can shape not just the magnitude of the immune response but also its balance: favoring antibody-producing B cells, virus-killing T cells, or some mix of the two.

With mRNA, “there’s quite a bit of flexibility,” she said.

Not so fast

For all the putative upsides, however, mRNA does carry some baggage. There are concerns about public acceptance given the intense backlash and misinformation campaigns that followed the rollout of Covid-19 vaccines. And though those shots ultimately proved remarkably safe, with very low rates of serious side effects, a peculiar skin problem has emerged in early-stage trials of mRNA vaccine candidates for HIV specifically. 

In two separate trials reported last year, around one in 12 participants who received mRNA-based HIV vaccines manufactured by Moderna developed chronic urticaria, a form of persistent hives that in some cases endured for years. The vaccines encoded different portions of HIV’s envelope protein, yet both produced the same unexpected side effect.

The fact that the reactions appeared across distinct vaccine designs — but never before in Moderna’s other mRNA vaccine programs — has fueled suspicion that something about HIV’s envelope protein itself may be involved. Even so, no clear explanation has emerged. 

“We’ve ruled a bunch of things out,” said William Schief, a professor at Scripps Research’s department of immunology and microbiology who doubles as vice president for protein design at Moderna, “but there’s no smoking gun.”

Schief is continuing to investigate the source of the immune reactions. But not wanting an unresolved safety signal to bring the program to a halt, he and his collaborators have pressed ahead with lower-dose versions of the vaccine, betting that the hives will fade while the desired immune response remains intact. 

That strategy is now being evaluated in an IAVI-backed trial led by Bekker in South Africa. Known as IAVI G004, it has yielded encouraging early results. (Unlike the African-developed vaccine whose launch was derailed by the USAID funding freeze, this study is testing a different mRNA vaccine candidate, manufactured by Moderna.)

At the lowest dose tested, just one-tenth of the amount used in the original studies, the hives that had troubled earlier trials never materialized, Bekker said. Her team has since moved on to a somewhat higher dose, seeking the sweet spot between safety and immune potency. 

All of these discoveries and challenges along the way have helped map a path forward. “We know what we need to do,” said Barton Haynes, director of the Human Vaccine Institute at the Duke University School of Medicine. The task for them now is to move through the necessary iterations as quickly as the science — and the funding and political landscape — allow.

“A black hole”

When Bekker and her team learned about the sudden funding cut that would halt their African-designed, USAID-funded vaccine study in January 2025, they were already in Tanzania to prepare its launch. They immediately had to stop work on the project, which had been years in the making. “It was like falling into a black hole of depression,” she said. 

And the setbacks kept coming. With prominent vaccine critic Robert F. Kennedy Jr. overseeing US health policy, the federal government moved to undermine both vaccine science broadly and mRNA technology in particular.

The NIH, in addition to terminating dozens of smaller HIV-related grants, began winding down its flagship Consortia for HIV/AIDS Vaccine Development (CHAVD) program, which has long served as a cornerstone of global HIV vaccine research, while other federal agencies curtailed support for mRNA vaccine projects across multiple disease areas.

At the same time, South Africa, the continent’s leading center for biomedical research, found itself in the Trump administration’s crosshairs over allegations of anti-white discrimination. New federal research grants were no longer permitted to support collaborations with South African scientists, severing ties that had underpinned years of international HIV research.

“That’s a perfect storm to prevent us from building on the most exciting science HIV vaccines have had in 45 years,” said Mitchell Warren, executive director of AVAC, a nonprofit dedicated to HIV prevention access and policy. 

Yet for all the financial and political disruption, the scientific momentum hasn’t stopped. Philanthropic organizations and governments elsewhere have stepped up to help fill the funding gap, allowing key trials to move forward, although in scaled-down forms with more modest ambitions. 

The Africa-led effort that Bekker had dreamed of was salvaged, with emergency backing from the South African Medical Research Council, albeit in diminished form and built, in the end, on the same protein-based technology that mRNA was meant to leapfrog.

The only mRNA-based HIV vaccine study that is actually underway in Africa is IAVI G004: a program designed by US scientists, not by locals, and funded largely by the Gates Foundation.

A longtime backer of HIV research, that foundation is estimated to invest around $70 million annually — with $64 million being invested in 2022, and $70 million in 2026 — across a global portfolio of HIV vaccine programs. That’s a substantial sum, though only a fraction of the hundreds of millions of dollars once provided by the NIH, USAID, and other federal agencies. 

For now, some of that funding continues to flow. But even what remains is far from assured. The Trump administration’s proposed 2026 budget would slash the National Institute of Allergy and Infectious Diseases — the NIH institute that has long anchored HIV vaccine science — along with the Office of AIDS Research that coordinates HIV research across the entire NIH, leaving the field’s longer-term future in doubt.

“We’re not going to be able to fill the gap that’s been left by the US government,” said Nina Russell, director of TB & HIV research and development at the Gates Foundation. Still, she says, the foundation remains determined to keep the most promising vaccine programs moving forward: “We are super committed to it.”

All of these changes have left the research field daunted, but not hopeless. “It’s been a very disruptive time,” said Burton, who leads one of the CHAVD research hubs. But he remains convinced the field is on the right track. “The pieces of the puzzle are in place,” he said. “It’s obviously been a long, long journey, but you can begin to see the end.”

A higher bar

The funding crisis and political challenges are not the only forces reshaping HIV vaccine development.

For much of the HIV epidemic, which has killed over 40 million people worldwide, even a partially effective vaccine might have been enough to transform the course of HIV. Today, however, vaccine researchers are also competing against long-acting preventive drugs that can protect people for months at a time with just two injections. 

These drugs are an enormous step forward for HIV protection, but they also raise the standard the vaccine field must meet, Warren said. “The bar for a licensed vaccine that is going to have a public health impact has gotten much higher,” he said.

But these prophylactic drugs, which began as daily pills and have evolved into long-acting injectables, are only as good as the systems that deliver them. Cost, stigma, and the need for regular clinic visits have limited access in many countries with the highest HIV burdens. A vaccine, by contrast, that provided years of protection after a handful of doses could overcome many of those barriers.

That is precisely why many scientists view the current retreat of the US government with such alarm. After decades of disappointments and billions of dollars in investment, the field finally believes it has a coherent strategy for building an effective HIV vaccine. The fear is that momentum could stall just as researchers have begun to see a path across the finish line. As a result, what once seemed like a scientific problem increasingly looks like a political one.

For Bekker, the current moment feels all too familiar. In the early 2000s, South Africa’s government embraced AIDS denialism, delaying the rollout of lifesaving treatments and forcing researchers and clinicians to battle both the virus and the state. A quarter-century later, she says, the political opponent has merely changed address to Washington, DC, threatening once again to undermine the fight against HIV and cost countless lives.

“When politics interferes in science,” Bekker said, “that is the death of scientific progress.”

Bekker still does not know whether the vaccine she watched being manufactured last year will ever reach the people it was designed to protect. She and her colleagues still hope to carry out the made-in-Africa mRNA vaccine trial they spent years designing — if they can find a way to pay for it. But Bekker remains convinced that the scientific strategy behind it is the right one, and that mRNA may yet do for HIV what it did for Covid-19, rapidly transforming decades of scientific groundwork into an effective shot.

She only hopes politics does not succeed where HIV itself has failed in slowing the field’s progress. “We should only be fighting the virus,” Bekker said. “But we’re fighting the administration and its policies, and that is a waste of our energy.”

How do we know when the world has changed?

On June 1, a team of scientists published a preprint scientific paper claiming they had edited human embryonic DNA with more precision than any previous attempt. As a technical achievement, the work is undoubtedly impressive, largely avoiding the errors that had accompanied earlier efforts to gene edit embryos. With further development, such embryonic editing could free future children from fatal or debilitating genetic diseases, but as the veteran science writer Carl Zimmer reported in the New York Times later that week, the real headline news was that the work “could open the way to babies engineered with particular characteristics” — designer children, in other words. 

The same day the Times piece published, the AI company Anthropic published a post asserting that AI was already accelerating AI development, which the authors argue may represent an early step toward recursive self-improvement (RSI) — AI systems that design and build their own successors, faster and faster. Already most of the code that runs Anthropic’s Claude was written by Claude itself, which has helped the company’s engineers ship eight times as much code as they did two years ago. While more is not automatically better, and Claude is still far from being able to guide itself, the possibility of self-improving AI is on the horizon — and “it could come sooner than most institutions are prepared for,” as Anthropic co-founder Jack Clark and Anthropic Institute head Marina Favaro wrote.   

These two writings were published by academic biologists and the employees of an AI company, in two wildly disparate disciplines, but they nonetheless point to a possible near future that is fundamentally different from the world we live in now. 

Both events are potential key steps toward unprecedented powers — not all of which we would have firm control over: newly designed intelligences and newly designed humans. What the two share is not just consequence, but bivalence — the possibility of both the miraculous and the catastrophic. The biological precision that could eradicate an inherited disease like Huntington’s could also pave the way to a genetic caste system. The AI capability that could accelerate decades of scientific progress could also utterly disempower its makers — us.

The world may have walked through a historic door with both of these advances last week. But we can’t yet know which kind.

Designing ourselves

Take the biology step first. Strip away the headlines — which come from the media, not from the scientists themselves — and the experiment is fairly narrow.

Using so-called base editors, which make a small nick in a gene strand rather than chopping out an entire segment, as CRISPR does, Columbia University geneticist Dieter Egli and his team edited two genes: PCSK9 and HBG. You might have heard of the first one; PCSK9 produces a protein that affects the body’s ability to clear cholesterol from the blood, and certain mutations in the gene can drive LDL cholesterol levels dangerously high. HBG encodes a form of hemoglobin that the body relies on before birth and normally switches off afterward. Being able to control these genes could prevent the mutations that increase heart disease risk (PCSK9) and reactivate that fetal hemoglobin in adulthood, easing — though not curing — sickle cell disease and beta-thalassemia (HBG).

The researchers delivered their base editors into fertilized eggs and into two-cell human embryos, and in some cases they managed to make the edits without the chromosomal damage that had been associated with earlier attempts to edit using CRISPR. 

The paper — which has yet to be peer-reviewed — is an impressive step forward in the effort to use gene editing technology on human embryo genes with greater precision. But impressive is still far from perfect, or even safe — some edits landed at the wrong spot in the genome, and relatively few of the embryos went on to develop normally. (The embryos, which had been donated by IVF patients, were developed no further than very early stages, and none were implanted.) Egli and his colleagues were clear in the paper that any notion of using the base editing technique as it is now for treatment is “premature.” But the paper does show such editing can now apparently be done without shredding chromosomes. 

When the Chinese scientist He Jiankui used conventional CRISPR to edit human embryos in 2018, producing three children, his work was widely rejected not just for moral reasons, but technical ones, as his clumsy gene editing did real genetic damage. Should the new paper’s results bear out, the technical obstacles to embryo engineering begin to vanish.  

No one knows what comes next. Certain genetic disorders like sickle-cell anemia can be fixed with a single gene edit, but preventing more complex health problems — or engineering the traits some people might dream about, like height or intelligence — would require editing hundreds or even thousands of genes in combinations we don’t fully understand yet. But if the technical barriers keep falling, that will only leave the moral ones — and the moral ones have rarely held back a technology for long. 

Designing intelligence

As revolutionary as the ability to truly engineer human beings would be, biology still moves slowly. The same can’t be said for the subject of the other document released last week.

Anthropic’s post uses over 5,000 words and plenty of (I’m guessing) Claude-produced graphics to make a single point: The proportion of human work that goes into building AI is shrinking at every stage. Engineers who once wrote the code now mostly review what Claude itself writes. Experiments once designed manually are now increasingly proposed and run by the model. While humans still make the judgment call about what is worth building, Anthropic argues that even that has started to change, as employees increasingly defer to what the model proposes to do next. 

A research loop that is increasingly dominated by AI itself is one that could move ever faster. Technology has always changed at the rate of human beings — how fast they can think, plan, and act. An AI capable of improving itself eliminates that speed limit, allowing for the very real possibility of it moving faster than any human or any human-run institution charged with governing it can follow. Intelligence itself goes critical — each smarter model building a smarter one, the reaction sustaining itself. 

That might seem like a lot to put on a few months of internal coding data from an AI company that has a vested interest in making its models look as strong and as smart as possible. (Especially if that AI company happens to have a potentially record-breaking IPO on the horizon.) In the post, Anthropic itself concedes that simply counting lines of code only goes so far, and that speed is only at best a partial metric of success. But independent research has shown that AI models are able to spend longer and longer on a single task, which allows them to work not just quicker but deeper. We can quibble over the speed, but not on the idea that AI is moving forward, and fast.

Powerful and blindingly quick AI could lead to rapid economic, scientific, and medical progress — all the dreams Anthropic CEO Dario Amodei has laid out in his own writing. 

But it also threatens to be existentially dangerous as well as profoundly disempowering for most of us, not unlike genetic human enhancement could be for those left out. And the potential speed of such change is so great that Anthropic makes the unusual proposal of calling for AI companies to consider collectively slowing down or even temporarily pausing frontier AI development, to enable societal structures and AI alignment research to keep up. The authors of the Anthropic post specifically cite the international regimes built to control past dangerous technology like nuclear weapons, which, for all their problems, have so far kept the world from annihilating itself. But those institutions, like the International Atomic Energy Agency, took decades of white-knuckling to build, and as the Anthropic leaders note, when it comes to self-improving AI: “We don’t have that long.”     

History’s hinge

How do we know when the world has changed?

Sometimes it’s immediate. When Otto Hahn and Fritz Strassmann achieved nuclear fission in December 1938, experts understood the implications almost immediately: A nuclear bomb would be possible. Sometimes the scientists see it, and the rest of the world doesn’t. When Jennifer Doudna and Emmanuelle Charpentier published the seminal paper detailing CRISPR in 2012, initial press attention was all but nonexistent, and the institutions that would eventually need to govern it had no idea what had just happened.

The hardest cases of all are the ones where even the experts can only see half of it. Fission pointed one way, toward a weapon, and the people who understood it could do little to stop it. Each of the two advances of last week points in two ways at once. The same editing technology that could spare a child from a fatal disease is one that could eventually sort children into genetic castes. The same intelligence that could give us “a country of geniuses in a data center,” as Amodei once put it, could also leave us as little more than spectators in the world. 

So we are left where we began, at a threshold we cannot see past. The danger is not just that we may have walked through the wrong door. It is that we’ve walked through without noticing there was one.

A version of this story originally appeared in the Future Perfect newsletter. Sign up here!

A flesh-eating parasite that the United States spent decades eradicating, and even longer trying to keep at bay, has now shown up in Texas.

Federal officials confirmed this week that New World screwworm, a fly whose larvae burrow into living tissue, had been found in a 3-week-old calf in Zavala County in Southwest Texas. It is the state’s first confirmed detection since the early 1980s, and the first in US livestock in several decades. This infestation marks a new stage in the parasite’s northward resurgence through Central America and Mexico that began in 2023.

Human infestations from these flies are rare in the United States, and the Centers for Disease Control and Prevention says there have been no locally acquired human cases reported in the country. But the unwelcome infestation in Texas could be a serious test for ranchers and animal agriculture in the US. Beef prices are already near record high, and if screwworm spreads beyond this single detection, it could push prices and ripple through the economy.

Texas officials are now trying to answer the most urgent question: Was this a single stray case, or a sign that adult screwworm flies are already in the area?

A spokesperson for the Texas Animal Health Commission (TAHC) told Vox that officials had not confirmed any additional cases and were conducting ranch-to-ranch animal surveillance and fly surveillance around the infested zone. That zone covers about 12 miles around the detection site. Warm-blooded animals, such as cattle, horses, and pets, cannot be moved out of this zone unless they are inspected.

Texas has been watching for this moment. The TAHC told Vox it has had fly traps along the Texas-Mexico border since July 2025, which has since collected over 54,000 suspicious flies. None of them were confirmed to be New World screwworm.

But the detection of this case in Zavala County has moved the state from precautionary work to containment. The TAHC told Vox that sterile flies are being deployed through ground release chambers where the infestation was detected, and aerial dispersal was expected to follow. The idea is to flood the area with sterilized flies, so wild screwworms mate without producing offspring — it’s the same strategy that the United States used to eradicate the parasite decades ago. Texas had already been doing these precautionary aerial sterile-fly drops over South Texas since late January, but after this case, officials said those releases were now being redirected toward the 20-kilometer response zone around the detection site.

What went wrong

While the containment efforts are on, it’s still unclear how the calf got infected. The TAHC told Vox that it was not aware of any recent animal movement off the ranch where the calf was found, or any known link to Mexico or another affected area.

If the calf had no movement history, Phillip Kaufman, an entomologist at Texas A&M University who has worked with state officials on screwworm response planning, said, “there certainly have to be adult flies in the area,” that laid eggs on it. Maxwell Scott, an entomologist at North Carolina State University who studies screwworm control, also said that if the livestock itself was not moved up from Mexico, “then the fly had to be here.”

That doesn’t mean that screwworms are established in Texas. Scott said it is possible the case came from a single female fly, and US Department of Agriculture says there have been no further detections so far. But it does mean that the US is no longer preparing for a hypothetical threat.

In Mexico, screwworms-related export restrictions have cost cattle exporters more than $1.3 billion, according to the country’s National Agricultural Council. And in Texas alone, a widespread outbreak could drain as much as $1.8 billion a year from ranchers and the wider economy, according to a USDA estimate.

The US has a history of eradicating screwworms before, and for years it kept the parasite at a distance through an invisible sterile-fly barrier near the Panama-Colombia border. But that barrier has cracked, and screwworm is now spread across a much wider front in Mexico and Central America. Livestock production is also vastly larger than it was when the US first eradicated the parasite. And the sterile-fly supply is limited. Scott, the NC State entomologist, said that the only current production plant in Panama is running at full capacity — 24/7, 365 days a year — and producing about 100 million flies a week, only half of which are males, the sex that actually suppresses the population.

The USDA is moving to raise that ceiling, including by renovating a facility in Metapa, Mexico, and building new production capacity in Texas. Newer genetic engineered strains, including a male-only fly known as Novofly, could also make existing plants more efficient by producing only the sex that actually suppress the wild population. But those tools still need regulatory approval and field testing before they could be deployed.

The response is unfolding after a bruising year for the agencies and programs that manage animal disease. More than 15,000 USDA employees accepted the Trump administration’s incentives to leave the department, while  the Animal and Plant Health Inspection Service, the USDA agency responsible for animal and plant health, lost more than 1,300 staff that included veterinarians and animal health personnel. The “Department of Government Efficiency,” which is officially scheduled to sunset next month, also listed an $84 million cut last year to a USAID grant that supported animal-disease surveillance and outbreak response. Agri-Pulse, an agriculture trade publication, reported that the terminated work included screwworm monitoring in Central America.

It is unclear whether those cuts have affected the current response in Texas or the US’s broader ability to track northward movement of screwworm, but it sharpens the question: whether the US has enough surveillance, staffing, and sterile-fly capacity to meet a fast-moving animal health threat.

What exactly is a New World screwworm?

The New World screwworm is a parasitic fly found today across parts of South America and the Caribbean, Central America, and Mexico. They have shiny blue-gray bodies and look similar to house flies that swarm your local dumpster. But unlike those ordinary flies, screwworm flies love fresh wounds.  

Female screwworm flies are attracted to warm-blooded animals, and lay their eggs in open cuts or natural openings like ears or nostrils. Each female can lay up to 200 eggs at a time, which hatch some 12 to 24 hours later. Upon hatching, the larvae twist into flesh like corkscrews tearing deeper as they feed, causing extreme pain and tissue damage. Their scientific name, Cochliomyia hominivorax, translates roughly to man-eater, and their common name, screwworm, capture their horror: a spiral larva that feeds on living flesh. 

After feeding for up to a week, the larvae wriggle back out of the wound and drop to the ground, where they pupate in the soil before emerging as adult screwworm flies — ready to repeat the cycle.

Most infestations – including livestock cases like the one in Zavala County — are treatable when caught early. But missed cases can allow the flies to reproduce and spread, making an outbreak much harder to contain.

What makes screwworms particularly brutal is they only consume living flesh. A single infested wound can attract more flies, leading to repeated infestations in the same animal. Infestations in humans are excruciating and disfiguring, but rarely fatal with treatment. In animals, untreated cases can be devastating, causing severe wounds, blood loss, secondary infections and sometimes death.

But there’s an Achilles’ heel: Female screwworms mate only once in their life — a unique biological quirk that has underpinned the US’s control strategy for decades.

How the US beat screwworms

Screwworms once terrorized the American South and the Western US, and killed millions of dollars’ worth of cattle each year. By the mid-20th century, the fly was costing America’s ranchers up to $100 million annually.

But starting in the 1950s, USDA scientists found a way to use the fly’s biology against itself. If they could find a way to get the female flies to mate with sterile mates, they could stop the flies’ population in its tracks. And that’s how the sterile insect technique (SIT) was developed.

The SIT is fairly straightforward: Rear huge numbers of screwworms in a lab and sterilize the pupae through radiation (a discovery from the post-war atomic age when scientists realized they could make flies infertile without killing them). Then these freshly sterilized pupae are packed onto twin-engine planes, timed so the flies hatch in the air. These flies are then sprayed out over the forest and ranchlands by the millions. They wake in warm air and do what flies do: They mate. Those pairings then produce nothing. If you do that at a sufficient scale and for a long enough time, the population will eventually collapse. 

The first eradication program in the American Southeast ran through the 1950s followed by a larger push across Southwest, costing roughly $42 million in total. Ranching groups pushed the USDA for eradication, Texas cattlemen even wrote letters to USDA urging the agency to expand SIT. And unlike today’s debates around genetically modified mosquitoes, screwworms never stirred much controversy. The technique was targeted, pesticide-free, and spared other insects, which is why it was an unusually “green” pest control, said Max Scott, a professor of entomology at NC State University. By 1966, the fly was gone. 

The technique then was adopted in Mexico and parts of Central America, pushing the flies all the way to a narrow band of dense rainforests between Panama and Colombia called the Darién Gap. The Pan-American Highway famously stops there, the region is sparsely populated, treacherous to cross, and light on livestock. It’s exactly the kind of chokepoint where a biological “firewall” can hold. 

Since 1998, a US-Panama program called Commission for the Eradication and Prevention of Screwworm (COPEG) has held the line at the Darién Gap. Planes drop off millions of sterile flies each week, and inspectors patrol the frontier town (not the deep Darién itself) to spot infestations, pluck out maggots manually, and treat wounds with insecticides — because SIT only works if you also knock down active infestations. 

The program costs about $15 million annually and is funded mostly by USDA, with Panama contributing a small share. “It was one of the greatest achievements of the USDA in the 20th century,” Scott said.

But, in 2023, the firewall cracked.

Smuggling of cattle through Central America seeded fresh outbreaks in new regions, and climate shifts — higher temperatures and humidity — aided their spread. By spring 2025, Mexico was reporting detections as far north as Oaxaca and Veracruz, a stretch of land far wider and difficult to contain than the narrow Darién. COPEG has been running flat out, turning out around 100 million larvae each week. But even at maximum capacity, the plant can only do so much. The screwworm front continued to advance, and has now reached continental US. 

What happens next

The response underway in Texas — animal movement restrictions, fly and animal surveillance, sterile-fly releases — is the standard screwworm playbook, and it may be enough if the Zavala County case remains to just one calf. 

The harder question is what happens if more cases appear.

SIT only works when sterile males vastly outnumber fertile wild males. Scott said earlier eradication programs often aimed for a 9-to-1 or 10-to-1 ratio of sterile to fertile males, because lab-reared flies that have been sterilized are not perfect competitors in the wild. Right now, the main production plant in Panama is producing about 100 million sterile flies a week. But only about half are males, and males are the ones that suppress reproduction.

That could become the bottleneck if the response has to expand. During the eradication campaign in Mexico, Scott said, officials had access to a plant producing roughly 500 million flies a week. That kind of capacity may not be necessary if Texas stamps out this case quickly. But Texas is vast, and the larger resurgence in Mexico and Central America has not gone away.

There’s also a trade-off. The sterile flies that are now being released in Texas are redirected from the Panama plant, and those flies would have otherwise been used in northern Mexico. That may be necessary to constrain the Zavala Country case. But the more flies officials have to pull north, the fewer flies they have to push back the broader front of screwworm moving through Mexico.

That capacity is coming but not immediately. USDA is renovating a facility in Metapa, Mexico, that is expected to add tens of millions of sterile flies per week, and it is building new production capacity in Texas. The Food and Drug Administration has also issued emergency authorizations for some animal treatments, bringing more tools to prevent and treat infestations while containment is underway.

And new genetic tools could eventually help too. Scott’s lab helped develop a male-only screwworm strain, called NovoFly, that could make sterile-fly production much more efficient. Instead of producing male and female flies, a plant using this strain could produce only the males needed for population control, effectively doubling the useful output of existing facilities.

But Novofly isn’t here yet. Scott said his lab developed the strain around 2018, and that it has spent years in storage because there was no urgent plan to use it. Now it is moving through EPA review, but it would need US approval, as well as approval from Panamanian regulators and field testing, before they could be deployed in the real world.

For now, the United States is relying on the basic strategies that worked decades ago, while racing to rebuild the capacity that made it work. The new few weeks will determine whether Texas is dealing with a contained incursion or something more serious.

Update, June 5, 1:25 pm ET: This story was originally published on September 7, 2025, and has been updated with the latest information about screwworm in Texas.