“Science,” says molecular virologist Seema Lakdawala, “needs to meet people where they are.” Her commitment to this principle means she not only spends her time investigating pathogens and pandemics in Emory University’s Lakdawala Lab in Atlanta, Georgia, but she also appears whenever she can on television, radio, and podcasts—or in print—to explain to the public what we need to know about influenza, COVID-19, and new threats like the H5N1 avian flu. “We never want to see the H5N1 virus become more successful infecting humans than it already is,” she cautions. “We need to consider ourselves at war with it, but we’re not doing nearly enough to fight it.”
After training at the Salk Institute and the National Institutes of Health, Lakdawala started an independent laboratory in Pennsylvania at the University of Pittsburgh School of Medicine in 2015. She moved the program to Emory University in Atlanta in 2022. Much of her research is focused on the airborne transmission of influenza viruses. During the COVID-19 pandemic she and her colleagues studied the importance of public health interventions in preventing the spread of viruses. She is a 2024 National Academy of Sciences Kavli Fellow and has been published in Science, Nature, and The Journal of Infectious Diseases.
We spoke in May 2025, about four months after the first human death from avian flu in the United States and while the Trump administration—including the head of the US Department of Health and Human Services, Robert F. Kennedy Jr.—was making major changes to the federal government’s approach to public health. By the end of the month, plans to develop a bird-flu vaccine had been canceled. Not long before I spoke to Lakdawala over video chat, the National Institutes of Health initiated a series of grant terminations amounting to $1.81 billion in cuts for ongoing scientific projects at many colleges and universities, including Emory, Yale, Johns Hopkins, and Columbia University—a withdrawal of funding that Lakdawala says is a “detriment to our society as a whole.”
Much of our conversation focused on how viruses become major pandemics, like the Spanish flu, which killed nearly seven hundred thousand Americans in 1918. We also talked about COVID-19, which continues to infect people years after it went pandemic in 2020. Despite the grim subject matter, Lakdawala stayed in good spirits as she explained complex science in terms the average person could understand.
Not all conversations are as linear and succinct as they appear. This interview has been condensed and edited for clarity.—Ed.
Seema Lakdawala
© Emory University
Leviton: Let’s start with some basic information. What’s the difference between an epidemic and a pandemic?
Lakdawala: Epidemics are regional outbreaks of diseases, like seasonal influenza. A pandemic is the introduction and spread of a novel pathogen—one that is new to the human population—across international borders and worldwide.
Leviton: Have epidemics and pandemics always been a part of human life?
Lakdawala: Yes. The ancient Greeks wrote about what they called “miasmas” [usually translated as “pollution” or “bad air”—Ed.]. The Greeks also described the symptoms of infectious diseases that we now know are caused by viruses. We find evidence of viruses as far back as we can go in human history.
Leviton: So there’s no golden age in the past, when hunter-gatherers happily roamed, eating perfectly nutritious food and coming in contact with a variety of animals without ever getting sick?
Lakdawala: I can’t imagine there was.
Leviton: I have friends who get the flu and colds nearly year-round, while I’ve gotten the flu only a handful of times in my life. What accounts for this?
Lakdawala: A lot of it probably has to do with immune responses. When you were first exposed to flu, you may have produced a strong immune response that can shut down the virus and never really let it take hold. Every time you experience influenza after that, your body recalls its response to your original exposure. That first response is driven in part by genetics, which helps determine how well you make an antibody against something that you’ve only just encountered. Most of us have encountered influenza in some fashion by the time we reach the age of five. Some people may make a strong response initially. For others, every time they see it, their immune system will respond in a slightly different way, which may impact the severity of their disease. As you get older, you are less likely to have a very strong immune response against the virus, which is why the flu vaccine is recommended for those over sixty-five.
Leviton: When you say “recall,” this is not happening in your brain, right? It’s what we might call a “body memory.”
Lakdawala: Exactly. The cells in our bodies can also remember things. I like to refer to the immune cells as “superheroes”—like Batman or the Justice League. In this case the superheroes are B-cells and T-cells and natural killer (NK) cells. The immune system can send up the Bat-Signal to tell all the hero cells to gather. But first it needs to recognize the threat. This is how vaccines work. They contain a weak or inactive flu virus. The immune cells see it and say, “I’m going to remember you.” The next time they see the pathogen, the Bat-Signal goes out, and the superheroes come to take care of it.
Leviton: I had chicken pox as a child, and I thought I had a lifelong immunity to the virus, but now my doctor advises I get a shingles vaccination. [Shingles is caused by the same virus that causes chicken pox.—Ed.] Did my body’s memory decay?
Lakdawala: I just had this conversation with my mother-in-law last night! I’m not a shingles expert, but, yes, there is likely a decay. In the case of the flu, you are probably reexposed to it every year, which serves as a constant reminder to your immune cells of the dangers out there. But what if you’re not exposed to a virus year after year? What’s the longevity of the immune response? You’d really have to ask an immunologist that.
Leviton: So influenza is a seasonal epidemic?
Lakdawala: Yes, but we also have sporadic flu pandemics, when a novel version of the virus infects humans. In 2009 the H1N1 strain, commonly called swine flu, made the leap from pigs to people. After H1N1 was introduced, it became an epidemic and now circulates through the human population year after year. The same can be said for SARS-CoV-2, which causes COVID-19. It was a pandemic in 2020, but it’s now an epidemic and unlikely to go anywhere, because there is sustained human-to-human transmission.
Leviton: We’ve had several other major flu pandemics in the last century or so: the Spanish flu in 1918, the Asian flu in 1957, and the Hong Kong flu in 1968.
Lakdawala: Right. The Spanish flu came from a bird source and was very lethal, with reportedly fifty million people dying around the world. There is evidence from archive tissues of influenza strains that circulated in humans prior to 1918.
Leviton: You study “enveloped viruses.” What are they?
Lakdawala: Influenza is an enveloped virus. So are other RNA viruses like hepatitis C, RSV, Ebola, HIV, and SARS. [RNA, or ribonucleic acid, is similar to DNA and found in all living organisms.—Ed.] Enveloped viruses mutate a lot. They are constantly evolving, trying new things. When one of these viruses comes out of a cell that it’s infected, instead of killing the cell, it goes to the edge of the cell and starts budding out from it. It uses your cell’s membrane to package its own genome. It’s like a parasite co-opting the host. It’s taken all the resources from your cell to create this virus-making factory.
The enveloped virus is very much like our human cells: It doesn’t stay for long periods of time on surfaces and can be easily inactivated, the way washing our hands with soap and water inactivates the flu.
Adenoviruses, which can cause the common cold and bronchitis, are different. They are DNA viruses with a protein capsid, or nonenveloped. When an adenovirus leaves an infected cell, that cell bursts, releasing all the newly made viruses inside. Adenoviruses are also very hardy in the environment and therefore harder to kill.
Leviton: You’re an expert in how the flu spreads from person to person. You’ve done a lot of research about the persistence of droplets in the air, for instance.
Lakdawala: Respiratory pathogens spread through many different modes. We think of the air as being the most important medium, but there are also what we call “fomites”—materials or surfaces that can carry infection. Every mode of transmission is possible.
When we are sick and we cough, sneeze, sing, shout, and so on, we are expelling virus into the air in aerosols of varying sizes. Some are really small and can stay suspended in the air for long periods of time and travel great distances. Some are larger and will fall onto nearby surfaces. Some are droplets and may fall onto the person we’re talking to.
The most effective modes of transmission will change depending on what location you are in. In day care centers, where kids touch everything—touch their faces, touch each other, put things in their mouth, the whole gamut—fomite transmission is highly likely, because contact with contaminated surfaces is so frequent. There’s also a higher level of surface contamination in confined spaces, such as hospital and nursing home rooms.
By contrast, at the grocery store, am I worried about touching the container of grapes that someone else may have touched? No, because the level of contamination on surfaces in public areas is very low. In an office building where there’s poor ventilation, the most likely mode of transmission is by the smaller, more long-range aerosols. High schools, the same.
Say you’re having a dinner party or chatting with an old friend over coffee. In that sort of scenario, all modes of transmission are possible. During the COVID pandemic everyone wanted to know the means of transmission, but it wasn’t just one of the above. You can’t have one type of intervention that’s going to be effective in every single location.
Leviton: Are certain surfaces more hospitable to viruses?
Lakdawala: We did a lab study and found that the flu virus is most stable on certain types of plastic, including the popular and easy-to-mold ones called ABS [acrylonitrile-butadiene-styrene]. It’s the least stable on things like copper.
Those are nonporous surfaces. On a porous surface, the virus may remain infectious, but the transfer of that virus from the surface to our skin is really hard.
When we talk about the bird-flu infections we’re seeing in the poultry and dairy industry, we’ll talk about farmworkers coming home with contaminated clothing and shoes, and pathogens coming off their person to infect cats or family members.
Leviton: What about the persistence of particles in the air? Do infectious particles stay around for days, weeks, months?
Lakdawala: In an office building or a private home, where there are HVAC systems that circulate the air and open doors and windows and cracks in the walls, the air gets exchanged fairly frequently for outside air, and particles eventually get diluted out. And, of course, aerosol dilution is even faster outdoors. It’s less important to think about how long aerosols persist than about how quickly they move.
With every breath you or I take, we are taking in and expelling pathogens. There are hundreds of pathogens circulating among people, plants, and animals in a typical environment, but most of the time we’re not getting sick. We breathe them in, and our immune system shuts them down. At my lab we’re working hard to figure out how much virus you have to inhale to become infected. It sounds simple, but there are a lot of factors. Do you have to inhale it all at once? What about sequential doses, like if you’re working with someone who is sick, and you see them several times a day?
I can do lab studies where I put different amounts of virus into animals and find you need very few cells to cause infection, but studies done with animals in labs don’t totally replicate the way humans get infected, which involves mucus, saliva, and other pathogens. We don’t know the full complexity of that interaction. The lab study showing that a hundred particles of flu virus can cause infection is a good starting point for sure, but if that was all we needed to become infected, we’d be getting infected all the time. And we’re not.
We’ve done experiments at Emory with aerosol inoculations: We place the subject in a kind of bubble and have them just sit there, naturally breathing in whatever we put into the bubble for ten minutes. And we’ve found that the dose necessary to get infected is not a hundred particles; in fact, it’s more on the order of ten thousand. Not everyone gets infected at that dose either, and those that do get infected often get only mildly sick, not severely ill. When we tell them they are testing positive, they’ll ask, “Are you sure?” We still haven’t figured everything out.
Leviton: The lack of outside-air circulation on an airplane must make it a prime environment for getting infections.
Lakdawala: I definitely wear an N95 mask every time I go on a plane. The interesting thing about airplane air is that the circulation is actually occurring within the row. In studies of where people get infections on a plane, it is found that they get them from the people they sat near. And the people with the highest potential for being infected are those sitting on the aisle, because they have more interactions with other passengers.
I also always reach up and turn on the air vent. If the person next to me sneezes, it makes this pool of air that’s carrying virus, but if I add more air current with a fan, I’ll dilute that pool and breathe in less of what they are expelling.
Leviton: In the early days of COVID, before we had much information about transmission, I used to come home from the grocery store, take my clothes off on the porch, and go straight into a shower, while every piece of packaging and fruit was being wiped down with antibacterial cloths.
Lakdawala: If people wanted to wipe down every apple, I was fine with them doing it, but I was surprised by how far some were going. My dad was quarantining his mail. I told him, “Dad, don’t worry about it. I promise you won’t get infected from your mail.” And he’d say he had heard it on the news.
There was a lot of fear out there. It was a new virus, and we didn’t have any licensed antivirals or vaccines that we could immediately use to fight it. The pandemic came fast, and science had to catch up. We’d been working on the SARS 1 coronavirus, which is similar to the COVID virus, since 2003, but there was a hesitancy, a fear of the unknown. And the communication by government agencies could have been better. Public health experts were giving one message, and one message only: Stay home. And not everybody had the luxury of staying home from their job or from school, or taking extra precautions as you and my father did. There was a lot of pushback on that stay-home advice, because the scientific community was not meeting people where they were.
In the early days I had ER physicians ask me how to protect their families after spending all day with sick patients. At that point I did recommend ER doctors should take their clothes off when they got home and take a shower, because they were probably covered in virus.
Leviton: In a typical flu season, how many people are infected, and how many get seriously ill?
Lakdawala: It varies from season to season, but I’d say there are between five and forty million influenza infections in the US every year, on average. Roughly 10 percent of those infected seek some sort of medical help. About 10 percent of those people end up in the hospital. And around 10 percent of hospitalized patients die. So, depending on the total infections, we’ve got somewhere between five thousand and forty thousand people dying in a typical year.
The 2017–2018 flu season was particularly severe. [The CDC estimates there were fifty-two thousand US deaths.—Ed.] Most of those who died were unvaccinated. Many were elderly—there were fewer than two hundred pediatric deaths, and 80 percent of the pediatric deaths were of unvaccinated children. Many of those could have been prevented. It wasn’t the best-matched vaccine that year, which is one reason we had so many infections.
Studies done with animals in labs don’t totally replicate the way humans get infected, which involves mucus, saliva, and other pathogens. We don’t know the full complexity of that interaction.
Leviton: What’s your work like in Emory’s Department of Microbiology and Immunology? I understand you use ferrets as test animals.
Lakdawala: In my lab we mostly use cells in a dish. They are actually canine kidney cells, which have a receptor that flu binds to really well. It’s not a dog; it’s not a kidney. It’s just cells in a dish. I can put the virus in there and study what proteins are important for the virus to grow, what antivirals are effective, and so on. It’s nice we can do this without using live animals, but we also want to study how the virus spreads from one person to another. We use ferrets for that, because they are naturally susceptible to the human influenza virus. If you have flu, you can give it to your pet ferret, and vice versa. We know that, as early as 1933, an individual got sick from a ferret sneezing on him. [Laughs.] Ferrets don’t die from the flu. They simply get lethargic and don’t want to eat hard pellet food. They want soft food—sometimes we give them canned cat food—and then within seven days they bounce back.
We also study the virus as it naturally infects humans. We enroll patients and look at how much virus is in them. And where is the virus? How much do you have in your nose, how much in your mouth? We also have them “talk into the tunnel,” so we can see how much infectious virus they’re sending out into the environment. That’s a big question: You might feel fine, but how much are you expelling? We can do that study with ferrets, but they don’t have the complex human immune response, and they haven’t encountered the flu decade after decade.
That’s the big goal of my work: to figure out how to stop the spread. We want vaccines, but if we can actually block transmission, we’d be so much better off.
Leviton: What about “gain of function” experiments?
Lakdawala: We don’t manipulate the virus to make it more transmissible. We might change the ventilation or expose the virus to ultraviolet light, but with gain of function you make a change in the genome of the virus that confers an additional phenotype [a characteristic produced by the interaction of genes with the environment—Ed.]. It’s gaining a function it didn’t already have.
Leviton: That sounds sort of dangerous. It could make a virus much stronger, for instance.
Lakdawala: It goes on whether humans conduct experiments or not. If there’s a virus duplicating in you, it’s evolving and gaining different functions, finding ways to escape your immune response. I think the term “gain of function” has become a lightning rod, because of the fear of a lab leak. But gain-of-function research has allowed us to develop vaccines and antivirals. It’s important that we understand how a virus mutates.
Some papers in 2012 started this whole gain-of-function controversy, which has only grown since COVID. [During the H5N1 outbreak, the Obama administration halted all federal funding for gain-of-function studies that altered pathogens, including influenza, SARS, and MERS, to make them more transmissible or deadly.—Ed.] Those papers identified some mutations and phenotypes of the virus that were important for transmission. And now, more than ten years later, we have a huge outbreak of avian flu, and we need to know if any of those mutations are arising in cows, cats, birds, and the people working on farms. Those are the infections we really need to be concerned about right now.
Leviton: In January of this year the CIA issued an assessment supporting the idea that the COVID pandemic may have begun with a lab leak in Wuhan, China, where gain-of-function experiments were being conducted, but it has “low confidence” in the assessment. What do you think happened?
Lakdawala: I have no idea what happens in labs in China, because I have never been to a lab in China, but what I do know really well is transmission. There were some beautiful studies early in the pandemic from a group led by epidemiologist and medical statistician Ben Cowling in Hong Kong. They looked at the forward-transmission potential of a single infected person.
At the beginning of the pandemic, COVID was a superspreader phenotype, meaning that a small percentage of people caused most of the infections. Ben found that if ten people were infected, only three of them would spread the virus, and just two of them would cause 80 percent of the infections. He looked at the contact networks of people who spread the disease and concluded that a COVID superspreader was only a superspreader for a short time. That person could have gone to dinner, and gone to a party the next day, and maybe spread the virus at only one of those locations.
So the chance of a single person being infected in a lab, and that person also being a superspreader and spreading it to enough people within that narrow window is very low. It’s likely there were multiple points where the virus was introduced to humans, not a single spark.
Leviton: So there’s no “patient zero.”
Lakdawala: Typically no, not with an influenza pandemic, or with coronaviruses, because there’s such a disparity in forward-transmission potential.
Leviton: Let’s talk about vaccines. You’ve said they are not intended to block infections but rather to block severe disease. So a vaccination is not designed to prevent you from getting COVID; the aim is to keep you alive when you get it?
Lakdawala: This is the crux of why people don’t trust vaccines: Scientists haven’t done a good job of explaining what they are designed to do. Say my lab has developed a new vaccine. To get it licensed by the FDA, we would need to vaccinate animals and then “experimentally challenge” them—put a really high dose of virus up their nose. And if they all survive, because the vaccine helped them develop antibodies against the pathogen, fantastic!
But you and I are not injecting a big bolus of disease up our noses. We’re going through the world, breathing in pathogens. We don’t test the vaccine for blocking infection in real-world environments. Of course there are going to be breakthrough infections. We’re not doing sterilizing immunity, where you get no infections. But the infections you get should be milder. That’s a fantastic outcome. That person’s not going to die! I hear people say, “I got the flu vaccine, and I still got the flu.” Yeah, but you didn’t get really sick, right? Maybe you had it for a couple of days instead of a week. The messaging needs to be not “You won’t get the flu” but rather “You’re not going to die of the flu.”
When it comes to the next generation of vaccines, the manufacturers need to be shooting for vaccines that actually block infection. The next-generation flu vaccines should also be universal, meaning they don’t target individual strains but are “whole-virus” weapons. [Clinical trials for universal influenza vaccines are scheduled to begin in 2026, with FDA approval possible in 2029. An internasal flu vaccine that blocks transmission is also on track for FDA review that year.—Ed.]
But I’m concerned that, even with universal flu vaccines, people will feel let down because one shot won’t protect you for ten or twenty years or against every type of infection. They want a total fix.
Leviton: The internet has made it harder than ever to get reliable health information, because of the amount of misinformation spread by nonscientists.
Lakdawala: Look, as scientists we’re not trained to be communicators. We’re all very good at what we do in the lab, but how to communicate our findings to the public is not part of our training. And it’s almost impossible to counteract misinformation on a social media platform. That’s why I do things like this interview.
Leviton: You mentioned the avian-flu outbreak. How do pathogens jump from animals to humans?
Lakdawala: When I do a slide presentation on this, I use the analogy of an Olympic hurdling event—one of my favorite Olympic competitions. The runners at the starting line represent flu in birds, pigs, seals, whales, cows, and so on—all the zoonotic viruses. At the finish line is pandemic infection in humans. When the pistol goes off, they start to run, and the first hurdle is “Can they find an opportunity to infect a human host?” The seal and whale viruses fall at that hurdle, because they don’t have enough access to humans. But pigs, cows, and poultry jump right over, because they interact with humans all the time.
The next hurdle is “Can the virus get inside the human body and replicate?” That’s hard. A number of viruses will fail that hurdle, but pig and avian viruses are actually pretty good at jumping it.
The third and highest hurdle is “Can the virus spread from person to person through the air?” Very few viruses can do that, and all the characteristics that go with clearing that hurdle are the things my lab has been studying for over a decade. Only those viruses that can jump that final high hurdle can become a pandemic.
This doesn’t mean you have to quarantine yourself and never breathe around animals, but sometimes those pathogens can be successful in infecting you. Take backyard poultry, for instance. They have lots of pathogens in them all the time. You inhale them when gathering eggs or feeding the chickens, and most of the time nothing happens. But in January of this year an elderly person in Louisiana became the first US citizen to die from the H5N1 avian flu. There’s also a teen in British Columbia who was close to death, and a three-year-old girl who died in Mexico. As we speak, the CDC is saying there have been around seventy human infections in the US. We probably have more than that, because people aren’t being tested. Most of the cases have produced mild respiratory symptoms with conjunctivitis—pink eye. That’s great, because with bird flu our biggest fear has always been that it would kill around 30 to 50 percent of the people infected.
Those fatality numbers come from when the World Health Organization identified the first human infections in 1997 in Hong Kong. Despite compulsory vaccinations for poultry, there was a big outbreak of bird flu in China in 2005, with high mortality and a spread to poultry and a handful of humans in Cambodia, Laos, and eventually more than fifty countries. We should be very thankful that we’re not seeing those high mortality rates now. There are different theories about why that is, but I can tell you the circulation of H1N1 in 2009, and its yearly circulation since then, may have given us some immunity against the bird flu. Those superhero cells I talked about are maybe remembering the N1 end of the virus they previously saw.
But because we don’t have a lot of people getting very sick, we’re also not taking every case seriously. My concern is that, if this virus is allowed to continue to infect humans and perhaps encounter someone who is immunocompromised, it might mutate into something worse.
Another concern is coinfections. Let’s say a farmer infected with H5N1 also contracts H1N1 from their kid at home. Those two strains of flu in that person can intermingle and make a reassortment. And that mingled virus will be very good at transmitting between humans.
Leviton: What’s happening with bird flu in cows’ milk?
Lakdawala: Prior to May 2024, if you’d asked me about cows and influenza, I would have said not to worry about it. No one, in my world, thought influenza in cows was a high risk to humans, and we definitely didn’t worry about it getting into milk. Now we know it’s found in crazy-high levels in cows’ milk—like ten to a hundred million virus particles per milliliter. A shot glass is about fifty milliliters. Cows give six to ten gallons of milk per day. The amount of virus coming out of these infected animals is astronomical. And milk splashes the farmworkers and moves through the waste streams on dairy farms, which I’ve learned so much about in the last few months.
When a cow gets sick with H5N1, her milk usually gets thick and yellow. That milk never goes on sale; it’s collected separately and disposed of through the wastewater streams on the farm. That wastewater does not enter our sewer systems or water-filtration systems; it stays on the farm, where it might go into what’s called a manure lagoon—a large pond that birds come to and raccoons drink from. That water is also used to irrigate crops, and in some cases it can also be used to clean out the barns, infecting more cows through the aerosols. We know the infection is getting to the cows’ udders. We just don’t know how.
If you’ve got, say, ten of your cows infected, and you’re trying to stop it from spreading, what do you do? Imagine trying to find, out of a thousand cows, the ten that are positive for bird flu. Not all infected cows show symptoms, like the yellow milk or fever or lethargy. I’ve been trying to tell the USDA for a long time now that they need to go into farms and find out how many cows are infected. We need a rapid test like we have for the regular flu—companies could have started developing one a year ago.
When it comes to the next generation of vaccines, the manufacturers need to be shooting for vaccines that actually block infection. The next-generation flu vaccines should also be universal, meaning they don’t target individual strains but are “whole-virus” weapons.
Leviton: We’re in the middle of an effort to transform, and in some cases handicap, the government’s health agencies, including the CDC, HHS, and FDA. What kind of communication are you having with government agencies right now?
Lakdawala: It’s kind of a blank screen at this point, a “communication pause” from people who make policy decisions. I still talk to scientists who are working hard in government facilities, trying to figure out what’s going on. They are still invested in the work.
Leviton: Are there tests for bird flu that could be administered to farmworkers and veterinarians?
Lakdawala: Yes, but they are not being widely administered. Dairy producers are commercial entities, and there’s little in place at the government level to incentivize them to search for bird flu in their cows. According to the USDA website, only lactating dairy cows being shipped to another state must be tested. Also most of the people who work on dairy farms are migrant workers, and right now there’s a fear of saying anything that might bring attention to that community. So if they weren’t getting tested before, they’re definitely not getting tested now.
Leviton: What should we be doing to protect ourselves as individuals?
Lakdawala: Number one, don’t drink or eat raw-milk products or raw meat. Just don’t do it. Number two, if you have backyard poultry and they seem sick—infected birds don’t walk well, and it affects their egg production—never touch them without proper protection. That means gloves, face shield, and mask, at a minimum. Or call the department of food and agriculture in your state. Number three, if you have an outdoor cat, and your cat starts acting sick, use personal-protection equipment. Your cat could have easily killed and eaten a bird that had H5N1. It’s getting really prevalent in cats. So be careful. Also don’t feed your cat raw milk or poultry feed. Finally, don’t touch cows.
Leviton: Over the summer all the 4-H kids will be getting their animals ready for the state fairs.
Lakdawala: Hopefully they are all wearing masks. My kids are not allowed to go to the petting zoo. We don’t want to have to respond to another pandemic. We want to keep this outbreak under control. Calling state departments of food and agriculture is important, because they have the mandate to do testing on dairy farms and ranches in their state. As a result of budget cuts and staff reductions, the FDA suspended its milk-testing program earlier this year. The public needs to demand action. These agencies should be working around the clock to figure out how to test the cow population. The farmers need to know which cows are infected, and we need to know how well the virus is spreading, to prevent it from spreading continuously. And we need H5N1 vaccines for individuals on the front lines, which aren’t the doctors and nurses this time but the veterinarians and farmworkers.
I’ve been trying to tell the USDA for a long time now that they need to go into farms and find out how many cows are infected. We need a rapid test like we have for the regular flu—companies could have started developing one a year ago.
Leviton: You’ve said we need to consider ourselves at war with H5N1, and that a vaccine is like armor; a mask is like a shield; but we need some sort of sword—a type of intervention that is more offensive. What might that be?
Lakdawala: Remember, every mode of transmission is possible, so you cannot have only one mitigation strategy. Vaccines are great. Like armor, they protect you from severe injuries. A mask is a shield that lets you block as many of the enemy’s blows as you can. But if you are in a poorly ventilated environment and a person is coughing in your face, you still won’t block all of the virus. So you need the sword to reduce the amount of virus in your space. This could be something like better ventilation, or antiviral medications like Paxlovid, or germicidal UV-C lamps that inactivate viruses in the environment, or cleaning surfaces. These all reduce the amount of contaminants. Then you’ve got a chance to win the battle.
Leviton: The Trump administration is also trying to cancel scientific grants, money that’s been appropriated by Congress but not spent yet. How is that affecting Emory and other universities?
Lakdawala: There’s great concern. I employ ten people in our lab. We use grant money to pay researchers and also to train the next generation of scientists: the graduate students and postdocs. As of today, no money has been cut from my lab, but we’re just going day by day. My colleagues at other universities are in the same position.
I personally don’t operate well under fear. I can’t be constantly afraid of what’s going to happen if and when they take away my funding. But until that day, we will do the best science we can do and answer questions the public needs answered.
Leviton: I imagine it’s one thing to apply for a grant and not get it, but to have money that’s already been granted get rescinded seems especially destabilizing.
Lakdawala: Yeah, it’s definitely impacted morale, for the students in particular. It’s very scary for them, because they are at the start of their careers and see a huge amount of uncertainty. Are we going to lose a generation of scientists, including those interested in infectious diseases? This work is not only being deprioritized, it’s being vilified a bit.
I recently met a student who’d always wanted to work in public health, to work with underprivileged, underserved groups, and to eliminate health inequities. This is a very bright student who now has to worry if they can ever get a job in that field. They may have to rethink their entire career trajectory because of what’s going on in Washington, DC. And that’s detrimental to our society as a whole. We want our brightest people working in public health. I don’t care where you are from or who you are—public health matters.
