For Many Americans, Covid Is Still a Chronic, Disabling Disease. These Scientists Are Working Tirelessly to Bring Them Relief

Long Covid saps the strength and vitality of patients, who have little recourse to fight it. A team of specialists—including an afflicted researcher working mostly from her bed—is looking for answers

Photographs by Rachel Bujalski and Kate Warren

September/October 2026

A sample of cerebrospinal fluid is processed at the University of California, San Francisco, long Covid research lab. Rachel Bujalski

Julia Moore Vogel was living with her husband, Bobby, and their 2-year-old daughter in the sun-drenched suburbs of San Diego when the Covid-19 pandemic swept into the United States on commercial airplanes and cruise ships. Vogel, who has both a PhD in computational biology and medicine and an MBA from Cornell University, worked for Scripps Research at its facilities in La Jolla. She cherished her job managing a part of an ambitious study funded by the National Institutes of Health (NIH) known as the All of Us Research Program, which gathers health information from a vast cross-section of Americans—collecting biological samples, health records and other medical data from nearly 750,000 people that might one day yield treatments for devastating diseases. Her career allowed her to “work at the interface of science and business,” Vogel told me, helping ensure that research discoveries broke through academia to affect drug development and how doctors practiced medicine.

A former college cross-country runner, Vogel spent afternoons jogging through the snaking footpaths of Torrey Pines state park or pushing a stroller around her neighborhood, and she relished weekends playing with her daughter in the sand while her husband surfed the breakers that careered into the shallows off Carmel Valley. “I used to squeeze so much into my days and weeks,” she said.

portrait of Julia Moore Vogel — Julia Moore Vogel, a prominent long Covid patient-researcher. Kate Warren

During the pandemic’s first few months, when people were confined to their homes under lockdown orders, schools were closed, and the country was struggling to source N95 masks and ventilators, Vogel and her family were extremely cautious. She only left her home to watch her daughter play outside while her husband went out for groceries. They wore masks everywhere. Nevertheless, one day that summer, Vogel noticed that she could not taste her morning peppermint tea. Her sense of smell faded, too. She was diagnosed with Covid a few days later. Even now, the exact date she got sick, July 8, 2020, remains impossible for her to forget.

Vogel’s infection laid her up with a fever, shortness of breath and intense fatigue. Just as she was expecting to recover, however, in the weeks that followed her body and mind faltered. She felt her energy being sapped away. She had battering migraines that left her reeling in bed, disoriented with pain. She took one week off from her position at Scripps, then another, and then a third. Finally, she returned to remote work in August. But within a few hours, she intuited that something wasn’t right. “I was looking at tasks that would normally take me a very short amount of time, and they just felt impossible.”

Vogel struggled with concentration and memory recall. She found herself mixing up words and phrases in everyday conversation. Perhaps most unsettling, whenever Vogel exerted herself—attending doctors’ appointments, taking her daughter to play dates, visiting a local park—her other symptoms grew worse afterward. She eventually learned of others who were similarly suffering—terms like “long-haulers” and “long Covid” were already in use by May 2020—but clinicians were hesitant about making such diagnoses, as the condition had yet to be fully defined. It was an early sign of the grueling, uphill battle facing long Covid patients. Still, by late August 2020 Vogel strongly suspected that she suffered from this chronic form of Covid, whatever it was.

Most Scripps staff members in La Jolla began returning to the office in March 2021. Vogel, who continued to work remotely, never did. By 2021, she had trouble walking around her neighborhood; by 2022, she avoided stairs for fear that the exertion would leave her bedridden. At 37, she moved with the frailty and deliberativeness of someone twice her age, and she eventually acquired a wheelchair to reduce the burden on her stamina. In two years, she’d gone from a spry scientist and an active wife and mother to somebody who spent 18 hours a day in her bedroom, a drab refuge where she slept, recovered and worked using a bed-desk that sat atop her mattress.

A researcher by nature and by training, Vogel started stealing what time she could to learn about her condition. She scoured online support groups, read all the scientific papers she could find and devoured the work of journalists like Ed Yong, who were chronicling the emergence of this baffling new condition. At a time when people were dying from Covid at almost unfathomable rates—by mid-2022, more than a million Americans had been killed by the virus—long Covid patients struggled to seize the narrative of their arguably less urgent condition from skeptics who accused them of malingering or of psychosomatic afflictions.

In the meantime, long Covid treatment clinics began sprouting up to cater to desperate patients. By 2022, one patient support group, the Covid-19 Longhauler Advocacy Project, had compiled a list of 400 such practices nationwide offering everything from rehabilitation and physical therapy to lifestyle modifications to help manage chronic illness. A handful of major medical centers, including New York’s Mount Sinai Hospital, Yale New Haven Hospital and Stanford University, offered more specialized care: Their clinicians embraced an improvisatory treatment approach, making off-label use of antivirals, immune system regulators and anti-inflammatory drugs in the hopes that they might reduce symptoms, if not directly address long Covid’s still-mysterious root causes. (To this day, no medications have been approved by the FDA to specifically treat long Covid.)

As patients clamored for the American medical establishment to recognize long Covid’s severity and commit resources and expertise to illuminating it, Vogel’s boss, renowned molecular scientist Eric Topol, invited her to participate in a landmark scientific literature review of the existing research. The project gave Vogel the opportunity to collaborate with Hannah Davis and Lisa McCorkell, co-founders of an influential cohort of patients working as researchers, scientists and advocates known as the Patient-Led Research Collaborative (PLRC).

The paper that collaboration yielded, “Long Covid: Major Findings, Mechanisms and Recommendations,” published in Nature Reviews Microbiology in January 2023, has since been viewed online two million times, and it has been cited 4,000 times by other scientists, putting it in the top tier of academic papers published that year. Topol told Vogel that it’s among the most cited papers he has worked on during a celebrated five-decade career. Not only did the paper serve as a crucial overview of the first three years of long Covid research, a scattershot landscape that outside researchers struggled to get a handle on, but, according to Vogel, patients also routinely brought copies of the paper to their doctors’ appointments, as a way of substantiating their symptoms and the validity of their disease.

Vogel with her mother, Theresa Moore. — Vogel with her mother, Theresa Moore, at her parents’ home in upstate New York. Vogel was a project director at Scripps Research when a July 2020 Covid infection left her with debilitating chronic symptoms—one of an estimated 21 million Americans affected by long Covid. Kate Warren

For Vogel, the paper proved to be a valuable professional segue. “Having co-authored such an influential and highly cited article instantly legitimized me as a long Covid researcher,” she told me. And yet, at home, Vogel and her husband were scrambling. Their house was rarely cleaned, with toys strewn on the floor, dirty dishes stacked up in the kitchen, laundry mingling in unwieldy piles. Even after her mother, Theresa Moore, began flying in from upstate New York every other month to help with cooking, cleaning, child care and other chores, the family was overwhelmed. “I was in survival mode all the time,” Vogel recalled.

Since those early days, when nobody knew how long “long-haulers” would be sick, or how many people were suffering, we have gained a much clearer picture of the condition. The Centers for Disease Control and Prevention’s oft-cited, if conceptually broad, definition describes long Covid as a “chronic condition” following a Covid infection that is “present for at least three months as a continuous, relapsing and remitting, or progressive disease state that affects one or more organ systems.” The PLRC and other like-minded groups have outlined more than 200 associated symptoms, including fatigue, muscle weakness, joint pain, sore throat, insomnia, difficulty concentrating, memory issues and post-exertional malaise, a uniquely punishing impairment that exacerbates other symptoms following what were once routine activities. Estimates vary widely about how many people are affected by long Covid, but conservative assessments suggest that perhaps 21 million American adults, or more than 8 percent, have experienced symptoms related to long Covid, and that the illness routinely keeps more than one million adults out of the workforce.

Vogel sorts her daily medications and supplements, a constantly evolving combination assembled to manage multiple symptoms. Kate Warren

A subset of patients suffers from a severe manifestation of the condition, languishing with chronic pain, cognitive dysfunction and debilitating fatigue. This subset, which includes Vogel, is relatively small: Amy Proal, a microbiologist and a co-founder of PolyBio, a nonprofit dedicated to seeking treatments for chronic conditions associated with infections like Covid, estimates that this extreme form affects perhaps 2 percent of people who get a Covid infection (a figure that could still represent over two million people). But, Proal says, for them it is “totally life-altering”—leaving them not only disabled but also struggling to work or carry out basic chores and often scrabbling to make ends meet.

Organizations like Proal’s and the PLRC have been essential in raising awareness about long Covid and in advancing research into the disease. Their aim has always been to bring more medical researchers into the field, so that scientists can more clearly define the disease by clarifying its pathology and identify biomarkers that doctors can use to definitively diagnose it. And in the past few years, virologists, microbiologists, infectious disease doctors and other medical researchers have answered that call, dedicating themselves to studying this stubbornly opaque condition with increasing success. There is still a ways to go, but the hope is that by tracing the labyrinthine pathways by which this acute viral infection becomes a chronic, multisystem illness, the vital first steps toward understanding long Covid—and to effectively treating it—are within reach.

The Zuckerberg San Francisco General Hospital and Trauma Center is a dense, towering cluster of brick and concrete buildings in the city’s Mission District, adjacent to the 101 freeway and less than two miles west of the bay. On a drizzly, overcast week in February, I traveled there to meet with Michael Peluso, an infectious disease clinician and researcher, and his team at the University of California, San Francisco. The university opened a sleek new facility called Pride Hall on the hospital campus in 2023, and many of its hospital faculty and researchers have their offices and labs in the building. The skies were scuffed with gray when I met Peluso and his colleagues in their offices there.

Peluso, a measured, even-keeled scientist with a mop of black hair, dark stubble and brown eyes, runs a program at the university called Long-term Impact of Infection With Novel Coronavirus, abbreviated as LIINC. In its Pride Hall headquarters, the program shares a floor with UCSF researchers working on the NIH’s Recover program, which is also investigating long Covid. Peluso began his career studying HIV, probing the virus’s complex effects on the brain and nervous system. “I was really interested in understanding how HIV persists in a person’s body, what the consequences of that persistence are and whether we can alter that,” he told me. He focused specifically on how HIV “viral reservoirs”—remnants of the virus that hid inside tissue cells throughout the body—drove neuroinflammation and vascular damage, among other impacts, and whether helping patients suppress the virus with antiretroviral drugs could alleviate its knock-on effects. “Then, you know, 2020 happened.”

portrait of Michael Peluso — Michael Peluso, a UCSF infectious disease clinician, oversees the LIINC study. An HIV specialist when Covid arrived, he shifted his research resources to focus on Covid’s long-term impacts. Rachel Bujalski

When Covid began spreading in San Francisco, Peluso asked his mentor, the distinguished HIV researcher Steven Deeks, to explore whether they could help address the public health crisis. The pair had been running a long-term observational study of HIV patients, but the San Francisco Department of Public Health abruptly paused it amid the city’s lockdown measures. With their study on hold and the city under strict stay-at-home orders, Peluso and Deeks devised an idea: What if they repurposed their existing resources and infrastructure—researchers, study protocols, access to state-of-the-art laboratories—to track Covid’s long-term impacts? “We had no idea how SARS-CoV-2 was going to affect health,” Deeks told me, referring to the specific coronavirus that causes Covid-19. But based on their experience with HIV, the researchers knew that infectious diseases are more complex than they at first appear. “Our assumption was that it was going to have some long-term implications.” Peluso said, “There was just something about the speed, scale and severity of SARS-CoV-2 as it emerged that made it clear that it wasn’t going to be simple.”

Indeed, within the study’s first month, in April 2020, Peluso and his team were already meeting patients who reported an uneven recovery, with their strength and vitality nowhere near their pre-illness baseline. In response, Peluso went on, “We brought together clinical researchers like me, epidemiologists, laboratory scientists, biostatisticians and lab medicine people, to try to understand all aspects of the post-acute phase of Covid.” The result was what Deeks believes to be “the first longitudinal cohort of nonhospitalized patients who had Covid.”

The LIINC offices are modern if unremarkable, a maze of white cubicles and cluttered desks anchored by an elegant break room with floor-to-ceiling windows overlooking the city’s billowing skyline. Peluso and I took an elevator down to the first floor, where a full wing is dedicated to seeing the 2,000 or so patients enrolled in LIINC’s large observational study or the program’s various long Covid studies: trials testing the effectiveness of monoclonal antibodies as well as drugs such as the antiviral Paxlovid and the rheumatoid arthritis medication baricitinib. Then we trudged through the rain to a neighboring building, where LIINC carries out lumbar punctures, tissue biopsies and other invasive procedures to collect biospecimens for study and experimentation.

In one hallway, we passed a bronze plaque dated July 25, 1983, commemorating “The First AIDS Ward,” where caregivers “gathered to confront a new epidemic.” The hospital was one of the country’s first to treat HIV/AIDS, and many UCSF clinicians became pioneers in researching the lethal virus, which was killing thousands of gay men in San Francisco at the time. With long Covid, Peluso sees another opportunity for the university and the hospital to serve as trailblazers. “Both research programs emerged from a time of chaos and uncertainty,” he said. “Working in a place that has not been afraid to tackle those types of hard problems amid that uncertainty and having that sort of legacy—that was really important in providing meaning and purpose at the beginning.”

During my trip, I was surprised to find that many researchers said that long Covid could ultimately prove to be a knottier, more elusive disease than HIV/AIDS. Tim Henrich, a translational virologist at UCSF, invoked a daunting analogy to convey its complexity. When Henrich was around 10, his cousins gave him a formidable gift for his birthday. “It was a thousand-piece puzzle,” he recalled. Rather than each piece having a fragment of an image on only one side, however, the pieces had the same image, rotated 90 degrees, on the back, requiring that he effectively complete two puzzles at once. “That’s like long Covid,” Henrich said. “It’s not just that we’re looking at one picture; we’re looking at multiple pictures that are offsetting.”

Did you know? The objects the Smithsonian collected related to the Covid pandemic

Among the artifacts acquired by the Smithsonian include:

The vial that held the first Covid vaccine administered in the United States and the recipient’s vaccination card.

A test kit designed to detect a patient with asymptomatic Covid

A Philadelphia-area emergency room surgeon’s cap, designed with cartoon characters, to put patients at ease when he was wearing full protective equipment.

Examples of hand-sanitizer produced by distilleries during the height of the pandemic.

portrait of Tim Henrich — Tim Henrich, a physician and leading long Covid virologist at UCSF. The first step toward solving the puzzle of long Covid, he says, is collecting the pieces. “We have the puzzle pieces basically strewn about the table.” But, he says, “I think they’re all there.” Rachel Bujalski

There are several hypotheses about how the SARS-CoV-2 virus takes root in the body and evolves into the chronic condition we call long Covid, and they are not necessarily mutually exclusive. One is that the body’s ongoing effort to eradicate an acute Covid infection can reactivate other latent viruses—the immune system is continuously keeping a host of low-level infections in check—including Epstein-Barr virus and cytomegalovirus. These reactivations, says Proal, of PolyBio, then “spread to new sites and drive more chronic symptoms themselves.”

A second theory is that the immune system’s efforts to combat a lingering Covid infection lead to immunological dysregulation, triggering neuroinflammation and other effects sometimes referred to as sickness behavior. This can leave sufferers feeling perpetually ill as the body’s sickness response washes over them in a broken cycle. A third is the notion that the infection disrupts cellular mitochondria, inhibiting their critical role in converting food into energy and powering the cells they inhabit.

Finally, there’s a hypothesis that the virus will sometimes burrow into tissues in different parts of the body, creating viral reservoirs that evade the immune system and trigger a cascade of adverse physiological responses. Much of the field has converged on this hypothesis to explain at least some of the pathology of long Covid, in part because early research found compelling evidence of viral persistence in the gut. Moreover, as Peluso explained to me, viral persistence offers the simplest, most straightforward hypothesis: “A pathogen invades, sticks around and causes trouble.” This is the area Peluso and his LIINC colleagues are now most focused on.

Perhaps surprisingly, Peluso was initially skeptical that viral persistence could be a key characteristic of long Covid. “We’re really trained to conceive of most pathogens as transient, especially RNA viruses like SARS-CoV-2,” he told me. But when Peluso and his colleagues began analyzing tissue from LIINC participants, they were stunned to find the virus’s RNA in the tissue of people with long Covid who were months or even years past their initial infection. “It was only when we started to see it in our own program that I began to realize that the truth might be more complicated than what the textbook said,” he recalled. “When you’re looking at that slide in front of you, it’s quite remarkable.”

Retrieving biospecimens from a liquid nitrogen storage tank at the long Covid research lab jointly run by UCSF and Zuckerberg San Francisco General Hospital and Trauma Center Rachel Bujalski

After meeting with Peluso, I went to see some of the program’s research in action in Henrich’s virology laboratory, one floor below LIINC’s operations in Pride Hall. Together with a separate, dedicated repository at UCSF, the lab makes up one of the largest banks of long Covid biospecimens in the country, and this is where Henrich and his colleagues analyze tissue, fluid and other samples to identify latent SARS-CoV-2 virus and piece together what ill effects those viral reservoirs may cause.

The biobank also operates as a kind of massive “lending library”: LIINC staff correspond with researchers all over the world and send out samples to sustain other studies and experimentation. Among other researchers, the lab has lent specimens to Yale University’s Akiko Iwasaki, who is investigating long Covid autoimmunity and potential tissue damage stemming from infection; the University of Pennsylvania’s Michela Locci, whose team is examining whether SARS-CoV-2 could be altering the immune response in lymphoid tissue; and Irini Sereti, a scientist at the National Institute of Allergy and Infectious Diseases who focuses on the specific immunological dysfunctions triggered by SARS-CoV-2, including in T cells. (Although Peluso and his UCSF colleagues focus primarily on viral persistence, Peluso believes the field “will need to think much broader —not because I don’t think that viral persistence is an answer, but because it may not be the only answer, or the answer for everyone.”)

Stepping into a large, white antechamber, Henrich and I donned paper gowns, booties, safety glasses and two layers of gloves. Finally, we dropped our phones into zip-top bags. “Don’t touch anything,” Henrich warned, his arms splayed out and his palms facing up to emphasize the risk. That morning, a LIINC participant had undergone a lumbar puncture, with clinicians using a long, hollow needle to extract a sample of cerebrospinal fluid. Researchers were now transporting that fluid to the lab, a large room with high ceilings and long, narrow rows of benches, each affixed to shelves cluttered with vials, pipettes and biohazard containers. The lab has processed tens of thousands of long Covid tissue specimens drawn from all over the human body, including the gut, lymph nodes, bone marrow and spinal cord. (Thus far, Peluso, Henrich and their colleagues at UCSF have found viral reservoirs only in the gut and bone marrow.)

Once the cerebrospinal fluid was delivered, a tall, broad-shouldered researcher named Emmanuel Velazquez sat down in front of a large metal workspace called a biosafety cabinet to begin processing it. “I know the protocol like the back of my hand,” he said. Wearing latex gloves, Velazquez pulled the sample out of a foam container filled with ice and transferred the fluid into a second tube. He then carried it across the room to a centrifuge, where he would “spin down” the sample to remove unwanted proteins, collagen and other biological material that could interfere with the cells.

While the centrifuge whirred quietly, Henrich explained how the LIINC researchers analyze these purified samples to identify signatures of viral persistence, including, for example, telltale antibodies, proteins or RNA. Like physical evidence at a crime scene, these signatures will hopefully shed light on the sequence of events they believe viral persistence may trigger: inflammation, clotting, neural injury or other harmful physiological responses.

Of course, if viral persistence is shown to cause long Covid, it may represent just the first link in a longer chain reaction. It’s possible, even likely, that one or more of the other explanations for long Covid’s pathology is also a part of that chain—viral persistence leading to immune dysfunction, for example, which then prompts inflammation or interferes with mitochondria and causes cellular damage. As Peluso put it to me, “If viral persistence is the most upstream mechanism, how does it trigger all of these downstream mechanisms that are thought to contribute to long Covid?”

Emmanuel Velazquez places a cerebrospinal fluid sample into a centrifuge for processing; the lab’s cell counter. Rachel Bujalski

The centrifuge started gently beeping, signaling that it was finished spinning down the cells. Velazquez pulled open the machine, took out the sample and carried it back to the safety cabinet. There, he used a pipette to distribute the specimen into 20 separate vials, squeezing individual droplets of isolated cells into clear plastic containers. Although routine, transferring specimens requires intense focus and a steady hand. “Do you remember the game Operation, where you try to pick things out without hitting the side?” Henrich joked.

Velazquez squeezed exactly one milliliter of the sample into each vial. The specimens are separated so that LIINC can offer them to other labs; by dividing the samples, Peluso had told me, the lab is able to provide different researchers with the biological material necessary to pursue specific research niches within the larger long Covid field. Over time, Peluso said, this could help yield “a broader set of therapeutic approaches that could be tested beyond just ‘targeting the virus.’”

Finally, Velazquez loaded the samples into a plastic orange rack and transferred them to an industrial freezer, where they fit snugly next to stacks of white boxes blanketed in frost that stored additional LIINC samples. Once the temperature gets low enough, lab members transport the samples to a liquid nitrogen tank that maintains temperatures of around minus 320 degrees Fahrenheit, cryogenically freezing them and allowing Henrich and his colleagues to keep the cells—and the complex biological records concealed within them—alive and ready for further experimentation.

a box containing cryogenically frozen biospecimens. — A box containing cryogenically frozen biospecimens. Rachel Bujalski

Indeed, in May, a few months after I met Henrich, he presented new research at a long Covid symposium organized by PolyBio, demonstrating what a chain reaction triggered by viral persistence might look like. Using a form of biological analysis known as transcriptomics—which records a snapshot of a cell’s RNA molecules at a given moment and reveals which genes are actively turned on and off (possibly by a viral infection)—Henrich showed how the gut tissue of long Covid patients revealed signs of immune dysregulation. Near viral reservoirs, certain immune signals weakened while others were amplified. This suggests that the immune system was detecting the virus but mounting a disordered response to it, possibly because the virus or proteins it released interfered with its defenses. These responses, he argued, could explain not only why the immune system was failing to fully clear the virus from the body but also how its persistence may be causing chronic inflammation.

Biospecimens from the lab’s “tissue bank,” which holds tissues drawn from the gut, lymph nodes, bone marrow and spinal cord. Rachel Bujalski

Cover image of the Smithsonian Magazine September/October 2026 issue

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This article is a selection from the September/October 2026 issue of Smithsonian magazine

The findings have yet to be published, and Peluso, a co-author of the paper with Henrich, was careful not to get ahead of the peer-review process. But he did allow that the research represented a meaningful step forward: “It suggests that there is biological activity that is occurring in these spaces that are either allowing these reservoirs to persist or are a consequence of the reservoirs.” PolyBio’s website goes so far as to describe the new findings, when combined with similar data sets presented by other researchers, as a “major working model of long Covid mechanism—gut viral persistence leading to incomplete clearance and immune dysregulation.”

A few weeks later, I traveled to visit Julia Moore Vogel. Despite—and in some perverse way because of—her own deteriorating health, she has emerged as a prominent patient-scientist in the long Covid field. In 2024, Vogel moved with her husband and daughter to upstate New York to be closer to her parents. Late last year, they bought a house in Schaghticoke, a quiet town of 7,000 hunched on the banks of the Hoosic River. When I pulled up to it, a canary-yellow colonial-style house with white shutters and a center gable framing an ice-glazed roof, the front yard was carpeted in snow.

I met Vogel in her kitchen, and from her wheelchair she led me through her new home and daily routine. Vogel still works at Scripps; her position remains fully remote. While she continues to work on the All of Us study, she is now also an assistant professor at the institute, focused on long Covid, where she works to get drug trials off the ground. “I have felt since 2020 that we need to be doing clinical trials to help people feel better,” she said.

Leading me out of the kitchen and into the dining room, Vogel pointed to a long wooden table with an iron, fabrics and a small machine with a silver needle plate: an embroidery station. “It’s a really good sedentary thing,” she said. “I make gifts for all my disabled friends that I’ve never met.” In the corner of the room was an elevator, installed after her family purchased the home. Vogel agonized over the decision for months, unnerved by the cost of the project. “I really waffled about it, because it was so expensive,” she told me. “I was like, ‘I really don’t want to spend my emergency fund on this.’ And my dad, who also uses a wheelchair, was like, ‘Julia, this is an emergency.’”

Vogel took the elevator upstairs, and I met her in her bedroom, an unembellished space where she spends most of her day. When we entered, the room was dimly lit—bright lights can induce post-exertional malaise, leaving her with painful migraines. She does most of her work from her mattress, and everything she needs during the day—medications, supplements, tea, notes—are an arm’s length from her bed.

Vogel, working from bed in upstate New York. She and her family relocated from California in 2024 to be closer to her parents, who help with day-to-day support. Kate Warren

Vogel is dogged in maintaining a demanding work life. She runs a clinical trial of her own design that repurposes the GLP-1 receptor agonist tirzepatide to see whether its anti-inflammatory effects can benefit long Covid sufferers. (She has already tried another GLP-1 and found that it wasn’t an effective treatment for her, but she is determined to see if the drug class can help others.) The trial is still underway, which means data is not yet available, and because she is a principal investigator, she remains completely blinded, but some participants have anecdotally reported marked improvements in their symptoms, and Vogel is hopeful that the data will bear out their experiences. (A few intrepid physicians already prescribe tirzepatide in an off-label capacity; one, David Kaufman, a leading HIV/AIDS physician and a co-founder, in 2017, of the Center for Complex Diseases, presented survey data last year showing that between 60 and 90 percent of patients responded positively to small doses of GLP-1.)

Vogel’s trial is one of around 90 long Covid drug trials that are underway or have concluded worldwide. (The NIH is also tracking hundreds of other trials that focus primarily on behavioral treatments such as diet and exercise.) In addition to studies of Paxlovid and baricitinib, which have yet to show convincing evidence that either is an effective treatment for long Covid, researchers are examining a range of other existing medications, including the diabetes drug metformin (meant to improve metabolic energy) and the antidepressant fluvoxamine (which has reduced fatigue in some patients). The heart disease drug ivabradine, meanwhile, failed to improve dizziness and fatigue in patients who developed heart problems after a Covid infection. Another study, which is expected to begin this fall, will investigate whether a combination of repurposed HIV and cholesterol drugs, maraviroc and atorvastatin, can improve both physical and neurocognitive symptoms, including brain fog, fatigue, dizziness and indigestion. At least one cancer-fighting biologic therapy, known as Anktiva, which may boost immune response, is in safety trials at UCSF. And Proal, Peluso and other researchers are working with a small pharmaceutical company called Invivyd to see if its experimental monoclonal antibody, which can neutralize diverse Covid variants, might be an effective treatment for long Covid. “It’s one of the most anticipated trials from both the patient community and the research side,” Proal told me.

As desperately needed as these drug trials are, however, none of the therapies was designed to treat long Covid. That’s what makes the work of Peluso, Henrich and other early-stage researchers so essential. The hope is that once scientists firmly establish long Covid’s pathology, and doctors can reliably diagnose the disease with bloodwork or other lab tests, researchers will have a much easier time persuading pharmaceutical companies to invest in developing new, targeted drugs. Only then, if all goes well, will long Covid patients see new experimental medications in the pipeline that may one day alleviate their symptoms—perhaps even return them to their pre-Covid baselines. That we may be approaching the end of the beginning phase of this long trajectory, nearly seven years on from Covid’s emergence, is a testament to the perseverance of patients and researchers like Vogel for whom advocacy is no easy task.

A LIINC participant departs after testing at the San Francisco hospital. Peluso says, “Seeing people from the beginning whose lives were really disrupted by this, I really wanted to understand what was causing this for them, and I really wanted to try to help them get better.” Rachel Bujalski

In her bedroom, Vogel reflected on why she maintains such a grueling professional load in spite of her severe physical limitations—a balancing act, she confessed, that requires her to “ruthlessly prioritize” her days, often giving most of them over to her job. Just the day before, in addition to her research duties, she’d participated in two video calls related to long Covid awareness and education: One was a panel with Nancy Klimas, an expert on infection-associated chronic conditions; on the other, she briefed officials from public health departments all over the country on the disease. “I’m self-conscious on Zoom,” she admitted. “You can tell I’m sitting in bed, because you can see the stuff behind me.”

But she fills her workdays with such talks and virtual meetings anyway, she says, because she believes that while progress is closer than many people realize, it is not inevitable. “Having the capability to help the community, I feel a moral obligation to use my skills for that purpose, because I feel like there’s reason for hope. And I want other people to know that—to feel that hope.”

For Many Americans, Covid Is Still a Chronic, Disabling Disease. These Scientists Are Working Tirelessly to Bring Them Relief

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