Researchers led by UVA School of Medicine scientist Jie Sun, PhD, discovered that severe respiratory infections can alter immune cells in the lungs in ways that support tumor growth months or even years later. Based on these findings, the scientists recommend that doctors closely watch patients who recover from severe COVID, flu, or pneumonia so lung cancer can be detected early, when treatment is most effective.

“A bad case of COVID or flu can leave the lungs in a long-lasting ‘inflamed’ state that makes it easier for cancer to take hold later,” said Sun, co-director of UVA’s Carter Center and a member of UVA’s Division of Infectious Diseases and International Health. “The encouraging news is that vaccination largely prevents those harmful changes for cancer growth in the lung.”

Severe Respiratory Infections and Long Term Lung Damage

Respiratory illnesses such as influenza and COVID are among the most common sources of lung injury. However, scientists have not fully understood how this type of damage might influence cancer risk years later. To explore this question, Sun and his team studied the effects of severe lung infections in both laboratory mice and human patients.

The findings were striking. Mice that experienced severe lung infections were more likely to develop lung cancer later and were also more likely to die from the disease. When the researchers analyzed patient data, they found a similar pattern. People who had previously been hospitalized with COVID-19 showed a higher rate of lung cancer diagnoses.

The analysis revealed a 1.24-fold increase in lung cancer incidence among patients who had been hospitalized for COVID-19. This elevated risk was seen regardless of whether the individuals smoked or had other medical conditions, which doctors refer to as “comorbidities.”

“These findings have important immediate implications for how we monitor patients after severe respiratory viral infection,” said Jeffrey Sturek, MD, PhD, a UVA physician-scientist who collaborated on the study. “We’ve known for a long time that things like smoking increase the risk for lung cancer. The results from this study suggest that we may need to think about severe respiratory viral infection similarly. For example, in some patients who are at high risk for lung cancer based on smoking history, we recommend close monitoring with routine screening CT scans of the lungs to catch cancer early. In future studies, we may want to consider a similar approach after severe respiratory viral infection.”

Immune Changes That Create a Pro Tumor Environment

Experiments in mice helped the researchers uncover why severe infections may increase cancer risk. The team observed major changes in immune cells known as neutrophils and macrophages, which normally help defend the lungs.

After severe infection, some neutrophils began behaving abnormally and contributed to a persistent inflammatory environment described as “pro-tumor,” meaning it supports cancer growth. The scientists also found significant changes in epithelial cells that line the lungs and the tiny air sacs responsible for breathing.

Vaccination May Protect the Lungs

The study also produced encouraging findings about prevention. Prior vaccination appeared to block many of the lung changes linked to cancer development. Vaccines help the immune system respond more effectively to infections, which reduces how severe the illness becomes.

The researchers observed the increased cancer risk mainly in people who had severe COVID-19. Individuals who experienced only mild infections did not show this elevated risk and actually had a slight decrease in lung cancer incidence.

Even so, the scientists warn that many people who survived severe COVID-19 or other serious respiratory infections could face a higher risk of lung cancer in the future.

“With tens of millions of people globally experiencing long-term pulmonary [COVID-19] sequelae, these findings carry significant implications for clinical care,” the researchers wrote in their scientific paper. “Individuals recovering from severe viral pneumonia, particularly those with smoking history, may benefit from enhanced lung cancer surveillance, and preventing severe infection through vaccination may confer indirect cancer protection benefits.”

Implications for Early Detection and Treatment

Sun and his colleagues hope their work will help doctors better identify patients who may face an increased risk of lung cancer after severe respiratory infections. Earlier detection could allow treatment to begin sooner and improve patient outcomes.

The team also believes their findings could guide the development of new strategies to prevent or treat lung cancer linked to prior lung infections.

“Our goal is to help doctors identify who may be at higher risk of lung cancer after a severe infection, and develop targeted ways to prevent and treat lung cancer after prior pneumonia,” Sun said. “We also believe that vaccines don’t just prevent acute hospitalization after contracting the virus. They may also reduce the long-term fallout of severe infection, including the kind of immune scarring that can increase cancer risk.”

Advancing Biomedical Research at UVA

Improving the understanding and treatment of complex diseases is a central mission of UVA’s Paul and Diane Manning Institute of Biotechnology. The institute focuses on accelerating innovative research like Sun’s work and helping translate laboratory discoveries into new treatments more quickly.

UVA’s Beirne B. Carter Center for Immunology Research (CIC) was established through the generosity of Beirne B. Carter, and the Beirne Carter Foundation continues to support its research efforts. Scientists at CIC study infections, cancer, cardiovascular disease, chronic lung conditions, the microbiome, and autoimmune disorders to develop new therapies and cures.

The UVA Comprehensive Cancer Center is one of only 57 cancer centers in the United States to receive the National Cancer Center’s “comprehensive” designation, recognizing excellence in patient care and advanced cancer research.

Findings Published in Cell

Sun and his collaborators published their findings in the scientific journal Cell. The research team included Wei Qian, Xiaoqin Wei, Andrew J. Barros, Xiangyu Ye, Haibo Zhang, Qing Yu, Samuel P. Young, Eric V Yeatts, Yury Park, Chaofan Li, Sijie Hao, Gislane Almeida-Santos, Jinyi Tang, Harish Narasimhan, Nicole A Kirk, Valeria Molinary, Ying Li, Li Li, Bimal N. Desai, Peter Chen, Kwon-Sik Park, Anny Xiaobo, Jeffrey M. Sturek, Wei Chen, In Su Cheon and Sun.

Funding for the research came from the National Institutes of Health, grants AI147394, AG069264, AI112844, HL170961, AI176171, AG090337, R01HL179312, F31HL170746, T32AI007496, T32CA009109, R01AI155808 and R01HL162783; a UVA Comprehensive Cancer Center Collaborative Grant, U01CA224293; a UVA Pinn Scholar Award; a UVA Shannon Fellowship; a UVA Comprehensive Cancer Center Lung TRT Pilot Grant; an American Lung Association Catalyst Grant, T32GM139787-01; and a UVA Parsons-Weber-Parsons Fellowship.

Scientists at the University of Queensland partnered with researchers from the University of Minnesota to examine levels of adenosine triphosphate (ATP) – known as the “energy currency” molecule – in the brains and blood cells of young people with depression.

Associate Professor Susannah Tye from UQ’s Queensland Brain Institute (QBI) said the findings mark the first time researchers have detected patterns in these fatigue related molecules in both the brain and bloodstream of young people with major depressive disorder (MDD).

“This suggests that depression symptoms may be rooted in fundamental changes in the way brain and blood cells use energy,” Dr. Tye said.

“Fatigue is a common and hard-to-treat symptom of MDD, and it can take years for people to find the right treatment for the illness.

“There has been limited progress in developing new treatments because of a lack of research, and we hope this important breakthrough could potentially lead to early intervention and more targeted treatments.”

Study Examines Brain Scans and Blood Samples

In the study, a team at the University of Minnesota gathered brain scans and blood samples from 18 participants between the ages of 18 and 25 who had been diagnosed with MDD.

Researchers at the Queensland Brain Institute then examined those samples and compared them with samples taken from individuals who did not have depression.

Unexpected Energy Patterns in Cells

QBI researcher Dr. Roger Varela said the team observed an unusual pattern in cells from participants with depression. The cells produced higher levels of energy molecules while resting but struggled to boost energy production when under stress.

“This suggests cells may be overworking early in the illness, which could lead to longer-term problems,” Dr. Varela said.

“This was surprising, because you might expect energy production in cells would be lower for people with depression.

“It suggests that in the early stages of depression, the mitochondria in the brain and body have a reduced capacity to cope with higher energy demand, which may contribute to low mood, reduced motivation, and slower cognitive function.”

Findings May Help Reduce Stigma and Improve Treatment

Dr. Varela said the research may also help change how people understand depression.

“This shows multiple changes occur in the body, including in the brain and the blood, and that depression impacts energy at a cellular level,” he said.

“It also proves not all depression is the same; every patient has different biology, and each patient is impacted differently.

“We hope this research will help lead to more specific and effective treatment options.”

The study was led by the University of Minnesota’s Katie Cullen MD, and the imaging method used to measure ATP production in the brain was developed by Professors Xiao Hong Zhu and Wei Chen.

The research is published in Translational Psychiatry.

Researchers at Scripps Research have now introduced a different type of blood test that focuses on how proteins are folded in the bloodstream rather than how much of them is present. Their findings, published in Nature Aging on February 27, 2026, show that structural differences in three plasma proteins are strongly linked to Alzheimer’s status. These changes allowed scientists to accurately distinguish cognitively normal individuals from those with Alzheimer’s and mild cognitive impairment (MCI). The method could eventually allow diagnosis and treatment to begin earlier.

“Many neurodegenerative diseases are driven by changes in protein structure,” says senior author John Yates, a professor at Scripps Research. “The question was, are there structural changes in specific proteins that might be useful as predictive markers?”

Protein Folding and the Breakdown of Proteostasis

For many years, Alzheimer’s disease has been closely associated with amyloid plaques and tau tangles that accumulate in the brain. However, scientists increasingly believe that the condition may involve a broader failure in proteostasis, the system responsible for keeping proteins properly folded and removing damaged ones.

As people age, this system becomes less effective. Proteins are then more likely to fold incorrectly during production or maintenance. Based on this idea, the researchers proposed that if proteostasis is disrupted in the brain, similar structural changes might also appear in proteins circulating through the blood.

Analyzing Structural Changes in Blood Proteins

To explore this possibility, the research team examined plasma samples from 520 participants divided into three groups: cognitively normal adults, individuals with mild cognitive impairment and patients diagnosed with Alzheimer’s.

The scientists used mass spectrometry to determine how exposed or buried certain locations within proteins were, which indicates changes in their structure. They then applied machine learning techniques to identify patterns connected to disease stage.

The results revealed a clear pattern across all groups. As Alzheimer’s progressed, some blood proteins became less structurally “open.” These structural changes proved to be more informative for identifying disease stage than simply measuring protein concentrations.

Three Proteins Linked to Alzheimer’s Progression

Among the many proteins analyzed, three showed the strongest association with disease status. These were C1QA, which plays a role in immune signaling; clusterin, which is involved in protein folding and amyloid removal; and apolipoprotein B, a protein that transports fats in the bloodstream and contributes to blood vessel health.

“The correlation was amazing,” says co author Casimir Bamberger, a senior scientist at Scripps Research. “It was very surprising to find three lysine sites on three different proteins that correlate so highly with disease state.”

Changes at specific sites within these proteins enabled researchers to classify participants as cognitively normal, MCI or Alzheimer’s with about 83% overall accuracy. When comparing two groups directly, such as healthy individuals versus those with MCI, accuracy rose above 93%.

Tracking Alzheimer’s Over Time

The three protein model remained reliable when tested in independent participant groups and when researchers analyzed blood samples collected months later.

In repeat tests taken months apart, the panel identified disease status with about 86% accuracy and reflected changes in diagnosis over time. The structural score also showed a strong relationship with cognitive test results and a more moderate association with MRI measurements of brain shrinkage.

Together, these findings suggest that analyzing protein structure in blood could complement existing amyloid and tau tests. Because this method focuses on structural changes connected to the underlying biology of the disease, it may help researchers identify disease stages, monitor progression and evaluate how well treatments are working.

Future Applications and Next Steps

“Detecting markers of Alzheimer’s early is absolutely critical to developing effective therapeutics,” says Yates. “If treatment can start before significant damage has been done, it may be possible to better preserve long-term memory.”

Before the blood test can be used in clinical settings, larger studies with longer follow up periods will be needed to confirm the results. Researchers are also exploring whether the same structural profiling method could be applied to other diseases, including Parkinson’s and cancer.

In addition to Yates and Bamberger, authors of the study “Structural signature of plasma proteins classifies the status of Alzheimer’s disease,” include Ahrum Son, Hyunsoo Kim and Jolene K. Diedrich of Scripps Research; Heather M. Wilkins, Jeffrey M. Burns, Jill K. Morris and Russell H. Swerdlow of the University of Kansas Medical Center; and Robert A. Rissman of the University of California San Diego.

Support for this study was provided by the National Institutes of Health (grants RF1AG061846-01, 5R01AG075862, P30AG072973 and P30-AG066530).

In a recent experiment, scientists successfully grew and harvested chickpeas using simulated “moon dirt.” This is the first time the crop has been produced in a material designed to mimic lunar soil. The research was carried out with collaborators from Texas A&M University and published in the journal Scientific Reports.

Sara Santos, the project’s principal investigator, said the findings represent an important step toward understanding how crops might be grown on the lunar surface.

“The research is about understanding the viability of growing crops on the Moon,” said Santos, who is a distinguished postdoctoral fellow at the University of Texas Institute for Geophysics (UTIG) at the Jackson School of Geosciences. “How do we transform this regolith into soil? What kinds of natural mechanisms can cause this conversion?”

Challenges of Growing Plants in Lunar Soil

Lunar regolith is the scientific name for the dusty material that covers the Moon’s surface. Unlike soil on Earth, it does not contain microorganisms or organic matter that plants depend on to grow. Although regolith includes minerals and nutrients that plants can use, it also contains heavy metals that may harm plant development.

To test whether crops could grow in these conditions, the researchers used a simulated lunar soil produced by Exolith Labs. This mixture is designed to closely resemble the composition of moon samples brought back during the Apollo missions.

Creating Better Soil With Worm Compost

To improve the growing environment, the team mixed the simulated moon dirt with vermicompost. This nutrient rich material is created by red wiggler earthworms as they digest organic waste. Vermicompost contains valuable plant nutrients and a diverse microbiome that supports plant health.

In a space mission setting, the worms could generate compost from discarded materials such as food scraps or cotton clothing and hygiene products that would otherwise be thrown away.

Before planting, the researchers coated the chickpea seeds with arbuscular mycorrhizae fungi. These fungi form a symbiotic relationship with plants. They help plants absorb key nutrients while also reducing the amount of heavy metals taken up from the soil.

Chickpeas Grow in Simulated Moon Dirt

Santos and her team planted the chickpeas in different mixtures of moon dirt and vermicompost.

The results showed that plants could grow successfully in mixtures containing up to 75% simulated lunar soil. When the amount of moon dirt increased beyond that level, the plants experienced stress and died sooner.

Even in difficult conditions, the plants treated with fungi survived longer than those that were not inoculated. This highlights how important the fungi were for supporting plant growth. The researchers also discovered that the fungi were able to establish themselves in the simulated lunar soil, which suggests they might only need to be introduced once in a real lunar farming system.

Are Moon Grown Chickpeas Safe to Eat?

Although harvesting chickpeas from simulated moon dirt is a significant milestone, several questions remain. Scientists still need to determine whether the plants absorb harmful metals from the soil and whether the chickpeas provide the nutrients astronauts would need.

“We want to understand their feasibility as a food source,” said Jessica Atkin, the first author on the paper and a doctoral candidate in the Department of Soil and Crop Sciences at Texas A&M University. “How healthy are they? Do they have the nutrients astronauts need? If they aren’t safe to eat, how many generations until they are?”

The project was originally funded by Santos and Atkin themselves. It has since received additional support through a NASA FINESST grant, which will help advance research on growing food for future missions to the Moon.