By Debbie Bunch
August 25, 2025
COVID-19 Linked to Chronic Respiratory Conditions, but Vaccination Mitigates the Risk
A recent study based on data from the TriNetX electronic health database in the U.S. suggests that COVID-19 can increase the odds of someone developing a new-onset condition linked to type 2 inflammation, including asthma, hay fever, and chronic sinusitis.
The epidemiological study, conducted by an international group of investigators, compared 973,794 individuals who had contracted COVID-19 with 691,270 individuals who had been vaccinated against the virus, and 4,388,409 healthy controls without documented infection or vaccination.
The researchers found:
- People who had experienced COVID-19 had a 66% higher risk of developing asthma, a 74% higher risk of developing chronic sinusitis, and a 27% higher risk of developing hay fever when compared with healthy controls.
- No increased risk was seen for atopic eczema or eosinophilic esophagitis.
- Vaccinated individuals had a 32% lower risk of asthma compared to healthy unvaccinated individuals, and risks of sinusitis and hay fever were slightly reduced as well.
- When comparing those who had COVID-19 with vaccinated individuals, those who had COVID had more than twice the risk of developing asthma or chronic sinusitis, and a 40% higher risk of hay fever.
Since no increased risk was found for atopic eczema or eosinophilic esophagitis, the authors speculate that COVID-19 triggers type-2 inflammation in the airways but not in other organs.
They believe the results of their study also show that vaccination against the virus may have benefits beyond preventing COVID-19.
“COVID-19 vaccination may reduce respiratory complications driven by type-2 inflammation, thereby diminishing disease burden,” they wrote. The study was published in the Journal of Allergy and Clinical Immunology. Read Article Read Abstract
COPD May Begin Much Earlier Than We Think
Could COPD be a disease rooted in childhood? Researchers from the University of Arizona plan to investigate in a new study how low levels of a lung protein called club cell secretory protein (CC16) may impact the long-term risk of the condition.
Produced by specialized cells that line the airways, CC16 helps to calm inflammation and protect lung tissue from irritants, infections, and environmental pollutants. Recent evidence suggests that nearly half of all COPD cases are due not to a rapid decline in lung function due to smoking and other factors, but because some people never reach peak lung function in young adulthood, which led the investigators to launch the study.
The goal is to find out whether low CC16 levels in childhood may be playing a role in COPD by leaving people vulnerable to lung damage later in life.
The researchers will analyze blood samples from diverse population studies conducted in the U.S. and Europe to determine CC16 levels in the participants when they were children and how low CC16 levels may have impacted their lung function as they aged. Airway samples will be taken via nasal swabs or sputum as well.
“The goal is to go back in time to childhood, measure CC16 levels between ages 4 and 16, and then follow what happened to lung function in the same individuals as they reach their 20s, 30s, and beyond,” said researcher Stefano Guerra, MD, PhD. “If we can pinpoint children at risk for early COPD, we might be able to intervene while they’re still young and push them onto a healthier lung growth path.”
Dr. Guerra says the long-term goal of the five-year study, which is being funded by the National Institute of Allergy and Infectious Diseases, is to prevent lung disease before it has a chance to develop. Read Press Release
How Respiratory Viruses May be Promoting the Spread of Cancer
According to an international group of researchers led by a team from the University of Colorado Anschutz Medical Campus, respiratory viruses may be partly to blame for cancer that spreads even years after a patient went into remission.
In experiments carried out in a mouse model of breast cancer, they studied the effects of influenza and COVID-19 infections on disseminated cancer cells (DCCs) and metastasis in the lungs.
Before infection with the respiratory viruses, the mouse lungs contained very few DCCs; however, within three days of infection with the flu virus, the number increased markedly and continued to grow over the next two weeks. Nine months after infection, DCC levels remained high, and a decrease in the proportion of DCCs in a dormant state was accompanied by an increase in the number of DCCs.
The same situation played out when the mice were infected with the COVID-19 virus.
What could be spurring this rise in DCCs after respiratory infections?
The authors went on to show that the virus-induced awakening of the DCCs relied on the inflammatory signaling molecule known as IL-6. Mice with lower levels of IL-6 had lower levels of activated DCCs and greater levels of DCCs that remained dormant. Organoids formed from the mice’s mammary glands grew significantly when treated with IL-6 as well.
Since DCCs tended to cluster near immune cells called CD4+ T cells, the researchers also explored that connection, finding that when CD4+ T cells were depleted, the number of DCCs present a month after infection was reduced. What’s more, depleting the number of CD4+ T cells caused the number of CD8+ T cells, which are known to kill both cancer and virus-infected cells, to rise, and those CD8+ T cells were better at killing breast cancer cells.
The authors believe these results suggest that CD4+ T cells help awaken DCCs by suppressing CD8+ T cell activity.
Is there any evidence that these lab studies are borne out in the real world?
Yes, report the investigators. When they examined electronic health records from the UK Biobank, which includes nearly 5,000 people with a prior cancer diagnosis who were thought to be in remission, they found that a positive test for COVID-19 almost doubled the risk for death from cancer.
Analysis of data in another database of more than 36,000 women with breast cancer found infection with COVID-19 increased the risk that the cancer would metastasize to the lungs by nearly 40%.
Study author Dr. James DeGregori summed it up like this. “Dormant cancer cells are like the embers left in an abandoned campfire, and respiratory viruses are like a strong wind that reignites the flames.” The study was published by Nature on July 30. Read Press Release Read Abstract
