Researchers grew tiny nose models and infected them with cold viruses. What they discovered could revolutionize the treatment of respiratory infections.
New Haven – When a cold hits a household, it can leave behind a wide variety of symptoms. The same rhinovirus that causes little more than a mild runny nose in one person can cause a stuffy nose for a week in another. In still others, it causes coughing and difficulty breathing, which may require hospitalization.
To understand how these winter ailments develop, why they can vary so much, and how to alleviate them, researchers at the Yale School of Medicine have grown miniature models of the nasal passages. Over a period of four weeks, they grew nasal stem cells into organoids. These are tiny versions of the interface between our nose and the air – complete with cells that produce mucus or hair-like structures called cilia. These pulsate in a wave-like rhythm to transport mucus and debris.
“Nose in the Petri dish” is infected with a rhinovirus – and reacts
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The scientists then infected their “nose in the petri dish” with a rhinovirus, a common cold cause. After studying thousands of individual cells, the researchers found that it is not the virus but the complexity of the reaction in thousands of nasal airway cells that determines whether a cold clears up quickly or develops into something more serious.
In one in the trade journal Cell Press Blue In a published study, researchers report that rapid production of a protein called interferon by the infected cells kept the rhinovirus in check. It was able to infect less than 2 percent of the cells. When they suppressed the interferon, about a third of the cells became infected and the rhinovirus multiplied. Another immune sensor kicked in. Molecules associated with inflammation increased, mucus production went into overdrive, and cilia slowed their pulsation.
Study reveals detailed choreography of immune system response to rhinovirus
“One reason their model system is so powerful is that it is reductionist. They can show how these pathways are connected or how one can take over in the absence of another,” said Patrick Mitchell, an assistant professor of microbiology at the University of Washington. He was not involved in the study.
Sebastian Johnston, professor of respiratory medicine and allergology at the National Heart and Lung Institute at Imperial College London, was not involved in the study. He said what’s new about the study isn’t individual findings, but the way it puts the pieces together to shed light on the detailed choreography of the immune system’s response to rhinovirus infection. “The study puts the story together in a very comprehensive and thorough way – using cutting-edge techniques,” Johnston said. “This is a very beautiful piece of work that gets right to the heart of the matter.”
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The long search for a cure for the common cold
It is no surprise that interferons play a key role in the initial response to infection. The idea that the family of proteins the body releases to fight disease could be used to cure the common cold first gained traction in the early 1980s. There was hope that a cure for all viral infections might be within reach. However, efforts to use interferon as a cure for the common cold have been complicated by side effects and the difficulty of administering interferon early enough in the infection.
“Rhinoviruses are challenging for research. It is probably the most common respiratory virus in humans, but it does not actually infect other animals,” said Ellen Foxman, associate professor of laboratory medicine and immunobiology at Yale. She led the work. The models she cultivates allow her to decipher, cell by cell, how infections progress and how they are kept under control. This gives hope for treatment options. “The key is how you trigger that response,” Foxman said.
Symptoms block the respiratory tract or cause a cold
Her team hopes to understand why some people experience a strong interferon response but not others. She also finds it fascinating that when the interferon response was blocked, the airway cells sensed the virus via another viral enzyme and triggered an inflammatory response. This could also be a goal. “It causes heavy mucus production, coughing and sneezing, and mucus production is how the virus spreads,” Foxman said. “When these symptoms occur in the lungs, they obstruct the airways, and when they occur in the nose, they cause a cold.”
There’s a reason the common cold is so difficult to fight: It’s not easy to disentangle immune responses to figure out which ones are useful, which ones help fight infection, and which ones contribute to the severity of symptoms. “If this were an easily solvable problem, it would have been solved a long time ago. The elegant way in which the body fights these infections very early and at very low levels before they spread is something we cannot replicate at this time,” Foxman said.
Carolyn Johnson is a science journalist. She previously reported on health care and health care affordability for consumers. Email: carolyn.johnson@washpost.com. Signal: carojo.55
This article was first published in English on January 19, 2026 at the “Washingtonpost.com” – as part of a cooperation, it is now also available in translation to readers of the IPPEN.MEDIA portals.
