Scientists may have found why some people escape the worst of a cold while others are laid up for days, and it may come down to how quickly the lining of the nose launches an antiviral defence after the virus arrives.
In a study published on January 19 in Cell Press Blue, researchers found that nasal cells act as a first line of protection against rhinovirus, the most common cause of the common cold, by rapidly coordinating antiviral responses that can contain infection before symptoms appear.
When that response is weakened or delayed, the virus spreads more widely and can trigger inflammation, excess mucus and breathing problems.
“As the number one cause of common colds and a major cause of breathing problems in people with asthma and other chronic lung conditions, rhinoviruses are very important in human health,” said senior author Ellen Foxman of Yale School of Medicine.
To study the early stages of infection, the team built a lab-grown model of human nasal tissue using nasal stem cells grown for four weeks and exposed to air so they matured into a structure resembling the lining of the nasal passages and lung airways. The model included mucus-producing cells and ciliated cells, which help move mucus and trapped particles out of the lungs.
The researchers found the early defence was coordinated by interferons, proteins that activate antiviral protection in infected cells and nearby healthy cells. When interferon activity began quickly, the infection was contained early.
But when the researchers blocked the sensors that detect rhinovirus, the virus spread rapidly, infecting more cells and causing significant damage, and some infected organoids did not survive.
“Our experiments show how critical and effective a rapid interferon response is in controlling rhinovirus infection, even without any cells of the immune system present,” said first author Bao Wang, also of Yale School of Medicine.
The study also found that as viral replication increases, rhinovirus can trigger a separate sensing system that drives heavy mucus production and inflammatory signals in both infected and uninfected cells, a response linked to airway inflammation and breathing difficulties.
Researchers noted the organoid model contains fewer cell types than real human tissue and does not capture the full role of immune cells and environmental factors. They said future work will examine how those influences shape the body’s response to rhinovirus.
“Our study advances the paradigm that the body’s responses to a virus, rather than the properties inherent to the virus itself, are hugely important in determining whether or not a virus will cause illness and how severe the illness will be,” Foxman said.
