When rhinovirus, the most common cause of the common cold, enters the nose, the body doesn’t wait around.
The cells lining the nasal passages immediately kick into action, working together to limit the infection and keep it from spreading. Research published January 19 (Cell Press Blue) shows that this early response may matter more than the virus itself.
How strongly and how quickly nasal cells react can determine whether someone gets sick at all and how severe their symptoms end up being.
Rhinovirus isn’t just responsible for sniffles. It’s also a major trigger for asthma flare-ups and breathing problems in people with chronic lung conditions.
Building a Mini Human Nose in the Lab
To study what actually happens during infection, the team created lab-grown human nasal tissue. They started with nasal stem cells and grew them for about four weeks, exposing the surface to air so the cells would mature naturally.
The result closely resembled the lining of real nasal passages and airways.
The tissue contained multiple cell types, including mucus-producing cells and ciliated cells. Cilia are tiny hair-like structures that help move mucus and trapped particles out of the airways.
This type of model allows researchers to observe human-specific viral responses much more accurately than with traditional lab cell lines.
Watching Cells Respond in Real Time
Using this lab grown tissue, the team tracked how thousands of individual cells responded during rhinovirus infection.
They also tested what happened when the sensors that detect the virus were blocked. These experiments revealed a strong, coordinated defense system driven by interferons.
Interferons are proteins that help block viruses from entering cells and reproducing.
When nasal cells sense rhinovirus, they release interferons that don’t just protect infected cells. They also warn nearby healthy cells, activating antiviral defenses across the tissue.
If this interferon response happens quickly, the virus struggles to spread.
When researchers blocked interferon signaling, the virus replicated rapidly, infected far more cells and caused major damage.
In some cases, the labgrown tissue didn’t survive the infection.
When the Response Turns Harmful
The study also found that when the virus manages to replicate more extensively, a different response kicks in.
This second pathway causes both infected and uninfected cells to release large amounts of mucus and inflammatory signals.
That reaction can contribute to airway swelling and breathing difficulties, especially in the lungs.
While meant to defend the body, this response may also drive many of the uncomfortable symptoms people associate with colds and asthma flare-ups — such as (with the former) having a constantly running, irritated nose and thus having to blow it repeatedly throughout the day.
The researchers suggest that these newly identified pathways could offer targets for future treatments.
Instead of only focusing on killing the virus, therapies might aim to support helpful early defenses while subduing the responses that cause inflammation, loss of smell and excess mucus.
This approach could reduce symptoms without interfering with the body’s ability to control the infection.
What the Model Can’t Yet Show
The lab grown tissue model doesn’t include every cell type found in the human body. During real infections, immune cells are recruited to the nasal passages and airways and play an important role in shaping the response.
Understanding how these additional cells and environmental factors interact with nasal tissue will be an important next step for future research.
The study reinforces a growing idea in infectious disease research: as mentioned, how the body responds to a virus often matters more than the virus itself.
According to the researchers, targeting the body’s defense mechanisms, especially early antiviral responses, could swing open the door to new ways of treating common viral infections such as the common cold.
