Every winter, rhinoviruses circulate widely, yet not everyone exposed comes down with a cold. New research suggests that the deciding factor may not be the virus itself, but how quickly and effectively the cells lining our noses respond to it.
New research, published in Cell Press Blue, shows that the body’s own antiviral defenses, activated within the nasal lining, largely predict whether a rhinovirus infection fizzles out or turns into a full-blown cold. The findings help explain why cold symptoms vary so widely and point toward new strategies for preventing illness by strengthening the body’s early defenses.
“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, in a press release. “This research allowed us to peer into the human nasal lining and see what is happening during rhinovirus infections at both the cellular and molecular levels.”
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Building a Human Nasal Model to Study the Common Cold
Image of the human nasal epithelial cell releasing rhinovirus, which is in blue.
(Image Credit: Lysenko Andrii/CC BY-SA)
Because rhinoviruses infect humans but not most other animals, they have been notoriously difficult to study in living systems. To overcome this challenge, the research team created lab-grown human nasal tissue that closely mimics the structure and function of real airway linings.
The team cultured human nasal stem cells for four weeks while exposing the upper surface to air. Under these conditions, the cells differentiated into a complex tissue containing many of the cell types found in the nose and lungs, including mucus-producing cells and ciliated cells, whose tiny hair-like structures normally help sweep pathogens out of the airways.
“This model reflects the responses of the human body much more accurately than the conventional cell lines used for virology research,” Foxman said. “Since rhinovirus causes illness in humans but not other animals, organotypic models of human tissues are particularly valuable for studying this virus.”
Interferons: The Fast-Acting Antiviral Alarm
Image of a differentiated human nasal epithelial organoid with multiciliated cells in blue.
(Image Credit: Julien Amat & Bao Wang/CC BY-SA)
When rhinovirus enters nasal cells, it triggers the production of interferons, signaling proteins that act as an antiviral alarm system. These interferons don’t just protect infected cells; they also alert neighboring cells, creating a hostile environment that blocks viral entry and replication.
When interferon responses were rapid, the virus failed to spread and caused little damage. But when researchers experimentally blocked the cells’ ability to sense the virus and produce interferons, rhinovirus quickly infected large numbers of cells, damaging and sometimes killing the nasal organoids.
“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 in a press release.
In other words, the nasal lining itself acts as a powerful frontline defense, capable of containing infection before the immune system even arrives.
When Defense Becomes the Problem
The research also revealed what happens when rhinovirus replication gains the upper hand. At higher viral levels, a different sensing system becomes active, triggering excessive mucus production and inflammation, responses that contribute to congestion, coughing, and breathing difficulties.
These later responses, while part of the body’s attempt to fight infection, may actually drive many of the symptoms people associate with colds and asthma flare-ups. The researchers suggest that future treatments could focus not only on stopping the virus but also on fine-tuning these defensive pathways to prevent them from becoming harmful.
Although the organoids lack immune cells found in real airways, the results support a key idea in virology: illness severity is shaped more by the body’s response than by the virus itself.
“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. “Targeting defense mechanisms is an exciting avenue for novel therapeutics.”
This article is not offering medical advice and should be used for informational purposes only.
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Article Sources
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- This article references information from a recent study published in Cell Press Blue: Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling
