Rapid interferon activity in nasal cells limits rhinovirus spread, explaining why some people escape cold symptoms while others develop inflammation and mucus buildup.
The intensity of common cold symptoms depends on how quickly nasal cells trigger an interferon response that limits the spread of rhinovirus (1✔ ✔Trusted Source
Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling
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Why does a cold virus leave some people exhausted while others hardly notice it?
A detailed investigation suggests the explanation lies in events unfolding inside the nose. How cells lining the nasal passages react when exposed to rhinovirus, the leading cause of the common cold, appears to determine whether symptoms develop and how severe they become.
The findings were published on Jan. 19 in the journal Cell Press Blue.
“This work provides a clearer and more detailed view of what happens during common cold infections than we have ever had before,” said senior author Dr. Ellen Foxman, an immunologist at Yale School of Medicine in New Haven, Connecticut.
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Did You Know?
Your nose can decide how bad a cold feels, because quick interferon action stops infection in most cells, while a slow response lets the virus spread and trigger classic cold symptoms.
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Nasal Cell Responses Shape Cold Severity
Although rhinovirus circulates more frequently during winter, not everyone who encounters it becomes ill. According to Foxman, only about half of infections actually result in noticeable symptoms.
To explore the reasons behind this difference, scientists cultivated human nasal tissue in laboratory conditions and then exposed it to rhinovirus. This approach allowed close examination of cellular and molecular changes occurring in the lining of the nose and lungs.
Fast Interferon Defense Versus Viral Spread
Two distinct response patterns emerged. In the first, the immune reaction occurred rapidly. Less than 1% of cells became infected because interferons, proteins released by the immune system, blocked viral entry and prevented further spread.
When this rapid response took place, the virus was contained before illness could develop.
In contrast, when interferon activity was delayed or impaired, the virus spread far more easily. In these cases, 30% or more of cells became infected, leading to inflammation and increased mucus production, the hallmark signs of a cold. That is when people actually begin to feel unwell.
Factors Influencing Immune Readiness
“What pushes the body toward one response or the other is still not fully clear,” Foxman noted.
Even so, the work highlighted several factors associated with stronger or weaker outcomes. Individuals who had recently experienced another viral infection may already have an active interferon response, allowing them to fend off a new virus more efficiently.
Temperature and Environmental Triggers
Temperature also appears to influence the process. Cooler air in the nose and lungs may slow interferon production, giving viruses more time to multiply. This effect could help explain why colds tend to occur more often during winter months.
Environmental exposures mattered as well. “Breathing in pollution or cigarette smoke significantly alters the immune response to the next exposure, such as a common cold virus, and often results in a more harmful inflammatory reaction,” Foxman explained.
While the findings do not point to a simple way to prevent colds, they shed light on why the same virus can affect people so differently.
In conclusion, the varied experience of a common cold can be traced to how swiftly nasal cells activate interferon defenses, influencing whether rhinovirus is stopped early or allowed to trigger inflammation and symptoms.
Reference:
- Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling (https:www.cell.com/cell-press-blue/fulltext/S3051-3839(25)00001-5 )
Source-Medindia