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He common cold It continues to be one of the most frequent infectious processes and, however, there are still aspects of its development that are surprising. For years it has been assumed that the virus is mainly responsible for whether a person gets sick or not. But new research suggests that the key may be in how the body itself reacts in the presence of rhinovirus.
The first defense wall is not in the gorge
The cells in the nose collaborate to defend us from the common cold, according to a study by researchers from the Yale University (United States), in which they suggest that our body’s defense against rhinovirus – not the virus itself – usually predicts whether we get a cold or not, as well as the severity of our symptoms.
In an article published in the magazine ‘Cell Press Blue‘, from Cell Press, researchers demonstrate how when a rhinovirus, the most common cause of the common cold, infects the lining of the nasal passages, our cells collaborate to fight it by activating an arsenal of antiviral defenses.
“As the main cause of common colds and one of the main causes of respiratory problems in people with asthma and other chronic lung diseases, rhinoviruses are very important for human health,” details the lead author, Ellen Foxmanfrom Yale School of Medicine.
“This research allowed us to look at the human nasal lining and see what happens during rhinovirus infections, both at the cellular and molecular level,” he adds.

When cells coordinate, the virus doesn’t stand a chance
To do this, the researchers created human nasal tissue grown in laboratory. They cultured human nasal stem cells for four weeks, while exposing the upper surface to air. Under these conditions, the stem cells differentiated into a tissue with many of the cell types present in the nasal passages and lining of the lung airways, including mucus-producing cells and cells with cilia (motile, hair-like structures that sweep mucus from the lungs).
“This model reflects the responses of the human body much more accurately than conventional cell lines used in virological research,” Foxman reports. “Since rhinovirus causes disease in humans, but not in other animals, organotypic models of human tissues are particularly valuable for the study of this virus.”
The model allowed the team to examine the coordinated responses of thousands of individual cells at a time and see how these responses changed when the cellular sensors that detect the rhinovirus were blocked. In this way, the researchers observed a defensive mechanism that keeps rhinovirus infections at baycoordinated by interferons, proteins that block the entry and replication of viruses.
Upon detecting rhinovirus, cells in the nasal lining produce interferons, which induce a coordinated antiviral defense of infected and neighboring cells, making the environment inhospitable to viral replication. If interferons act quickly enough, the virus cannot spread. When the researchers experimentally prevented this response, the virus quickly infected many more cells, causing damage and, in some cases, death of the infected organoids.
“Our experiments show how crucial and effective a rapid interferon response is in controlling rhinovirus infection, even without any immune system cells present,” adds the first author. Bao Wang of the Yale School of Medicine.
The key is not the virus… but how your body responds
The research also revealed other responses to rhinovirus that are activated when increases viral replication. For example, rhinovirus can activate a different sensing system that causes infected and uninfected cells to synergistically produce excess mucus, increase inflammation, and sometimes cause breathing problems in the lungs. These responses could be good targets to intervene in rhinovirus infection and promote a healthy antiviral response, the researchers say.
The team recognizes that the organoids used contain limited cell types compared to those in the body, as an infection in the body attracts other cells, including those of the immune system, to join the defense against rhinovirus infection. They say that understanding how other cell types and environmental factors in the nasal passages and airways calibrate the body’s response to rhinovirus infection is an important step in this work.
“Our study reinforces the paradigm that the organism’s responses to a virus, rather than the inherent properties of the virus itself, are crucial in determining whether or not a virus will cause disease and its severity,” concludes Foxman. “Tackling defense mechanisms is a promising avenue for new therapies.”
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