Scientists have long struggled to understand why some people are able to shrug off a cold with just a sniffle, while others end up hospitalized with life-threatening complications. A new study published in Cell Press Blue has shed some light on this mystery.
According to the researchers at Yale Medicine, it's not the virus itself that determines how severe or mild a person's symptoms will be. Instead, it's the body's early immune response that plays a crucial role in determining the outcome of an infection like the common cold.
In order to understand this process, the researchers created miniature 3D tissue structures called organoids from human nasal cells. These tiny models acted remarkably like actual noses and lungs, even producing mucus when infected with rhinovirus - the most common cause of colds.
What they found was that the production of interferons, proteins produced by the body to fight off infections, plays a key role in determining whether a cold will be mild or severe. Interferons work like a firebreak to keep the virus from spreading and causing damage. However, when these proteins are weakly produced or inhibited, the virus becomes more aggressive and can lead to serious complications.
But why do some people produce sufficient interferons to keep their cold at bay, while others have a weaker response? The researchers still don't know for sure, but it's clear that this is an important area of further study.
As for prevention, hand washing remains the best defense against rhinovirus. People who experience symptoms such as nasal congestion, coughing, and fever should seek medical attention if they persist or worsen over time. And while there may not be a vaccine available for rhinovirus just yet, scientists are working to develop new treatments that can help people manage their symptoms more effectively.
The study's lead author, Ellen Foxman, noted that the human body is driven by an early immune response that determines the disease outcome, but the mechanisms behind this process are not well understood. Her team's work has shed some light on these mechanisms and highlights the need for further research into this complex topic.
According to the researchers at Yale Medicine, it's not the virus itself that determines how severe or mild a person's symptoms will be. Instead, it's the body's early immune response that plays a crucial role in determining the outcome of an infection like the common cold.
In order to understand this process, the researchers created miniature 3D tissue structures called organoids from human nasal cells. These tiny models acted remarkably like actual noses and lungs, even producing mucus when infected with rhinovirus - the most common cause of colds.
What they found was that the production of interferons, proteins produced by the body to fight off infections, plays a key role in determining whether a cold will be mild or severe. Interferons work like a firebreak to keep the virus from spreading and causing damage. However, when these proteins are weakly produced or inhibited, the virus becomes more aggressive and can lead to serious complications.
But why do some people produce sufficient interferons to keep their cold at bay, while others have a weaker response? The researchers still don't know for sure, but it's clear that this is an important area of further study.
As for prevention, hand washing remains the best defense against rhinovirus. People who experience symptoms such as nasal congestion, coughing, and fever should seek medical attention if they persist or worsen over time. And while there may not be a vaccine available for rhinovirus just yet, scientists are working to develop new treatments that can help people manage their symptoms more effectively.
The study's lead author, Ellen Foxman, noted that the human body is driven by an early immune response that determines the disease outcome, but the mechanisms behind this process are not well understood. Her team's work has shed some light on these mechanisms and highlights the need for further research into this complex topic.