Scientists Have Cracked Part of the Cold Mystery, But There's Still Much to Be Learned.
The common cold has long been a mystery to scientists, with some people suffering from mild sniffles and others falling ill with severe complications. A new study published in Cell Press Blue has shed some light on why this is the case, revealing that it's not just the virus itself that determines the severity of the illness, but rather an early immune response within the body.
According to the researchers at Yale Medicine, who grew miniature tissue structures called organoids from human nasal cells and introduced rhinovirus into these models, a protein called interferon plays a crucial role in determining the outcome. Interferons are proteins produced by the body to fight off infections, and when they're produced in adequate amounts, they can keep the virus mild. However, if these proteins are weak or inhibited, the virus becomes more severe, leading to complications such as asthma attacks, bronchitis, and pneumonia.
But why do some people produce sufficient interferons to block rhinovirus while others don't? Researchers say it's still unclear, but they're working to understand this phenomenon. In their study, they found that when the interferon response was inhibited with a drug, the virus became more severe in the lab models, similar to what happens in people with chronic airway diseases who have lower levels of interferons.
The good news is that prevention remains key. The best defense against rhinovirus is hand washing, and people should seek medical attention if they experience shortness of breath, wheezing, or a high fever for more than three days. Currently, there's no vaccine available to prevent the common cold, but research into this area continues.
While scientists have made progress in understanding the immune response behind the common cold, much work remains to be done. By studying the mechanisms that drive disease outcomes and identifying potential treatments, researchers hope to develop new strategies for preventing and treating this widespread illness.
The common cold has long been a mystery to scientists, with some people suffering from mild sniffles and others falling ill with severe complications. A new study published in Cell Press Blue has shed some light on why this is the case, revealing that it's not just the virus itself that determines the severity of the illness, but rather an early immune response within the body.
According to the researchers at Yale Medicine, who grew miniature tissue structures called organoids from human nasal cells and introduced rhinovirus into these models, a protein called interferon plays a crucial role in determining the outcome. Interferons are proteins produced by the body to fight off infections, and when they're produced in adequate amounts, they can keep the virus mild. However, if these proteins are weak or inhibited, the virus becomes more severe, leading to complications such as asthma attacks, bronchitis, and pneumonia.
But why do some people produce sufficient interferons to block rhinovirus while others don't? Researchers say it's still unclear, but they're working to understand this phenomenon. In their study, they found that when the interferon response was inhibited with a drug, the virus became more severe in the lab models, similar to what happens in people with chronic airway diseases who have lower levels of interferons.
The good news is that prevention remains key. The best defense against rhinovirus is hand washing, and people should seek medical attention if they experience shortness of breath, wheezing, or a high fever for more than three days. Currently, there's no vaccine available to prevent the common cold, but research into this area continues.
While scientists have made progress in understanding the immune response behind the common cold, much work remains to be done. By studying the mechanisms that drive disease outcomes and identifying potential treatments, researchers hope to develop new strategies for preventing and treating this widespread illness.