New research shows how body temperature can affect the immune system’s response to the common cold virus.
In an earlier study, researchers found that the cold virus replicated more readily when the temperature in the nose dipped below core body temperature (98.6 degrees Fahrenheit). They determined that at a slightly cooler temperature (91.4 degrees Farhenheit), key immune system proteins—interferons—were impaired, allowing the cold virus to reproduce and spread in mouse airway cells.
For the current study, published in the Proceedings of the National Academy of Sciences, researchers focused on human airway cells, which make little interferons in response to the cold virus. While examining infected cells incubated at 98.6 or 91.4 degrees F (37 or 33 degrees C), researchers observed that even in the absence of interferon, cells still controlled the virus, raising the possibility of additional cold-fighting mechanisms.
Further investigation, including mathematical modeling, revealed two additional mechanisms: At core body temperature, infected cells die more rapidly, preventing viral replication. Second, an enzyme that attacks and degrades viral genes, RNAseL, is enhanced at the higher temperature. Each pathway independently contributes to the immune system’s defense against the cold virus.
“In this study, we found that there are two additional mechanisms at play,” in addition to interferon, says Akiko Iwasaki, professor of immunobiology at Yale University. “All are more optimal at 37 degrees.”
The findings underscore the impact of temperature on the immune system’s defenses. They also offer further approaches for therapeutically tackling the cold virus, which is a key trigger of asthma, Iwasaki says. “There are three ways to target this virus now.”
The Howard Hughes Medical Institute, the National Institutes of Health, and the American Asthma Foundation.
Source: Yale University