A group of Yale researchers study the role of body temperature in the response of the immune system to common cold virus. In addition to their prior discoveries, the researchers found two new mechanisms in which body temperature affects the immune system’s response, published in Proceedings of the National Academy of Sciences.
Previously, the Yale team discovered in mouse airway cells that the cold virus replicates more quickly when the nose’s temperature is lower than 37°C, which is the core body temperature. According with the observations of the team lead by Akiko Iwasaki, Professor of Immunobiology, this is caused because interferons (key immune system proteins) get impaired at a cooler temperature (33°C), which allows the virus to replicate and spread in the airway cells.
Now, Iwasaki and colleagues focus their studies in human airway cells, which in response to the common cold virus only produce little interferons, according with the authors. Nevertheless, the group observed that even on the absence of interferon, they found a relationship between the body temperature and the immune system capability to fight the cold virus, suggesting that the possibility of additional cold-fighting mechanisms.
The team then conducted additional studies, which include a mathematical model, revealing two new mechanisms: First, infected cell die more rapidly at the core body temperature, preventing viral replication. Second, RNAseL (n enzyme that attacks and degrades viral genes) enhances at higher temperature.
“In this study, we found that there are two additional mechanisms at play,” in addition to interferon, Iwasaki said. “All are more optimal at 37 degrees.”
The study may provide further strategies for developing therapies against common cold infections. With these findings, “there are three ways to target this virus now,” said Iwasaki.
Source: Yale News