A pretty cool (pun intended) story’s cropped up about the influence of cold temperatures on the body’s response to Rhinovirus infection – one of the viruses that leads to the common cold.
In brief, the interferon response pathway (which counteracts virus infection inside cells) doesn’t work as well at temperatures colder than 37°C. When the research team at Yale University School of Medicine compared interferon production in mouse cells at 33°C and 37°C, they found far more at the hotter temperature. Conversely, when they looked at Rhinovirus growth, surprise surprise, the virus grew better in the low temperature / low interferon environment.
This is neat, because it suggests that cold temperature may actually increase your susceptibility to getting a cold, just like your family always told you. I say may, because this study was conducted in mouse cells using a mouse-adapted strain of Rhinovirus, but this is intriguing evidence that your nose may be a frosty gateway to virus misery.
This is also interesting given a wonderful talk I listened to by Cardiff University’s Prof. Ron Eccles at the Society of General Microbiology conference in Liverpool last year, in which he discussed the symptoms behind the common cold. Most notable to me was his mention of how the insides of our nostrils reciprocally expand and relax, due to the dilation of large veins in our nose. This expansion becomes exaggerated during infection due to inflammation, which results in a horrible blocked nose (here’s a cool paper – not Open Access, sorry).
Not only was this interesting enough, but he hypothesised that this could be a defence against virus infection. How? The blocked nostril steadily increases in temperature and the poor sucker of a virus has a hard time growing as it finds itself out of its comfort-zone. If this is true, perhaps it also gives the innate immune response the jump-start it needs to get to work.