Past research has clearly demonstrated that most of the rhinoviruses – agents responsible for the “common cold” symptoms – prefer cooler temperatures over warmer ones. This explains why they replicate more successfully in the nose and the upper respiratory tract (with a normal temperature of 33-35 °C) than in the lungs (37 °C). Despite this observation, studies dealing with the effects of cold weather patterns on the likelihood of contracting the infection produced mixed results.
A study from 1968 published in the New England Journal of Medicine “demonstrated no effect of exposure to cold on host resistance to rhinovirus infection and illness that could account for the commonly held belief that exposure to cold influences or causes common colds.”
In 2005, however, a study in the journal Family Practice found that subjects who immersed their feet in ice water were more likely to self-report catching the cold in the days after the procedure.
There are at least three different hypotheses as to why the common cold is most prevalent during wintertime. One hypothesis holds that indoor crowding, rather than the cold weather itself, makes it easier for the virus to spread. Another maintains that its transmission is enhanced by cold, dry air. And the third hypothesis, raised by Ron Eccles from the Common Cold Centre in Cardiff, UK, proposes that the constriction of nose and upper airway blood vessels inhibits the immune system, thus making way for the infection to take hold.
In an attempt to solve the mystery once and for all, a group of researchers lead by a Yale immunobiologist Ellen Foxman, studied mouse airway epithelial cells which they incubated with a mouse-adapted rhinovirus (RV-1BM).
What they found was that at warmer temperatures the genes that produce the virus-fighting protein interferon were significantly more active, leading to an effective immune response, which successfully fought off the cold. At cooler temperatures, however, the animals produced lower amounts of the protein and were therefore unable to resist infection.
Then the team grew some human airway cells under cold and warm conditions and infected them with a human-specific strain of the virus. It soon transpired that the warm-grown cells were much more likely to undergo programmed cell death, mediated by the immune system to limit the spread of infection.
“That proves it’s not just virus intrinsic, but it’s the host’s response that’s the major contributor. In general, the lower the temperature, it seems the lower the innate immune response to viruses”, said study co-author Akiko Iwasaki.
The team hopes that their findings, published in the Proceedings of the National Academy of Sciences, will also help to explain how temperature fluctuations affect other conditions, such as childhood asthma.