The common cold has forever been a diminutive b2ut 1unrelenting nemesis of mankind. Countless generations of grandmothers, worldwide, have endeavoured to counter the common cold with home remedies ranging from chicken broth to steam inhalations, to no avail. You might even dismiss the idea of keeping warm and covering yourself during a cold as unscientific hokum. However, a recent Yale study redeems this age-old bit of housewife wisdom and sheds new light on how body temperature affects common cold outcomes.
The pathbreaking new study, published in the Proceedings of the National Academy of Sciences, studied the effect of temperature on live, infected human airway cells.
The study, led by Dr.Akiko Iwasaki of Yale University, follows an earlier 2015 study (conducted on mice airway cells), by the same team, which examined the effect of temperature on the replication of rhinoviruses and the subsequent host immune response. The researchers were then able to establish that cooler temperatures in the nose, of 33°C [91.4°F],compared to the core body temperature of 37°C [98.6 °F], allowed the viruses to multiply more rampantly and spread faster, due to weakened production of immune proteins, called interferons.
The new study went a step further and established that when incubated at 37°C [98.6 °F], human airway cells could control the spread of the virus, even in the absence of interferons (airway cells produce little to no interferons).
"We found that the innate immune response to the rhinovirus is impaired at the lower body temperature compared to the core body temperature," Iwasaki said.
While examining two sets of infected human airway cells, incubated at 33°C [91.4°F] and 37°C [98.6 °F] respectively, the researchers were made aware of the exciting possibility of unearthing previously unknown infection-fighting mechanisms at play.
After it was confirmed that the second batch of cells, incubated at core body temperature were resisting the spread of the virus significantly better than the first batch, further investigation was carried out using mathematical modeling. These investigations revealed two additional virus-fighting mechanisms that were previously unknown.
Firstly, it was found that at core body temperature, infected cells die off much faster, hence curtailing the replication of the virus. Additionally, an enzyme called RNAseL, which targets and degrades viral DNA has been shown to function most optimally at core body temperature, i.e 37°C [98.6 °F].
"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."
This study is revolutionary for a number of reasons. Although we have long suspected a link between temperature and viral mechanisms, this study opens up the link between temperature and host response mechanisms. Additionally, the two newly discovered host mechanisms mentioned before, show us that warmer temperatures affect not only interferon production but hitherto unknown processes, that are crucial in resisting and fighting infection.
These newly discovered mechanisms, which now add up to three unique virus-fighting mechanisms, all operate best at 37°C [98.6 °F]. They open us up to possibilities of newer and more advanced strategies to combat the dreaded common cold and its more sinister cousins such as asthma, which hamper an enormous number of lives worldwide and cost healthcare setups hundreds of millions of dollars to manage.
