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Recent Study: Temperature-dependent defense against the common cold virus

In a recent study1, we found that temperature can alter the ability of the airway cells to mount an effective innate immune response against rhinovirus, the common cold virus.

Airway epithelial cells, the cells that form the lining of the nose and the other airways, are the main target of rhinovirus infection. In order to amplify, spread, and cause disease, the virus must enter these cells and make more copies of itself. By studying airway cells incubated at different temperatures, we discovered that mechanisms used by the innate immune system to protect cells against this virus are quite effective at core body temperature (37°C), but are greatly diminished at slightly cooler temperatures, such as temperatures that might be found in the nasal passages upon inhaling cool ambient air (33°C).

The temperature-dependent signals included those involved in the recognition of the replicating virus inside the cell (the RIG-I like receptor pathway) as well as the signals required for turning on antiviral defenses following viral recognition (the Type I interferon response.) These signals are important in immune defense against many viruses, and future studies may reveal that lower temperature provides an opportunity for other viruses that infect the airways or other cool areas of the body to evade antiviral defenses.

1 Foxman et al. (2015) Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells. PNAS .In press.

Catching a Cold

Does the temperature really matter?

Rhinovirus infection of airway epithelial cells results in accumulation of double stranded RNA (dsRNA; blue) during viral genome replication. This dsRNA triggers RNA sensors, RIG-I-like receptors (RLRs), to induce type I interferons (IFNs) through the adaptor MAVS located on mitochondria (red). At the core body temperature of 37°C, three factors contribute to block in rhinovirus replication, rapid dsRNA accumulation, enhanced RLR signaling, and enhanced IFN receptor signaling. The photograph depicts dsRNA (stained with antibody specific to dsRNA; blue) surrounded by mitochondria (stained with Mitotracker red; red), 7 hours after infection of human bronchial epithelial cells with rhinovirus 1B.

Photograph courtesy of Ulysses Isidro.