Abstract
Currently available data are consistent with increased severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) replication at temperatures encountered in the upper airways (25–33°C when breathing room temperature air, 25°C) compared to those in the lower airways (37°C). One factor that may contribute to more rapid viral growth in the upper airways is the exponential increase in SARS‐CoV‐2 stability that occurs with reductions in temperature, as measured in vitro. Because SARS‐CoV‐2 frequently initiates infection in the upper airways before spreading through the body, increased upper airway viral growth early in the disease course may result in more rapid progression of disease and potentially contribute to more severe outcomes. Similarly, higher SARS‐CoV‐2 viral titer in the upper airways likely supports more efficient transmission. Conversely, the possible significance of air temperature to upper airway viral growth suggests that prolonged delivery of heated air might represent a preventative measure and prophylactic treatment for coronavirus disease 2019.
Highlights
Data on viral load are consistent with this hypothesis: SARS-CoV-2 upper respiratory tract viral load is strongly correlated with adverse outcomes and has been hypothesized to be a predictor of disease severity.[27]
The temperature-dependent decay rate suggests that cool air temperatures might enable increased rates of SARS-CoV-2 growth in the upper airways.[15,16,17]
The concept is supported by currently available data: In epithelial cell cultures, SARS-CoV-2 replicates more efficiently at temperatures encountered in the lower airways than those in the upper airways (33 and 37°C, respectively).[21,22,23]
Summary
The stability of viruses is affected by changes in temperature, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), is no exception.[1,2,3,4,5,6,7,8,9,10] Heat denatures the proteins that comprise each SARS-CoV-2 virion, inactivating it.[3,8] Laboratory data indicate that, as temperatures increase, the rate at which virions are inactivated increases exponentially.[3,9] These in vitro data suggest that lower temperatures within the body might result in lower rates of thermal inactivation and higher rates of viral growth, potentially affecting viral shedding, viral load densities, transmission rates, and patient outcomes. Complicating factors preclude the trivial extension of SARS-CoV-2 in vitro decay rates to the in vivo environment, currently available data support increased viral replication at the cooler temperatures of the upper airways relative to the warmer temperatures of the upper airways.[21,22,23]. While presently available data do not permit quantification of the impact of air temperature on COVID-19 transmission and disease progression, this article suggests that the potential for such an effect warrants further study
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