Abstract
Preliminary evidence suggests that climate may modulate the transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Yet it remains unclear whether seasonal and geographic variations in climate can substantially alter the pandemic trajectory, given that high susceptibility is a core driver. Here, we use a climate-dependent epidemic model to simulate the SARS-CoV-2 pandemic by probing different scenarios based on known coronavirus biology. We find that although variations in weather may be important for endemic infections, during the pandemic stage of an emerging pathogen, the climate drives only modest changes to pandemic size. A preliminary analysis of nonpharmaceutical control measures indicates that they may moderate the pandemic-climate interaction through susceptible depletion. Our findings suggest that without effective control measures, strong outbreaks are likely in more humid climates and summer weather will not substantially limit pandemic growth.
Highlights
Climate affects the transmission of several directly-transmitted pathogens [8]
Respiratory syncytial virus (RSV), a childhood pathogen, has been found to be dependent on specific humidity [13] and exhibits latitudinal correlations with climate [14]. For both influenza and RSV, low specific humidity increases transmission and epidemics tend to peak in the wintertime in northern latitudes
We do not yet know the climate sensitivity of SARS-CoV-2 transmission directly, data exists on four other coronaviruses that currently circulate in human populations
Summary
Climate affects the transmission of several directly-transmitted pathogens [8]. Specific humidity (the mass of water vapor in a unit mass of moist air) has been shown to be important for influenza transmission in both laboratory settings [9,10,11], and in population-level studies [12]. The relative importance of climate drivers when compared to high population susceptibility during the pandemic stage of an emerging infection such as SARS-CoV-2, has not been fully characterized. In the second and third scenarios, we assume SARS-CoV2 has the same climate dependence and length of immunity as HCoV-OC43 and HCoV-HKU1 respectively.
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