ARTICLE | doi:10.20944/preprints202006.0373.v1
Subject: Life Sciences, Virology Keywords: COVID-19; SARS-CoV-2; ambient temperature; risk level; mortality
Online: 30 June 2020 (13:10:27 CEST)
COVID-19 is a pandemic with no cure. There is an urgent need for low-cost interventions. Macroclimate work through microclimate. In many situations, man-made microclimate, such as air conditioning, may override the effect of natural macroclimate in determining the pathogenicity of SARS-CoV-2. This study aimed to determine if there is a ‘safe’ temperature that is comfortable to human beings while significantly inhibitory for SARS-CoV-2 pathogenicity. Data on monthly new deaths or new cases per million population (MDPM or MCPM) and monthly cumulated days with more cases than the previous day (DI) from March 2 to June 15, 2020 were collected from all 118 countries with population over five million. Monthly average AT negatively correlated with the transmission parameters. A significant decrease in transmission was observed when AT reached above 20 ºC. Monthly average (not average high) AT of countries with MDPM <2, MCPM<10, or DI<=7 was found to be between 24.54 and 25.90 ºC (25.00 ºC on average) with average standard error of 4.97. Thus, average AT <20, 20-25, >25 ºC were considered as high, medium, and low risk AT. Furthermore, MDPM in countries with AT <20 ºC were 80.93, 50.23, 13.52, and 7.72 times of those in countries with AT >25 ºC in March, April, May, and June 1-15, respectively. MDPM high-risk rates in countries with AT >25 ºC were 0, 6.25, 14.55, and 9.84%, and the low-risk rates were 100, 83.33, 52.73, and 81.97%, respectively. In countries with AT <20 ºC, the trends were opposite. Setting indoor temperature to 25 ºC could decrease the need of social distancing for containing SARS-CoV-2 transmission. Cooling indoor temperature too low may be a reason of COVID-19 outbreak in some high AT countries. Authorities and the general population can evaluate COVID-19 risk level and manipulate microclimate to reduce the risk anywhere anytime based on local day average AT.
ARTICLE | doi:10.20944/preprints202006.0369.v1
Subject: Life Sciences, Biophysics Keywords: temperature extreme; warm climate; low-and middle-income economies; COVID-19; mortality; mixed effect modelling
Online: 30 June 2020 (11:38:15 CEST)
We performed a global analysis with data from 149 countries to test whether temperature can explain the spatial variability of the spread rate and mortality of COVID-19 at the global scale. We performed partial correlation analysis and linear mixed effect modelling to evaluate the association of the spread rate and motility of COVID-19 with maximum, minimum, average temperatures and temperature extreme (difference between maximum and minimum temperature) and other environmental and socioeconomic parameters. After controlling the effect of the duration after the first positive case, partial correlation analysis revealed that temperature was not related with the spatial variability of the spread rate of COVID-19. Mortality was negatively related with temperature in the countries with high-income economies. In contrast, temperature extreme was significantly and positively correlated with mortality in the low-and middle-income countries. Taking the country heterogeneity into account, mixed effect modelling revealed that inclusion of temperature as a fixed effect in the model significantly improved model skill predicting mortality in the low-and middle-income countries. Our analysis suggest that warm climate may reduce the mortality rate in high-income economies but in low and middle-income countries temperature extreme may increase the mortality risk.
Mon, 29 June 2020
ARTICLE | doi:10.20944/preprints202006.0352.v1
Online: 29 June 2020 (10:40:07 CEST)
Mitochondria are classically termed as powerhouse of a mammalian cell. Most of the cellular chemical energy in the form of adenosine tri phosphate (ATP) is generated by mitochondria and dysregulation of mitochondrial functions thus can be potentially fatal of cellular homeostasis and health. Acute respiratory distress has been earlier linked to mitochondrial dysfunction. SARS-CoV-2 infection severity leads to acute respiratory distress syndrome (ARDS) and can be fatal. We tried to investigate possible connection between SARS-CoV-2, ARDS and mitochondria. Here, we report identification of SARS-CoV-2 non-structural proteins (particularly Nsp12 and 13) that have recognition sequence with respect to mitochondrial entry. We also report that these proteins can potentially shuttle between cytoplasm and mitochondria based on the localization signals and help in downstream maintenance of the virus. Their properties to use ATP for enzymatic activities may cause ATP scavenging allowing viral RNA functions in lieu of host cell health.