Abstract
Although vaccines have become available, emergence and rapid transmission of new variants have added new paradigm in the coronavirus disease-2019 (COVID-19) pandemic. Weather, population and host immunity have been detected as the regulatory elements of COVID-19. This study aims to investigate the effects of weather, population and host factors on the outcome of COVID-19 and mutation frequency in Japan. Data were collected during January 2020 to February 2021. About 92% isolates were form GR clades. Variants 501Y.V1 (53%) and 452R.V1 (24%) were most prevalent in Japan. The strongest correlation was detected between fatalities and population density (rs = 0.81) followed by total population (rs = 0.72). Relative humidity had the highest correlation (rs = -0.71) with the case fatality rate. Cluster mutations namely N501Y (45%), E484K (30%), N439K (16%), K417N (6%) and T478I (3%) at spike protein have increased during January to February 2021. Above 90% fatality was detected in patients aged >60 years. The ratio of male to female patients of COVID-19 was 1.35:1. This study will help to understand the seasonality of COVID-19 and impact of weather on the outcome which will add knowledge to reduce the health burden of COVID-19 by the international organisations and policy makers.
Highlights
The ongoing pandemic namely, coronavirus disease-2019 (COVID-19) has been triggered by the infection of a novel species of coronavirus called severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) of genera Betacoronavirus, family Coronaviridae [1,2,3]
The principal objective of this study is to investigate the impact of regulatory factors specially, weather on mutation frequency in SARS-CoV-2 in Japan
Temperature, UV ray intensity, relative humidity (RH), rainfall, snowfall, wind speed, atmospheric pressure and sun hours were analysed for their role in COVID-19
Summary
The ongoing pandemic namely, coronavirus disease-2019 (COVID-19) has been triggered by the infection of a novel species of coronavirus (named 2019-novel coronavirus, 2019-nCoV) called severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) of genera Betacoronavirus, family Coronaviridae [1,2,3]. Human coronavirus 229E and OC43 were the first members of Coronaviridae detected in patients with the symptoms of respiratory system infection and common cold during early 1960s [4]. Other members of the same genus Coronavirus namely, SARS-CoV, HCoV NL63, HKU1 and MERS-CoV had caused local outbreaks with human respiratory system infections in 2003, 2004, 2005 and 2012, respectively [1,2,3,4,5]. First two ORFs from 5′ end namely ORF-1ab comprise of ∼20 000 bases and encode for non-structural proteins (nsps) (replicase proteins). Major structural proteins of SARS-CoV-2 are encoded by the later ORFs of 3′ end (∼10 000 bases) [1, 2, 7,8,9,10,11]
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