From John Ray's shorter notes
April 03, 2020
Does warm weather inhibit the Coronavirus?
A study suggests the coronavirus outbreak could be stifled by warm English weather in May. Researchers from University College London found infections from three common coronaviruses followed a seasonal pattern in England, with large numbers in winter at the same time as influenza.
The academic study below is a one of a number that suggest that coronaviruses may be destroyed by heat. And if the mild heat of an English summer destroys them, how much greater must be the effects of a warmer climate?
Heat is in fact the only good explanation of the extraordinarily low coronavirus death toll in Australia. Australia is an advanced Western society very similar to Britain and the USA but differs in that it is located in the Southern hemisphere. For that reason, Australia is only now coming out of a very hot summer. And in any case Australia has a hot climate, with around a third of it being in the tropics
So for just about the whole period of the coronavirus outbreak, Australia has been distinctly hot. And there is no obvious other way in which Australia differs from other advanced countries
It may be noted that Singapore is also an advanced economy in the tropics -- and so far, its infection and death rates have been lower than most other countries, despite schools and universities remaining open.
Seasonality and immunity to laboratory-confirmed seasonal coronaviruses (HCoV-NL63, HCoV-OC43, and HCoV-229E): results from the Flu Watch cohort study
Robert W. Aldridge et al
Background: There is currently a pandemic caused by the novel coronavirus SARS-CoV-2. The intensity and duration of this first wave in the UK may be dependent on whether SARS-CoV-2 transmits more effectively in the winter than the summer and the UK Government response is partially built upon the assumption that those infected will develop immunity to reinfection in the short term. In this paper we examine evidence for seasonality and immunity to laboratory-confirmed seasonal coronavirus (HCoV) from a prospective cohort study in England.
Methods: In this analysis of the Flu Watch cohort, we examine seasonal trends for PCR-confirmed coronavirus infections (HCoV-NL63, HCoV-OC43, and HCoV-229E) in all participants during winter seasons (2006-2007, 2007-2008, 2008-2009) and during the first wave of the 2009 H1N1 influenza pandemic (May-Sep 2009). We also included data from the pandemic and ‘post-pandemic’ winter seasons (2009-2010 and 2010-2011) to identify individuals with two confirmed HCoV infections and examine evidence for immunity against homologous reinfection.
Results: We tested 1,104 swabs taken during respiratory illness and detected HCoV in 199 during the first four seasons. The rate of confirmed HCoV infection across all seasons was 390 (95% CI 338-448) per 100,000 person-weeks; highest in the Nov-Mar 2008/9 season at 674 (95%CI 537-835). The highest rate was in February at 759 (95% CI 580-975). Data collected during May-Sep 2009 showed there was small amounts of ongoing transmission, with four cases detected during this period. Eight participants had two confirmed infections, of which none had the same strain twice.
Conclusion: Our results provide evidence that HCoV infection in England is most intense in winter, but that there is a small amount of ongoing transmission during summer periods. We found some evidence of immunity against homologous reinfection.
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