Temporal dynamic in the impact of COVID- 19 outbreak on cause-specific mortality in Guangzhou, China.

BACKGROUND: Studies related to the SARS-CoV-2 spikes in the past few months, while there are limited studies on the entire outbreak-suppressed cycle of COVID-19. We estimate the cause-specific excess mortality during the complete circle of COVID-19 outbreak in Guangzhou, China, stratified by sociodemographic status. METHODS: Guangzhou Center for Disease Control Prevention provided the individual data of deaths in Guangzhou from 1 January 2018 through 30 June 2020. We applied Poisson regression models to daily cause-specific mortality between 1 January 2018 and 20 January 2020, accounting for effects of population size, calendar time, holiday, ambient temperature and PM2.5. Expected mortality was estimated for the period from 21 January through 30 June 2020 assuming that the effects of factors aforementioned remained the same as described in the models. Excess mortality was defined as the difference between the observed mortality and the expected mortality. Subgroup analyses were performed by place of death, age group, sex, marital status and occupation class. RESULTS: From 21 January (the date on which the first COVID-19 case occurred in Guangzhou) through 30 June 2020, there were three stages of COVID-19: first wave, second wave, and recovery stage, starting on 21 January, 11 March, and 17 May 2020, respectively. Mortality deficits were seen from late February through early April and in most of the time in the recovery stage. Excesses in hypertension deaths occurred immediately after the starting weeks of the two waves. Overall, we estimated a deficit of 1051 (95% eCI: 580, 1558) in all-cause deaths. Particularly, comparing with the expected mortality in the absence of COVID-19 outbreak, the observed deaths from pneumonia and influenza substantially decreased by 49.2%, while deaths due to hypertension and myocardial infarction increased by 14.5 and 8.6%, respectively. In-hospital all-cause deaths dropped by 10.2%. There were discrepancies by age, marital status and occupation class in the excess mortality during the COVID-19 outbreak. CONCLUSIONS: The excess deaths during the COVID-19 outbreak varied by cause of death and changed temporally. Overall, there was a deficit in deaths during the study period. Our findings can inform preparedness measures in different stages of the outbreak.

Genomic surveillance of a resurgence of COVID-19 in Guangzhou, China (preprint)

In the middle of March, the World Health Organization declared the outbreak of COVID-19 caused by SARS-CoV-2 infection a global pandemic. While China experienced a dramatic decline in daily growth rate of COVID-19, multiple importations of new cases from other countries and their related local infections caused a rapid rise. Between March 12 and April 15, we collected nasopharyngeal samples from 109 imported cases from 25 countries and 69 local cases in Guangzhou, China. In order to characterize the transmission patterns and genetic evolution of this virus among different populations, we sequenced the genome of SARS-CoV-2. The imported viral strains were assigned to lineages distributed in Europe (33.0%), America (17.4%), Africa (25.7%), or Southeast/West Asia (23.9%). Importantly, 10 imported cases from Africa formed two novel sub-lineages not identified in global tree previously. A detailed analysis showed that the imported viral strains from Philippines and Pakistan were closely related and within the same sub-lineage, whereas Ethiopia had varied lineages in the African phylogenetic tree. In spite of the diversity of imported SARS-CoV-2, 60 of 69 local infections could be traced back to two specific small lineages imported from Africa. A combined genetic and epidemiological analysis revealed a high-resolution transmission network of the imported SARS-CoV-2 in local communities, which might help inform the public health response and genomic surveillance in other cities and regions. Finally, we observed in-frame deletions on seven loci of SARS-CoV-2 genome, some of which were intra-host mutations, and they exhibited no enrichment on the S protein. Our findings provide new insight into the viral phylodynamics of SARS-CoV-2 and beta coronavirus.