The Different Impacts of Emissions and Meteorology on PM2.5 Changes in Various Regions in China: A Case Study

Emissions and meteorology are significant factors affecting aerosol pollution, but it is not sufficient to understand their relative contributions to aerosol pollution changes. In this study, the observational data and the chemical model (GRAPES_CUACE) are combined to estimate the drivers of PM2.5 changes in various regions (the Beijing–Tianjin–Hebei (BTH), the Central China (CC), the Yangtze River Delta (YRD), and the Pearl River Delta (PRD)) between the first month after COVID-19 (FMC_2020) (i.e., from 23 January to 23 February 2020) and the corresponding period in 2019 (FMC_2019). The results show that PM2.5 mass concentration increased by 26% (from 61 to 77 µg m−3) in the BTH, while it decreased by 26% (from 94 to 70 µg m−3) in the CC, 29% (from 52 to 37 µg m−3) in the YRD, and 32% (from 34 to 23 µg m−3) in the PRD in FMC_2020 comparing with FMC_2019, respectively. In the BTH, although emissions reductions partly improved PM2.5 pollution (−5%, i.e., PM2.5 mass concentration decreased by 5% due to emissions) in FMC_2020 compared with that of FMC_2019, the total increase in PM2.5 mass concentration was dominated by more unfavorable meteorological conditions (+31%, i.e., PM2.5 mass concentration increased by 31% due to meteorology). In the CC and the YRD, emissions reductions (−33 and −36%) played a dominating role in the total decrease in PM2.5 in FMC_2020, while the changed meteorological conditions partly worsened PM2.5 pollution (+7 and +7%). In the PRD, emissions reductions (−23%) and more favorable meteorological conditions (−9%) led to a total decrease in PM2.5 mass concentration. This study reminds us that the uncertainties of relative contributions of meteorological conditions and emissions on PM2.5 changes in various regions are large, which is conducive to policymaking scientifically in China.

A framework for predicting potential host ranges of pathogenic viruses based on receptor ortholog analysis (preprint)

Viral zoonoses are a serious threat to public health and global security, as reflected by the current scenario of the growing number of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cases. However, as pathogenic viruses are highly diverse, identification of their host ranges remains a major challenge. Here, we present a combined computational and experimental framework, called REceptor ortholog-based POtential virus hoST prediction (REPOST), for the prediction of potential virus hosts. REPOST first selects orthologs from a diverse species by identity and phylogenetic analyses. Secondly, these orthologs is classified preliminarily as permissive or non-permissive type by infection experiments. Then, key residues are identified by comparing permissive and non-permissive orthologs. Finally, potential virus hosts are predicted by a key residue-specific weighted module. We performed REPOST on SARS-CoV-2 by studying angiotensin-converting enzyme 2 orthologs from 287 vertebrate animals. REPOST efficiently narrowed the range of potential virus host species (with 95.74% accuracy).

The accessible promoter–mediated supplementary effect of ACE2 provides new insight into the tissue tropism of SARS-CoV-2 (preprint)

Background：Angiotensin-converting enzyme 2 (ACE2) has been confirmed to be a receptor for the newly discovered severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, cell surface ACE2 expression is reported to be inconsistent with clinical tissue tropism of SARS-CoV-2, which complicates understanding of the pathogenesis of 2019 novel coronavirus disease (COVID-19). The consumption of ACE2 by internalization and shedding processes may explain this discordance. Results：To understand the discordance between ACE2 expression and the tissue tropism of SARS-CoV-2, we examined the chromatin accessibility of ACE2 promoter in hundreds of tissues and cell lines using public DNase-seq and assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) data. We find that ACE2 promoter is only accessible in three tissues including lung, large intestine and placenta. Also, we examined tumors tissues and ACE2 promoter is observed accessible in five tumors with reported SARS-CoV-2 susceptibility. We confirmed the susceptibility by performing SARS-CoV-2 pseudovirus infection in several cell lines. Conclusions：We propose that open chromatin at the promoter mediates the ACE2 supplementary effect and ensures the entry of SARS-CoV-2. This hypothesis provides a new view and potential clues for further investigation of COVID-19 pathogenesis.