Network approach reveals the spatiotemporal influence of traffic on air pollution under COVID-19.

Air pollution causes widespread environmental and health problems and severely hinders the quality of life of urban residents. Traffic is critical for human life, but its emissions are a major source of pollution, aggravating urban air pollution. However, the complex interaction between traffic emissions and air pollution in cities and regions has not yet been revealed. In particular, the spread of COVID-19 has led various cities and regions to implement different traffic restriction policies according to the local epidemic situation, which provides the possibility to explore the relationship between urban traffic and air pollution. Here, we explore the influence of traffic on air pollution by reconstructing a multi-layer complex network base on the traffic index and air quality index. We uncover that air quality in the Beijing-Tianjin-Hebei (BTH), Chengdu-Chongqing Economic Circle (CCS), and Central China (CC) regions is significantly influenced by the surrounding traffic conditions after the outbreak. Under different stages of the fight against the epidemic, the influence of traffic in some regions on air pollution reaches the maximum in stage 2 (also called Initial Progress in Containing the Virus). For the BTH and CC regions, the impact of traffic on air quality becomes bigger in the first two stages and then decreases, while for CC, a significant impact occurs in phase 3 among the other regions. For other regions in the country, however, the changes are not evident. Our presented network-based framework provides a new perspective in the field of transportation and environment and may be helpful in guiding the government to formulate air pollution mitigation and traffic restriction policies.

Single-cell immune profiling reveals distinct immune response in asymptomatic COVID-19 patients.

While some individuals infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) present mild-to-severe disease, many SARS-CoV-2-infected individuals are asymptomatic. We sought to identify the distinction of immune response between asymptomatic and moderate patients. We performed single-cell transcriptome and T-cell/B-cell receptor (TCR/BCR) sequencing in 37 longitudinal collected peripheral blood mononuclear cell samples from asymptomatic, moderate, and severe patients with healthy controls. Asymptomatic patients displayed increased CD56briCD16- natural killer (NK) cells and upregulation of interferon-gamma in effector CD4+ and CD8+ T cells and NK cells. They showed more robust TCR clonal expansion, especially in effector CD4+ T cells, but lack strong BCR clonal expansion compared to moderate patients. Moreover, asymptomatic patients have lower interferon-stimulated genes (ISGs) expression in general but large interpatient variability, whereas moderate patients showed various magnitude and temporal dynamics of the ISGs expression across multiple cell populations but lower than a patient with severe disease. Our data provide evidence of different immune signatures to SARS-CoV-2 in asymptomatic infections.