An in-depth annotation of the newly discovered coronavirus (2019-nCoV) genome has revealed differences between 2019-nCoV and severe acute respiratory syndrome (SARS) or SARS-like coronaviruses. A systematic comparison identified 380 amino acid substitutions between these coronaviruses, which may have caused functional and pathogenic divergence of 2019-nCoV.

People across the world have been greatly affected by the ongoing coronavirus disease (COVID-19) pandemic. The high infection risk of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in hospitals is particularly problematic for recently delivered mothers and currently pregnant women who require professional antenatal care. Online antenatal care would be a preferable alternative for these women since it can provide pregnancy-related information and remote clinic consultations. In addition, online antenatal care may help to provide relatively economical medical services and diminish health care inequality due to its convenience and cost-effectiveness, especially in developing countries or regions. However, some pregnant women will doubt the reliability of such online information. Therefore, it is important to ensure the quality and safety of online services and establish a stable, mutual trust between the pregnant women, the obstetric care providers and the technology vis-a-vis the online programs. Here, we report how the COVID-19 pandemic brings not only opportunities for the development and popularization of online antenatal care programs but also challenges.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a widespread outbreak of highly pathogenic coronavirus disease 2019 (COVID-19). It is therefore important and timely to characterize interactions between the virus and host cell at the molecular level to understand its disease pathogenesis. To gain insights, we performed high-throughput sequencing that generated time-series data simultaneously for bioinformatics analysis of virus genomes and host transcriptomes implicated in SARS-CoV-2 infection. Our analysis results showed that the rapid growth of the virus was accompanied by an early intensive response of host genes. We also systematically compared the molecular footprints of the host cells in response to SARS-CoV-2, SARS-CoV, and Middle East respiratory syndrome coronavirus (MERS-CoV). Upon infection, SARS-CoV-2 induced hundreds of up-regulated host genes hallmarked by a significant cytokine production, followed by virus-specific host antiviral responses. While the cytokine and antiviral responses triggered by SARS-CoV and MERS-CoV were only observed during the late stage of infection, the host antiviral responses during the SARS-CoV-2 infection were gradually enhanced lagging behind the production of cytokine. The early rapid host responses were potentially attributed to the high efficiency of SARS-CoV-2 entry into host cells, underscored by evidence of a remarkably up-regulated gene expression of TPRMSS2 soon after infection. Taken together, our findings provide novel molecular insights into the mechanisms underlying the infectivity and pathogenicity of SARS-CoV-2.