This article reviews the correlation between angiotensin-converting enzyme 2 (ACE2) and severe risk factors for coronavirus disease 2019 and the possible mechanisms. ACE2 is a crucial component of the renin-angiotensin system (RAS). The classical RAS ACE-Ang II-AT1R regulatory axis and the ACE2-Ang 1-7-MasR counter-regulatory axis play an essential role in maintaining homeostasis in humans. ACE2 is widely distributed in the heart, kidneys, lungs, and testes. ACE2 antagonizes the activation of the classical RAS system and protects against organ damage, protecting against hypertension, diabetes, and cardiovascular disease. Similar to SARS-CoV, SARS-CoV-2 also uses the ACE2 receptor to invade human alveolar epithelial cells. Acute respiratory distress syndrome (ARDS) is a clinical high-mortality disease, and ACE2 has a protective effect on this type of acute lung injury. Current research shows that the poor prognosis of patients with COVID-19 is related to factors such as sex (male), age (>60 years), underlying diseases (hypertension, diabetes, and cardiovascular disease), secondary ARDS, and other relevant factors.

Approaches to preventing or mitigating the impact of the COVID-19 pandemic have varied markedly between nations. We examined the approach up to August 2020 taken by two jurisdictions which had successfully eliminated COVID-19 by this time: Taiwan and New Zealand. Taiwan reported a lower COVID-19 incidence rate (20.7 cases per million) compared with NZ (278.0 per million). Extensive public health infrastructure established in Taiwan pre-COVID-19 enabled a fast coordinated response, particularly in the domains of early screening, effective methods for isolation/quarantine, digital technologies for identifying potential cases and mass mask use. This timely and vigorous response allowed Taiwan to avoid the national lockdown used by New Zealand. Many of Taiwan's pandemic control components could potentially be adopted by other jurisdictions.

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Herpes simplex virus type 1 (HSV-1) infection of the murine cornea results in a tissue-destructive inflammatory response. In this study we show that virus infection induces the synthesis of macrophage inflammatory protein-2 (MIP-2), MIP-1alpha, and monocyte chemoattractant protein-1 (MCP-1). However, only the production of MIP-2 and MIP-1alpha coincided with the influx of leukocytes into the cornea. IL-10 treatment markedly suppressed chemokine message and protein synthesis in vivo. Local administration of IL-10 also dramatically reduced the number of T cells and neutrophils migrating into the cornea and suppressed the severity of corneal disease. The inflammatory response could also be suppressed by the passive transfer of neutralizing antibody to MIP-1alpha but not MCP-1. We conclude that local IL-10 administration can suppress chemokine synthesis, thereby ameliorating corneal disease. Furthermore, our results indicate that MIP-1alpha plays a major role in herpes stromal keratitis development, whereas MCP-1 does not.

Highlights Robust contact tracing with an integrated system effectively intervene early transmission of COVID-19 in Taiwan. Develop an integrated management system to support traditional contact tracing is critical in response to control the spread of COVID-19. Management tools augment the capacity and decreased workloads of contact tracers, which improve contact tracing effectiveness.