The most effective way to control newly emerging infectious disease, such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, is to strengthen preventative or therapeutic public health strategies before the infection spreads worldwide. However, global health systems remain at the early stages in anticipating effective therapeutics or vaccines to combat the SARS-CoV-2 pandemic. While maintaining social distance is the most crucial metric to avoid spreading the virus, symptomatic therapy given to patients on the clinical manifestations helps save lives. The molecular properties of SARS-CoV-2 infection have been quickly elucidated, paving the way to therapeutics, vaccine development, and other medical interventions. Despite this progress, the detailed biomolecular mechanism of SARS-CoV-2 infection remains elusive. Given virus invasion of cells is a determining factor for virulence, understanding the viral entry process can be a mainstay in controlling newly emerged viruses. Since viral entry is mediated by selective cellular proteases or proteins associated with receptors, identification and functional analysis of these proteins could provide a way to disrupt virus propagation. This review comprehensively discusses cellular machinery necessary for SARS-CoV-2 infection. Understanding multifactorial traits of the virus entry will provide a substantial guide to facilitate antiviral drug development.

The most effective way to control newly emerging infectious disease, such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, is to strengthen preventative or therapeutic public health strategies before the infection spreads worldwide. However, global health systems remain at the early stages in anticipating effective therapeutics or vaccines to combat the SARS-CoV-2 pandemic. While maintaining social distance is the most crucial metric to avoid spreading the virus, symptomatic therapy given to patients on the clinical manifestations helps save lives. The molecular properties of SARS-CoV-2 infection have been quickly elucidated, paving the way to therapeutics, vaccine development, and other medical interventions. Despite this progress, the detailed biomolecular mechanism of SARS-CoV-2 infection remains elusive. Given virus invasion of cells is a determining factor for virulence, understanding the viral entry process can be a mainstay in controlling newly emerged viruses. Since viral entry is mediated by selective cellular proteases or proteins associated with receptors, identification and functional analysis of these proteins could provide a way to disrupt virus propagation. This review comprehensively discusses cellular machinery necessary for SARS-CoV-2 infection. Understanding multifactorial traits of the virus entry will provide a substantial guide to facilitate antiviral drug development.

Objective: Endoscopic hemostasis is a key treatment for variceal upper gastrointestinal bleeding. However, the effects of early endoscopy in variceal upper gastrointestinal bleeding have not been sufficiently studied. This study investigated the effects of the use of the critical pathway (CP) for upper gastrointestinal bleeding. Methods: The study was designed as a ‘before and after’ study. A group of patients diagnosed with variceal upper gastrointestinal bleeding from January 1, 2011, to December 31, 2014, and CP activated patients from January 1, 2015, to December 31, 2018, were reviewed retrospectively. The study endpoints included an analysis of the following in the two groups: time from emergency department (ED) arrival to endoscopy, number of blood transfusions, hospitalization period, intensive care unit (ICU) admission, 30-day mortality. Results: From January 1, 2011, to December 31, 2018, 207 patients were admitted with variceal upper gastrointestinal bleeding, and 137 patients with a Blatchford score of 7 or higher were included in the study. Of these, 88 patients visited before the implementation of CP and 49 patients visited thereafter. The time from ED arrival to endoscopy was 218.1±201.7 minutes in the CP activated group, which was about 200 minutes shorter (P=0.046) than the non-CP group. There was no statistical difference in 30-day mortality, transfusion, emergency room hospitalization time, number of ICU admissions, and hospitalization days (P=0.348, P=0.394, P=0.651, P=0.164, and P=0.069). Conclusion After CP, the time to endoscopy was significantly shortened, but it did not reduce mortality.