Insight into the mechanisms of coronaviruses evading host innate immunity

The SARS-CoV-2 induced coronavirus disease (COVID-19) has recently caused a pandemic. Patients with COVID-19 presented with a wide spectrum of symptoms for the disease, from entirely asymptomatic to full-blown pneumonia and multiorgan failures. More evidence emerged, showing the production of interferons (IFNs) in the severe cases were significantly lower than their milder counterparts, suggesting linkage of COVID-19 to impaired innate immunity. This review presents a brief overview of how coronaviruses evade innate immunity, based on the information from SARS-CoV and MERS-CoV. The coronaviruses manage to block, escape, or dampen the innate immune response by antagonizing double-stranded RNA (dsRNA) sensor, stimulator of IFN genes (STING) and mitochondrial antiviral-signaling protein (MAVS) pathways, epigenetic modification, posttranslational modifications, and host mRNA translation. We provide novel insights into a comprehensive therapy to combat SARS-CoV-2 infection.

Insight into the mechanisms of coronaviruses evading host innate immunity.

The severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) induced coronavirus disease 2019 (COVID-19) has recently caused a pandemic. Patients with COVID-19 presented with a wide spectrum of symptoms for the disease, from entirely asymptomatic disease to full-blown pneumonia and multiorgan failures. More evidence emerged, showing the production of interferons (IFNs) in the severe cases were significantly lower than their milder counterparts, suggesting linkage of COVID-19 to impaired innate immunity. This review presents a brief overview of how coronaviruses evade innate immunity, according to the current studies about SARS-CoV and middle-east respiratory syndrome-coronavirus (MERS-CoV). The coronaviruses manage to block, escape, or dampen the innate immune response by antagonizing double-stranded RNA (dsRNA) sensor, mitochondrial antiviral-signaling protein (MAVS) and stimulator of IFN genes (STING) pathways, epigenetic modification, posttranslational modifications, and host mRNA translation. We provide novel insights into a comprehensive therapy to combat SARS-CoV-2 infection.

Automatic range of motion measurement via smartphone images for telemedicine examination of the hand.

BACKGROUND: Telemedicine support virtual consultations and evaluations in hand surgery for patients in remote areas during the COVID-19 era. However, traditional physical examination is challenging in telemedicine and it is inconvenient to manually measure the hand range of motion (ROM) from images or videos. Here, we propose an automatic method using the hand pose estimation technique, aiming to measure the hand ROM from smartphone images. METHODS: Twenty-eight healthy volunteers participated in the study. An eight-hand gestures measurement protocol and the Google MediaPipe Hands were used to analyze images and calculate the ROM automatically. Manual goniometry was also performed according to the guideline of the American Medical Association. The correlation between the automatic and manual methods was analyzed by the intraclass correlation coefficient and Pearson correlation coefficient. The clinical acceptance was testified using Bland-Altman plots. RESULTS: A total of 32 parameters of each hand were measured by both methods, and 1792 measurement results were compared. The mean difference between automatic and manual methods is -2.21 ± 9.29° in the angle measurement and 0.48 ± 0.48 cm in the distance measurement. The intraclass correlation coefficient of 75% of parameters was higher than 0.75, the Pearson correlation coefficient of 84% of parameters was over 0.6, and 40.6% of parameters reached well-accepted clinical agreements. CONCLUSIONS: The proposed method provides a helpful protocol for automatic hand ROM measurement based on smartphone images and the MediaPipe Hands pose estimation technique. The automatic measurement is acceptable and comparable with existing methods, showing a possible application in the telemedicine examination of hand surgery.

Removal and toxic forecast of microplastics treated by electrocoagulation: Influence of dissolved organic matter.

In recent years, the break of COVID-19 makes the large use of disposable products, which causes the removal of microplastics become an imperative problem. Electrocoagulation is one of the effective removal technologies, but there is hardly research concentrating on the effect of substrate in the actual water on the microplastics removal with electrocoagulation. As an important role of water bodies, dissolved organic matter (DOM) has a vital and inevitable effect on the efficiency of electrocoagulation. In this study, the effect of DOM in tailwater on microplastics during electrocoagulation is elucidated by comparing the electrocoagulation treatment results between simulated wastewater and tailwater, using parallel factor analysis (PARAFAC), Scanning Electron Microscopy (SEM), Fourier Transform Infrared Spectrometer (FTIR) and zeta potential analyzer. Three kinds of microplastic particles (i.e. polypropylene, polyethylene, and polymethyl methacrylate) were added into each of the two kinds of wastewaters to form six electrocoagulation systems. Results show that DOM in tailwater promotes the production of flocs and free radicals during electrocoagulation process. Fe2+ and Fe3+ are adsorbed on the surface of DOM molecules and combined with •OH form flocs. Although DOM accelerates the production of free radicals and thus promotes the aging of microplastics, flocs with DOM as crystal nucleus can prevent toxic substances and small-sized microplastics from leaching into water again. Therefore, electrocoagulation is preferred to removal microplastics in water with high concentration of DOM. This study provides a significant reference for microplastics removal by electrocoagulation in actual water, and promote the practical application of electrocoagulation for microplastics removal in water treatment.

The study of antiviral drugs targeting SARS-CoV-2 nucleocapsid and spike proteins through large-scale compound repurposing.

Contributing to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) clinical treatment, a drug library encompassing approximately 3,142 clinical-stage or FDA-approved small molecules is profiled to identify the candidate therapeutic inhibitors targeting nucleocapsid protein (N) and spike protein (S) of SARS-CoV-2. 16 screened candidates with higher binding affinity are evaluated via virtual screening. Comparing to those under trial/temporarily used antivirus drugs (i.e., umifenovir, lopinavir), ceftriaxone, cefotaxime, and cefuroxime show higher binding affinities to the N-terminal domain of N protein (N-NTD), C-terminal domain of N protein (N-CTD), and receptor-binding domain of S protein (S-RBD). Cefotaxime and cefuroxime have high binding affinities towards S-RBD with angiotensin-converting enzyme 2 (ACE2) complex via influence the critical interface sites at the interface of S-RBD (Arg403, Tyr453, Trp495, Gly496, Phe497, Asn501and Tyr505) and ACE2 (Asn33, His34, Glu37, Asp38, Lys353, Ala386, Ala387, Gln388, Pro389, Phe390 and Arg393) complex.