Exploitation of N-Gene of SARS-CoV-2 to Develop a New Rapid Assay by ASOs@AuNPs.

A naked-eye (equipment-free), label-free (cost-effective), and RNA extraction-free (to speed up) method for SARS-CoV-2 (as a case study of RNA viruses) detection is developed. Here, the DNA is being used as a template for in situ formation of anisotropic gold nanoparticles (AuNPs) without any chemical modification or DNA labeling. In this study, synthesized AuNPs for the direct detection of N-gene (nucleocapsid phosphoprotein) of SARS-CoV-2 are exploited. To this aim, antisense oligonucleotides (ASOs) with an extra poly guanine tail (G12) were designed. Thus, in the presence of its viral target RNA gene and ASOs@AuNPs-RNA hybridization, there was a red shift in its localized surface plasmon resonance (LSPR), and the intensity of the LSPR peak at 690 nm of throat swab samples was compared to the threshold cycle (Ct) of a reverse-transcriptase real-time polymerase chain reaction (RT-qPCR) (as a gold standard). Results suggested that the plasmonic biosensor can detect a very low amount of SARS-CoV-2 with a detection limit close to RT-qPCR. Simplicity of the new conjugation method with hybridization and annealing without amplification and denaturation steps enabled it to perform in a microfluidic paper-based analytical device.

Inflammatory Response Leads to Neuronal Death in Human Post-Mortem Cerebral Cortex in Patients with COVID-19.

The recent coronavirus disease of 2019 (COVID-19) pandemic has adversely affected people worldwide. A growing body of literature suggests the neurological complications and manifestations in response to COVID-19 infection. Herein, we explored the inflammatory and immune responses in the post-mortem cerebral cortex of patients with severe COVID-19. The participants comprised three patients diagnosed with severe COVID-19 from March 26, 2020, to April 17, 2020, and three control patients. Our findings demonstrated a surge in the number of reactive astrocytes and activated microglia, as well as low levels of glutathione along with the upregulation of inflammation- and immune-related genes IL1B, IL6, IFITM, MX1, and OAS2 in the COVID-19 group. Overall, the data imply that oxidative stress may invoke a glial-mediated neuroinflammation, which ultimately leads to neuronal cell death in the cerebral cortex of COVID-19 patients.