De novo design of a stapled peptide targeting SARS-CoV-2 spike protein receptor-binding domain.

Although effective vaccines have been developed against SARS-CoV-2, many regions in the world still have low rates of vaccination and new variants with mutations in the viral spike protein have reduced the effectiveness of most available vaccines and treatments. There is an urgent need for a drug to cure this disease and prevent infection. The SARS-CoV-2 virus enters the host cell through protein-protein interaction between the virus's spike protein and the host's angiotensin converting enzyme (ACE2). Using protein design software and molecular dynamics simulations, we have designed a 17-residue peptide (pep39), that binds to the spike protein receptor-binding domain (RBD) and blocks interaction of spike protein with ACE2. We have confirmed the binding activity of the designed peptide for the original spike protein and the delta variant spike protein using micro-cantilever and bio-layer interferometry (BLI) based methods. We also confirmed that pep39 strongly inhibits SARS-CoV-2 virus replication in Vero E6 cells. Taken together these data suggest that a newly designed spike protein RBD blocking peptide pep39 has a potential as a SARS-CoV-2 virus inhibitor.

A label-free aptasensor FET based on Au nanoparticle decorated Co3O4 nanorods and a SWCNT layer for detection of cardiac troponin T protein.

Acute myocardial infarction (AMI) is a serious health problem that must be identified in its early stages. Considerable progress has been made in understanding the condition of AMI through ascertaining the role of biomarkers, such as myoglobin, cardiac troponin proteins (T and I), creatine kinase-MB, and fatty acid-binding protein (FABP). A field-effect transistor (FET) is an effective platform; however, innovations are required in all layers of the FET for it to become robust and highly sensitive. For the first time, we made use of the synergistic combination of noble metal nanoparticles (AuNPs) with Co3O4 for the detection of cardiac troponin T (cTnT) in a FET platform. We determined the morphology of Au-decorated Co3O4 NRs and their electronic properties by characterizing the channel layer using electron microscopies and transient measurements. Subsequently, we performed the detection of cardiac troponin T by immobilizing its complementary biotinylated DNA aptamer on the channel surface using a drop-casting method. To understand the changes in drain current caused by this interaction, we probed our SWCNT-Co3O4 NR transistor with limited gate and drain bias (≤1 V), achieving a sensitivity of 0.5 µA µg-1 mL-1 for the Au-decorated NRs. A 250% increase in the sensitivity and a limit of detection (LOD) of 0.1 µg mL-1 were achieved by using this device. Finally, selectivity studies proved that this synergistic combination works well in the FET configuration for the successful detection of cTnT.