ABSTRACT
Field-effect transistors (FET) composed of transition metal dichalcogenide (TMDC) materials have gained huge importance as biosensors due to their added advantage of high sensitivity and moderate bandgap. However, the true potential of these biosensors highly depends upon the quality of TMDC material, as well as the orientation of receptors on their surfaces. The uncontrolled orientation of receptors and screening issues due to crossing the Debye screening length while functionalizing TMDC materials is a big challenge in this field. To address these issues, we introduce a combination of high-quality monolayer WSe2 with our designed Pyrene-based receptor moiety for its ordered orientation onto the WSe2 FET biosensor. A monolayer WSe2 sheet is utilized to fabricate an ideal FET for biosensing applications, which is characterized via Raman spectroscopy, atomic force microscopy, and electrical prob station. Our construct can sensitively detect our target protein (streptavidin) with 1 pM limit of detection within a short span of 2 min, through a one-step functionalizing process. In addition to having this ultra-fast response and high sensitivity, our biosensor can be a reliable platform for point-of-care-based diagnosis.
ABSTRACT
Since the global outbreak of SARS-CoV-2 (COVID-19), infections of diverse human organs along with multiple symptoms continue to be reported. However, the susceptibility of the brain to SARS-CoV-2, and the mechanisms underlying neurological infection are still elusive. Here, we utilized human embryonic stem cell-derived brain organoids and monolayer cortical neurons to investigate infection of brain with pseudotyped SARS-CoV-2 viral particles. Spike-containing SARS-CoV-2 pseudovirus infected neural layers within brain organoids. The expression of ACE2, a host cell receptor for SARS-CoV-2, was sustained during the development of brain organoids, especially in the somas of mature neurons, while remaining rare in neural stem cells. However, pseudotyped SARS-CoV-2 was observed in the axon of neurons, which lack ACE2. Neural infectivity of SARS-CoV-2 pseudovirus did not increase in proportion to viral load, but only 10% of neurons were infected. Our findings demonstrate that brain organoids provide a useful model for investigating SARS-CoV-2 entry into the human brain and elucidating the susceptibility of the brain to SARS-CoV-2.