Since the outbreak of the coronavirus disease 2019 (COVID-19) pandemic, there have been a few variants of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), one of which is the Omicron variant (B.1.1.529). The Omicron variant is the most mutated SARS-CoV-2 variant, and its high transmissibility and immune evasion ability have raised global concerns. Owing to its enhanced transmissibility, Omicron has rapidly replaced Delta as the dominant variant in several regions. However, recent studies have shown that the Omicron variant exhibits reduced pathogenicity due to altered cell tropism. In addition, Omicron exhibits significant resistance to the neutralizing activity of vaccines, convalescent serum, and most antibody therapies. In the present review, recent advances in the molecular and clinical characteristics of the infectivity, pathogenicity, and immune evasion of Omicron variant was summarized, and potential therapeutic applications in response to Omicron infection were discussed. Furthermore, we highlighted potential response to future waves and strategies to end the pandemic. 

/pdf/sars-cov-2-omicron-variant-recent-progress-and-future-rymk2gdz.pdf

SARS-CoV-2 Omicron variant: recent progress and future perspectives

Solution-processed organic light-emitting diodes (s-OLEDs) have received a great deal of interest owing to the huge market application potentials as large-size, flexible, high-quality self-luminous display panels and lighting sources. It is anticipated that those electronic products can be easily manufactured by modern wet-processing techniques, e.g. ink-jet printing and ‘roll-to-roll’ coating methods. However, issues related to power efficiency (PE) are highly hampering the progress of s-OLEDs towards real applications. Herein, we will demonstrate current development of s-OLEDs targeting for high PE with emphasis on introducing (i) theoretical and practical significance in simultaneously achieving close-to-unity (∼100 %) exciton emission and low driving voltage realized by advanced interface modification, bipolar-transporting-type host, all-exciton-harvesting emissive material and customized device architectures to integrate their functions, (ii) novel low-driving-voltage techniques for phosphorescent and thermally activated delayed fluorescence (TADF) s-OLEDs, i.e. barrier-free exciplex host or bipolar co-host scaffold, and charge-trapping- or charge-scattering-free emissive layer (EML) structures by matching the frontier molecular orbitals (FMOs) between host and dopant emitters, (iii) a variety of tactics to effectively alleviate the efficiency roll-off issue at the practically high luminance value, e.g. removing or largely restraining exciton-quenching in the EML and/or interfaces, the utilization of novel emitters with fast radiative decay rate and/or the EML architectures with prompt and efficient Forster energy transfer process.

Towards high-power-efficiency solution-processed OLEDs: Material and device perspectives

http://www.cell.com/article/S0092867422004561/pdf

Efficient recall of Omicron-reactive B cell memory after a third dose of SARS-CoV-2 mRNA vaccine

Omicron is the evolutionarily most distinct severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variant of concern (VOC) to date. We report that Omicron BA.1 breakthrough infection in BNT162b2-vaccinated individuals resulted in strong neutralizing activity against Omicron BA.1, BA.2, and previous SARS-CoV-2 VOCs but not against the Omicron sublineages BA.4 and BA.5. BA.1 breakthrough infection induced a robust recall response, primarily expanding memory B (BMEM) cells against epitopes shared broadly among variants, rather than inducing BA.1-specific B cells. The vaccination-imprinted BMEM cell pool had sufficient plasticity to be remodeled by heterologous SARS-CoV-2 spike glycoprotein exposure. Whereas selective amplification of BMEM cells recognizing shared epitopes allows for effective neutralization of most variants that evade previously established immunity, susceptibility to escape by variants that acquire alterations at hitherto conserved sites may be heightened. Description BA.1 infection after BNT162b2 vaccination drives cross-variant neutralization and memory B cell formation against conserved epitopes.

https://www.science.org/cms/asset/5060d037-7a97-43b3-8fc3-3e1a9574c730/sciimmunol.abq2427.v1.pdf

Omicron BA.1 breakthrough infection drives cross-variant neutralization and memory B cell formation against conserved epitopes

Immunological memory is the basis of protective immunity provided by vaccines and previous infections. Immunological memory can develop from multiple branches of the adaptive immune system, including CD4 T cells, CD8 T cells, B cells, and long‐lasting antibody responses. Extraordinary progress has been made in understanding memory to SARS‐CoV‐2 infection and COVID‐19 vaccines, addressing development; quantitative and qualitative features of different cellular and anatomical compartments; and durability of each cellular component and antibodies. Given the sophistication of the measurements; the size of the human studies; the use of longitudinal samples and cross‐sectional studies; and head‐to‐head comparisons between infection and vaccines or between multiple vaccines, the understanding of immune memory for 1 year to SARS‐CoV‐2 infection and vaccines already supersedes that of any other acute infectious disease. This knowledge may help inform public policies regarding COVID‐19 and COVID‐19 vaccines, as well as the scientific development of future vaccines against SARS‐CoV‐2 and other diseases.

https://zenodo.org/record/6410210/files/Crotty%20Immune%20Memory%20Review%20COVID%202022.pdf

Immunological memory to SARS‐CoV‐2 infection and COVID‐19 vaccines

Multiple SARS-CoV-2 variants have mutations in the spike receptor binding domain (RBD) with potential to evade neutralizing antibody. In particular, the Beta and Omicron variants escape from antibody neutralizing activity in those who received two doses of BNT162b2 mRNA vaccine. Nonetheless, boosting with a third vaccine dose or by breakthrough infection improves the overall breadth of the neutralizing antibodies, but the mechanism remains unclear. Here, we longitudinally profiled the cellular composition of RBD-binding memory B cell subsets and their antibody binding and neutralizing activity against SARS-CoV-2 variants after the second dose of mRNA vaccine. Two doses of the mRNA vaccine elicited plasma neutralizing antibodies with a limited activity against Beta and Omicron but induced an expanded antibody breadth overtime, up to 4.9 months after vaccination. In contrast, more than one-third of RBD-binding IgG+ memory B cells with a resting phenotype initially bound the Beta and Omicron variants and steadily increased the B cell receptor breadth overtime. As a result, a fraction of the resting memory B cell subset secreted Beta and Omicron-neutralizing antibody when stimulated in vitro. The neutralizing breadth of the resting memory B cell subset helps us understand the prominent recall of Omicron-neutralizing antibodies after an additional booster or breakthrough infection in fully vaccinated individuals. Description Memory B cells elicited by two doses of mRNA vaccine preserve broadly neutralizing antibodies against Omicron variant. mRNA vaccines induce Omicron neutralizing memory B cells Two doses of the mRNA SARS-CoV-2 vaccines are less effective at inducing neutralizing antibodies against the Omicron variant, but a third dose or breakthrough infection rescues those poor antibody responses. Here, Kotaki et al. profiled the antibody and memory B cell responses of 40 health care workers vaccinated with two doses of the BNT162b2 mRNA vaccine. Confirming multiple reports, they found reduced neutralizing antibodies against Omicron; however, they found that memory B cells were still able to generate strong neutralizing antibody responses against Omicron ex vivo due to their expanded breadth overtime. These data suggest that SARS-CoV-2–specific memory B cells contribute to the increase of Omicron neutralizing antibodies after a breakthrough infection or booster mRNA vaccination.

SARS-CoV-2 Omicron-neutralizing memory B-cells are elicited by two doses of BNT162b2 mRNA vaccine

The synthesis and photoluminescence properties of three-coordinate Au(I) complexes with rigid diphosphine ligands LMe {1,2-bis[bis(2-methylphenyl)phosphino]benzene}, LEt {1,2-bis[bis(2-ethylphenyl)phosphino]benzene}, and LiPr {1,2-bis[bis(2-isopropylphenyl)phosphino]benzene} are investigated. The LMe and LEt ligands afford two types of complexes: dinuclear complexes [μ-LMe(AuCl)2] (1d) and [μ-LEt(AuCl)2] (2d) with an Au(I)–Au(I) bond and mononuclear three-coordinate Au(I) complexes LMeAuCl (1) and LEtAuCl (2). On the other hand, the bulkiest ligand, LiPr, affords three-coordinate Au(I) complexes, LiPrAuCl (3) and LiPrAuI (4), but no dinuclear complexes. X-ray analysis suggests that both 3 and 4 possess a highly distorted trigonal planar geometry. Moreover, luminescence data reveal that at room temperature, 3 and 4 exhibit yellow-green thermally activated delayed fluorescence in the crystalline state with maximum emission wavelengths at 558 and 549 nm, respectively. The emission yields are close to unity. Quantum chemical calculations suggest that the emission of 4 originates from the (σ + X) → π* excited state that possesses strong intraligand charge-transfer character. The luminescent properties of four-coordinate Au(I) complex (5) possessing a tetrahedral geometry are discussed on the basis of the emission spectra and decay times measured in a temperature range of 309–77 K.

Near-unity thermally activated delayed fluorescence efficiency in three- and four-coordinate Au(i) complexes with diphosphine ligands.

Severe acute respiratory syndrome coronavirus 2–neutralizing antibodies primarily target the spike receptor binding domain (RBD). However, B cell antigen receptors (BCRs) on RBD-binding memory B (Bmem) cells have variation in the neutralizing activities. Here, by combining single Bmem cell profiling with antibody functional assessment, we dissected the phenotype of Bmem cell harboring the potently neutralizing antibodies in coronavirus disease 2019 (COVID-19)–convalescent individuals. The neutralizing subset was marked by an elevated CD62L expression and characterized by distinct epitope preference and usage of convergent VH (variable region of immunoglobulin heavy chain) genes, accounting for the neutralizing activities. Concordantly, the correlation was observed between neutralizing antibody titers in blood and CD62L+ subset, despite the equivalent RBD binding of CD62L+ and CD62L− subset. Furthermore, the kinetics of CD62L+ subset differed between the patients who recovered from different COVID-19 severities. Our Bmem cell profiling reveals the unique phenotype of Bmem cell subset that harbors potently neutralizing BCRs, advancing our understanding of humoral protection.

https://www.science.org/doi/pdf/10.1126/sciadv.adf0661?download=true

Takaki Nagakura

Papers

SARS-CoV-2 Omicron-neutralizing memory B-cells are elicited by two doses of BNT162b2 mRNA vaccine

Near-unity thermally activated delayed fluorescence efficiency in three- and four-coordinate Au(i) complexes with diphosphine ligands.

CD62L expression marks SARS-CoV-2 memory B cell subset with preference for neutralizing epitopes