[from Science, First Release Notification for July 21]
Proton-Coupled Energy Transfer in Molecular Triads
Abstract
A photochemical mechanism was experimentally discovered and denoted proton-coupled energy transfer (PCEnT). A series of anthracene–phenol–pyridine triads formed the local excited anthracene state after light excitation at ca. 400 nm, which led to fluorescence around 550 nm from the phenol–pyridine unit. Direct excitation of phenol–pyridine would have required light around 330 nm, but the coupled proton transfer within the phenol–pyridine unit lowered its excited state energy so that it could accept excitation energy from anthracene. Singlet-singlet energy transfer thus occurred despite the lack of spectral overlap between the anthracene fluorescence and the phenol–pyridine absorption. Moreover, theoretical calculations indicated negligible charge transfer between the anthracene and phenol–pyridine units. PCEnT was suggested as an elementary reaction of possible relevance to biological systems and future photonic devices.
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Omicron Spike Function and Neutralizing Activity Elicited by a Comprehensive Panel of Vaccines
Abstract
The SARS-CoV-2 Omicron variant of concern comprises several sublineages with BA.2 and BA.2.12.1 having replaced the previously dominant BA.1, and BA.4 and BA.5 increasing in prevalence worldwide. We show that the large number of Omicron sublineage spike mutations lead to enhanced ACE2 binding, reduced fusogenicity, and severe dampening of plasma neutralizing activity elicited by infection or seven clinical vaccines relative to the ancestral virus. Administration of a homologous or heterologous booster based on the Wuhan-Hu-1 spike sequence markedly increased neutralizing antibody titers and breadth against BA.1, BA.2, BA.2.12.1, and BA.4/5 across all vaccines evaluated. Our data suggest that although Omicron sublineages evade polyclonal neutralizing antibody responses elicited by primary vaccine series, vaccine boosters may provide sufficient protection against Omicron-induced severe disease.
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