SARS-CoV-2 has undergone progressive change with variants conferring advantage rapidly becoming dominant lineages e.g. B.1.617. With apparent increased transmissibility variant B.1.617.2 has contributed to the current wave of infection ravaging the Indian subcontinent and has been designated a variant of concern in the UK.
We recently reported vaccine effectiveness (VE) estimates against symptomatic disease with the Delta (B.1.617.2) variant.(1) After a full course, VE reached 88% with the Pfizer/BioNTech BNT162b2 vaccine and 67% with the AstraZeneca ChAdOx1 AZD1222 vaccine. This provided important evidence that despite modest reductions in protection, vaccines remain effective against Delta. However, the very recent emergence of the variant and the relatively low case numbers meant that it was not possible to estimate VE against severe disease.
Abstract SARS-CoV-2 VOCs immune evasion is mainly due to lower cross-reactivity from previously elicited class I/II neutralizing antibodies, while increased affinity to hACE2 plays a minor role. The affinity between antibodies and VOC is impacted by remodeling of the electrostatic surface potential of the Spike RBDs. P.3 variant is a putative VOC.
The dynamics underlying severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfection remain poorly understood. We identified a small cluster of patients in Brazil who experienced 2 episodes of coronavirus disease (COVID-19) in March and late May 2020. In the first episode, patients manifested an enhanced innate response compared with healthy persons, but neutralizing humoral immunity was not fully achieved. The second episode was associated with different SARS-CoV-2 strains, higher viral loads, and clinical symptoms. Our finding that persons with mild COVID-19 may have controlled SARS-CoV-2 replication without developing detectable humoral immunity suggests that reinfection is more frequent than supposed, but this hypothesis is not well documented.
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