Key result
Prophylactic neutralizing mAbs reduce SARS-CoV-2 lung viral load and prevent weight loss in animal models.
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Why the study?
SARS-CoV-2 variants of concern with multiple spike protein mutations can exhibit neutralization resistance, potentially affecting antibody-based therapeutics effectiveness.
A panel of 91 human monoclonal antibodies targeting the SARS-CoV-2 RBD demonstrates dose-dependent protection in animal models and identifies specific antibodies resistant to variants of concern.
Animal model findings should not guide clinical prophylaxis; leaves open translation and variant resistance testing in humans.
Potent neutralizing monoclonal antibodies are one of the few agents currently available to treat COVID-19. SARS-CoV-2 variants of concern (VOCs) that carry multiple mutations in the viral spike protein can exhibit neutralization resistance, potentially affecting the effectiveness of some antibody-based therapeutics. Here, the generation of a diverse panel of 91 human, neutralizing monoclonal antibodies provides an in-depth structural and phenotypic definition of receptor binding domain (RBD) antigenic sites on the viral spike. These RBD antibodies ameliorate SARS-CoV-2 infection in mice and hamster models in a dose-dependent manner and in proportion to in vitro, neutralizing potency. Assessing the effect of mutations in the spike protein on antibody recognition and neutralization highlights both potent single antibodies and stereotypic classes of antibodies that are unaffected by currently circulating VOCs, such as B.1.351 and P.1. These neutralizing monoclonal antibodies and others that bind analogous epitopes represent potentially useful future anti-SARS-CoV-2 therapeutics.
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Wheatley et al. (2021) studied SARS-CoV-2 infection. Neutralizing monoclonal antibodies (e.g., PDI 96, PDI 222) vs. Isotype control was evaluated on Viral titers in lung homogenates and weight loss. Prophylactic administration of neutralizing monoclonal antibodies, either singly or in cocktails, significantly reduced SARS-CoV-2 viral load in the lungs and prevented weight loss in mice and hamster models.
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