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Articles by Sandra E. Dross
Computationally designed proteins mimic antibody immune evasion in viral evolution
Keywords protein design machine learning viral evolution antibody escape generative protein models vaccine evaluation immune landscape Introduction The emergence of viral variants that evade protective immunity induced by prior infections, vaccines, and therapeutics is a challenge for the control of viral spread. This is exemplified by recurrent breakthrough infections observed with SARS-CoV-2 and influenza.
Mosaic sarbecovirus nanoparticles elicit cross-reactive responses in pre-vaccinated animals
Highlights • Pan-sarbecovirus vaccine evaluated in pre-vaccinated monkeys and mice • Mosaic nanoparticles elicited broad antibody responses after COVID-19 vaccinations • Epitope and molecular fate mapping revealed cross-reactive recall responses • Original antigenic sin did not diminish immune responses to a mosaic vaccine Summary Immunization with mosaic-8b (nanoparticles presenting 8 SARS-like betacoronavirus [sarbecovirus] receptor-binding domains [RBDs]) elicits more broadly...
Mosaic sarbecovirus nanoparticles elicit cross-reactive responses in pre-vaccinated animals
Abstract Immunization with mosaic-8b [60-mer nanoparticles presenting 8 SARS-like betacoronavirus (sarbecovirus) receptor-binding domains (RBDs)] elicits more broadly cross-reactive antibodies than homotypic SARS-CoV-2 RBD-only nanoparticles and protects against sarbecoviruses.
Mosaic sarbecovirus vaccination elicits cross-reactive responses in pre-immunized animals
Abstract Immunization with mosaic-8b [60-mer nanoparticles presenting 8 SARS-like betacoronavirus (sarbecovirus) receptor-binding domains (RBDs)] elicits more broadly cross-reactive antibodies than homotypic SARS-CoV-2 RBD-only nanoparticles and protects against sarbecoviruses.
Kinetics of Myeloid-Derived Suppressor Cell Frequency and Function during Simian Immunodeficiency Virus Infection, Combination Antiretroviral Therapy, and Treatment Interruption
During chronic lentiviral infection, poor clinical outcomes correlate both with systemic inflammation and poor proliferative ability of HIV-specific T cells; however, the connection between the two is not clear. Myeloid-derived suppressor cells (MDSC), which expand during states of elevated circulating inflammatory cytokines, may link the systemic inflammation and poor T cell function characteristic of lentiviral infections.
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