JCI Insight (Dec 2022)

Bamlanivimab therapy for acute COVID-19 does not blunt SARS-CoV-2–specific memory T cell responses

  • Sydney I. Ramirez,
  • Alba Grifoni,
  • Daniela Weiskopf,
  • Urvi M. Parikh,
  • Amy Heaps,
  • Farhoud Faraji,
  • Scott F. Sieg,
  • Justin Ritz,
  • Carlee Moser,
  • Joseph J. Eron,
  • Judith S. Currier,
  • Paul Klekotka,
  • Alessandro Sette,
  • David A. Wohl,
  • Eric S. Daar,
  • Michael D. Hughes,
  • Kara W. Chew,
  • Davey M. Smith,
  • Shane Crotty,
  • for the Accelerating COVID-19 Therapeutic Interventions and Vaccines–2/A5401 (ACTIV-2/A5401) Study Team

Journal volume & issue
Vol. 7, no. 24

Abstract

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Despite the widespread use of SARS-CoV-2–specific monoclonal antibody (mAb) therapy for the treatment of acute COVID-19, the impact of this therapy on the development of SARS-CoV-2–specific T cell responses has been unknown, resulting in uncertainty as to whether anti–SARS-CoV-2 mAb administration may result in failure to generate immune memory. Alternatively, it has been suggested that SARS-CoV-2–specific mAb may enhance adaptive immunity to SARS-CoV-2 via a “vaccinal effect.” Bamlanivimab (Eli Lilly and Company) is a recombinant human IgG1 that was granted FDA emergency use authorization for the treatment of mild to moderate COVID-19 in those at high risk for progression to severe disease. Here, we compared SARS-CoV-2–specific CD4+ and CD8+ T cell responses of 95 individuals from the ACTIV-2/A5401 clinical trial 28 days after treatment with bamlanivimab versus placebo. SARS-CoV-2–specific T cell responses were evaluated using activation-induced marker assays in conjunction with intracellular cytokine staining. We demonstrate that most individuals with acute COVID-19 developed SARS-CoV-2–specific T cell responses. Overall, our findings suggest that the quantity and quality of SARS-CoV-2–specific T cell memory were not diminished in individuals who received bamlanivimab for acute COVID-19. Receipt of bamlanivimab during acute COVID-19 neither diminished nor enhanced SARS-CoV-2–specific cellular immunity.

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