Evidence map›Paper›PMID 38133292›Full record

ArticlePathogens (Basel, Switzerland)2023

The Therapeutic Monoclonal Antibody Bamlanivimab Does Not Enhance SARS-CoV-2 Infection by FcR-Mediated Mechanisms.

Robert W Cross, Christopher M Wiethoff, Patricia Brown-Augsburger, Shawn Berens, Jamie Blackbourne, Ling Liu, Xiaohua Wu, Jonathan Tetreault, Carter Dodd, Ramtin Sina and 20 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathogens (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. [Human monkeypox (Mpox)].Dermatologie (Heidelberg, Germany) · 2024
    Review
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

30 authors at 5 institutions in 1 country.

Robert W CrossDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Christopher M WiethoffEli Lilly and Company, Indianapolis, IN 46285, USA.
Patricia Brown-AugsburgerEli Lilly and Company, Indianapolis, IN 46285, USA.
Shawn BerensEli Lilly and Company, Indianapolis, IN 46285, USA.
Jamie BlackbourneEli Lilly and Company, Indianapolis, IN 46285, USA.
Ling LiuEli Lilly and Company, Indianapolis, IN 46285, USA.
Xiaohua WuEli Lilly and Company, Indianapolis, IN 46285, USA.
Jonathan TetreaultEli Lilly and Company, Indianapolis, IN 46285, USA.
Carter DoddEli Lilly and Company, Indianapolis, IN 46285, USA.
Ramtin SinaEli Lilly and Company, Indianapolis, IN 46285, USA.
Derrick R WitcherEli Lilly and Company, Indianapolis, IN 46285, USA.
Deanna NewcombCharles River Laboratories, Inc., Reno, NV 89511, USA.
Denzil FrostCharles River Laboratories, Inc., Reno, NV 89511, USA.
Angela WilcoxCharles River Laboratories, Inc., Reno, NV 89511, USA.
Viktoriya BorisevichDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Krystle N AgansDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Courtney WoolseyDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0003-3389-0137
Abhishek N PrasadDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0002-4147-2077
Daniel J DeerDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Joan B GeisbertDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Natalie S DobiasDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Karla A FentonDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Beth StriflerEli Lilly and Company, Indianapolis, IN 46285, USA.
Philip EbertEli Lilly and Company, Indianapolis, IN 46285, USA.
Richard HiggsEli Lilly and Company, Indianapolis, IN 46285, USA.
Anne BeallImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Sumit ChandaDepartment of Immunology and Microbiology, Scripps Research, La Jolla, CA 92037, USA.
Laura RivaImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.ORCID 0000-0003-2414-7341
Xin YinImmunity and Pathogenesis Program, Infectious and Inflammatory Disease Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.ORCID 0000-0003-2357-6718
Thomas W GeisbertDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0003-0858-1877
Eli Lilly (United States) · USThe University of Texas Medical Branch at Galveston · USCharles River Laboratories (United States) · USSanford Burnham Prebys Medical Discovery Institute · USScripps Institution of Oceanography · US

Funding

Regulatory Compliance Core - Galveston National Laboratory BSL4 OperationsUC7AI094660 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI Gene Garrard Olinger · 2011 to 2026
$208.8M
NIAID NIH HHS UC7 AI094660
6 · The paper itself

Abstract

As part of the non-clinical safety package characterizing bamlanivimab (SARS-CoV-2 neutralizing monoclonal antibody), the risk profile for antibody-dependent enhancement of infection (ADE) was evaluated in vitro and in an African green monkey (AGM) model of COVID-19. In vitro ADE assays in primary human macrophage, Raji, or THP-1 cells were used to evaluate enhancement of viral infection. Bamlanivimab binding to C1q, FcR, and cell-based effector activity was also assessed. In AGMs, the impact of bamlanivimab pretreatment on viral loads and clinical and histological pathology was assessed to evaluate enhanced SARS-CoV-2 replication or pathology. Bamlanivimab did not increase viral replication in vitro, despite a demonstrated effector function. In vivo, no significant differences were found among the AGM groups for weight, temperature, or food intake. Treatment with bamlanivimab reduced viral loads in nasal and oral swabs and BAL fluid relative to control groups. Viral antigen was not detected in lung tissue from animals treated with the highest dose of bamlanivimab. Bamlanivimab did not induce ADE of SARS-CoV-2 infection in vitro or in an AGM model of infection at any dose evaluated. The findings suggest that high-affinity monoclonal antibodies pose a low risk of mediating ADE in patients and support their safety profile as a treatment of COVID-19 disease.

Indexed as

antibody-dependent enhancementbamlanivimabCOVID-19monoclonal antibodiesSARS-CoV-2

Identifiers

PMID38133292
PMCPMC10746090
OpenAlexW4389203890

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.