Evidence map›Paper›PMID 40627384›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

Optimization of a sarbecovirus llama nanobody-antigen binding interface via a combined computational and phage display protein engineering approach.

Kevin E Ramos, Prithviraj Nandigrami, Ahmad Najafian, Jonathan R Lai, Andras Fiser

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Kevin E Ramos *Department of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461.
Prithviraj Nandigrami *Department of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461.ORCID 0000-0002-2269-9292
Ahmad NajafianDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461.ORCID 0000-0003-3802-8538
Jonathan R LaiDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461.ORCID 0000-0002-4863-0015
Andras FiserDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY 10461.ORCID 0000-0003-0085-5335

Funding

Geographic Medicine and Emerging InfectionsT32AI070117 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WEISS, LOUIS M. · 2008 to 2023
$5.1M
Molecular basis of recognition in the Immunological SynapseR35GM136357 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI FISER, ANDRAS · 2020 to 2024
$2.7M
Interdisciplinary protein engineering approach to design high affinity antibodies for flavivirusesR01AI141816 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI FISER, ANDRAS · 2019 to 2023
$2.1M
HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI141816HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) T32-AI070117HHS | NIH | National Institute of General Medical Sciences (NIGMS) GM136357NIAID NIH HHS R01 AI141816NIAID NIH HHS T32 AI070117NIGMS NIH HHS R35 GM136357
6 · The paper itself

Abstract

Single-domain antibodies, such as variable heavy domain of heavy chain (VHH) domains from camelids, are an attractive platform for therapeutic purposes. VHHs have a smaller size than traditional antibodies, which harbors certain advantages such as tissue penetration or accessing epitopes that may be shielded by protein domains. However, the smaller size of VHHs typically involves a smaller binding site, which can limit the scope of related antigens they are able to bind and, in the specific case of antiviral VHHs, render them susceptible to escape by a single point mutation. Here, we present a combined computational and experimental protein engineering approach to broaden the reactivity of SARS-CoV-1 receptorbinding domain (RBD)-specific VHH-72 for SARS-CoV-2 and Delta. Our strategy focuses on increasing the size of the binding site by imparting "second site" interactions toward heterologous antigens. We utilized the residue-based pharmacophore modeling approach, Protein-ligandinterface design (ProtLID), to identify potential productive side chain interactions in this second site and then encoded the ProtLID-predicted restricted diversity into a VHH-72-based phage library, which we then screened for cross-reactive SARS-CoV-1/2 RBD clones. Based on sequence analysis from the resulting population of functional VHH clones, we identified a VHH-72 triple mutant (T60P.D61P.D100eY), which maintained high affinity for SARS-CoV-1 RBD but was enhanced by 18- and 20-fold for RBDs from SARS-CoV-2 and Delta relative to WT VHH-72. These results highlight the potential of computationally customizing phage display diversity for single-domain binding proteins and provide a strategy for designing extension of protein binding interfaces.

Indexed as

Protein EngineeringSingle-Domain AntibodiesAnimalsAntibodies, ViralBinding SitesBinding Sites, AntibodyCamelids, New WorldCOVID-19HumansPeptide LibraryProtein BindingSARS-CoV-2Spike Glycoprotein, CoronavirusAntibodies, ViralPeptide LibrarySingle-Domain AntibodiesSpike Glycoprotein, Coronavirusantibody engineeringphage displayprotein engineeringresidue-based pharmacophore

Identifiers

PMID40627384
PMCPMC12280912

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LicenceCC BY-NC-ND
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Registered trials

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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.