Variant-proof high affinity ACE2 antagonist limits SARS-CoV-2 replication in upper and lower airways

SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would main...

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Published inNature communications Vol. 15; no. 1; pp. 6894 - 13
Main Authors Gagne, Matthew, Flynn, Barbara J., Honeycutt, Christopher Cole, Flebbe, Dillon R., Andrew, Shayne F., Provost, Samantha J., McCormick, Lauren, Van Ry, Alex, McCarthy, Elizabeth, Todd, John-Paul M., Bao, Saran, Teng, I-Ting, Marciano, Shir, Rudich, Yinon, Li, Chunlin, Jain, Shilpi, Wali, Bushra, Pessaint, Laurent, Dodson, Alan, Cook, Anthony, Lewis, Mark G., Andersen, Hanne, Zahradník, Jiří, Suthar, Mehul S., Nason, Martha C., Foulds, Kathryn E., Kwong, Peter D., Roederer, Mario, Schreiber, Gideon, Seder, Robert A., Douek, Daniel C.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 12.08.2024
Nature Publishing Group
Nature Portfolio
Subjects
13/1
13/106
13/31
38/88
631/154
631/250/24
631/250/255/2514
631/250/347
631/326/596/4130
64
ACE2
Affinity
Angiotensin-converting enzyme 2
Angiotensin-Converting Enzyme 2 - antagonists & inhibitors
Animal models
Animals
Antiviral agents
Antiviral Agents - pharmacology
Antiviral drugs
Binding
Chlorocebus aethiops
COVID-19
COVID-19 - immunology
COVID-19 - prevention & control
COVID-19 - virology
COVID-19 Drug Treatment
Disease Models, Animal
Drug efficacy
Effectiveness
Evolution
Humanities and Social Sciences
Humans
Immunity
Inhalation
Lymphocytes B
Macaca mulatta
Male
multidisciplinary
Pharmacology
Protein folding
Proteins
Replication
Respiration
SARS-CoV-2 - drug effects
SARS-CoV-2 - immunology
SARS-CoV-2 - physiology
Science
Science (multidisciplinary)
Severe acute respiratory syndrome coronavirus 2
Spike Glycoprotein, Coronavirus - genetics
Spike Glycoprotein, Coronavirus - immunology
Spike Glycoprotein, Coronavirus - metabolism
Vaccines
Vero Cells
Viral diseases
Virus Replication - drug effects
Viruses
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Abstract SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta—the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant. SARS-CoV-2 evolution poses a risk to vaccine and antiviral drug efficacy. Here, Gagne et al. report the development of a variant-agnostic protein, RBD-62, with enhanced ACE2 binding obtained through in vitro evolution and show that RBD-62 inhalation protects nonhuman primates against SARS-CoV-2 Delta challenge.
AbstractList SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta—the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant.
SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta—the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant. SARS-CoV-2 evolution poses a risk to vaccine and antiviral drug efficacy. Here, Gagne et al. report the development of a variant-agnostic protein, RBD-62, with enhanced ACE2 binding obtained through in vitro evolution and show that RBD-62 inhalation protects nonhuman primates against SARS-CoV-2 Delta challenge.
SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta-the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant.SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta-the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant.
SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta—the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant.SARS-CoV-2 evolution poses a risk to vaccine and antiviral drug efficacy. Here, Gagne et al. report the development of a variant-agnostic protein, RBD-62, with enhanced ACE2 binding obtained through in vitro evolution and show that RBD-62 inhalation protects nonhuman primates against SARS-CoV-2 Delta challenge.
Abstract SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent that protects against severe disease without putting selective pressure on the virus would thus be a valuable biomedical tool that would maintain its efficacy despite the ongoing emergence of new variants. Here, we challenge male rhesus macaques with SARS-CoV-2 Delta—the most pathogenic variant in a highly susceptible animal model. At the time of challenge, we also treat the macaques with aerosolized RBD-62, a protein developed through multiple rounds of in vitro evolution of SARS-CoV-2 RBD to acquire 1000-fold enhanced ACE2 binding affinity. RBD-62 treatment equivalently suppresses virus replication in both upper and lower airways, a phenomenon not previously observed with clinically approved vaccines. Importantly, RBD-62 does not block the development of virus-specific T- and B-cell responses and does not elicit anti-drug immunity. These data provide proof-of-concept that RBD-62 can prevent severe disease from a highly virulent variant.
ArticleNumber 6894
Author Douek, Daniel C.
Todd, John-Paul M.
Suthar, Mehul S.
Wali, Bushra
Li, Chunlin
Dodson, Alan
Flebbe, Dillon R.
Van Ry, Alex
Schreiber, Gideon
Kwong, Peter D.
Roederer, Mario
Jain, Shilpi
Pessaint, Laurent
Provost, Samantha J.
Seder, Robert A.
McCormick, Lauren
Marciano, Shir
Teng, I-Ting
McCarthy, Elizabeth
Bao, Saran
Flynn, Barbara J.
Andrew, Shayne F.
Foulds, Kathryn E.
Gagne, Matthew
Cook, Anthony
Rudich, Yinon
Andersen, Hanne
Lewis, Mark G.
Zahradník, Jiří
Nason, Martha C.
Honeycutt, Christopher Cole
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/39134521$$D View this record in MEDLINE/PubMed
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CitedBy_id crossref_primary_10_3390_v17020143
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– reference: 37503026 - bioRxiv. 2023 Jun 12:2023.06.09.544432. doi: 10.1101/2023.06.09.544432
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Score 2.455191
Snippet SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic therapeutic agent...
Abstract SARS-CoV-2 has the capacity to evolve mutations that escape vaccine- and infection-acquired immunity and antiviral drugs. A variant-agnostic...
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SubjectTerms 13/1
13/106
13/31
38/88
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631/250/24
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631/250/347
631/326/596/4130
64
ACE2
Affinity
Angiotensin-converting enzyme 2
Angiotensin-Converting Enzyme 2 - antagonists & inhibitors
Animal models
Animals
Antiviral agents
Antiviral Agents - pharmacology
Antiviral drugs
Binding
Chlorocebus aethiops
COVID-19
COVID-19 - immunology
COVID-19 - prevention & control
COVID-19 - virology
COVID-19 Drug Treatment
Disease Models, Animal
Drug efficacy
Effectiveness
Evolution
Humanities and Social Sciences
Humans
Immunity
Inhalation
Lymphocytes B
Macaca mulatta
Male
multidisciplinary
Pharmacology
Protein folding
Proteins
Replication
Respiration
SARS-CoV-2 - drug effects
SARS-CoV-2 - immunology
SARS-CoV-2 - physiology
Science
Science (multidisciplinary)
Severe acute respiratory syndrome coronavirus 2
Spike Glycoprotein, Coronavirus - genetics
Spike Glycoprotein, Coronavirus - immunology
Spike Glycoprotein, Coronavirus - metabolism
Vaccines
Vero Cells
Viral diseases
Virus Replication - drug effects
Viruses
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Title Variant-proof high affinity ACE2 antagonist limits SARS-CoV-2 replication in upper and lower airways
URI https://link.springer.com/article/10.1038/s41467-024-51046-w
https://www.ncbi.nlm.nih.gov/pubmed/39134521
https://www.proquest.com/docview/3092133902
https://www.proquest.com/docview/3092365235
https://pubmed.ncbi.nlm.nih.gov/PMC11319446
https://doaj.org/article/398a2dfd9ac6483f881f1a81f6f17840
Volume 15
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