Chemical proteomics tracks virus entry and uncovers NCAM1 as Zika virus receptor

The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host ce...

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Published inNature communications Vol. 11; no. 1; pp. 3896 - 10
Main Authors Srivastava, Mayank, Zhang, Ying, Chen, Jian, Sirohi, Devika, Miller, Andrew, Zhang, Yang, Chen, Zhilu, Lu, Haojie, Xu, Jianqing, Kuhn, Richard J., Andy Tao, W.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 04.08.2020
Nature Publishing Group
Nature Portfolio
Subjects
631/326/596/2557
631/45/475
631/92/96
82/58
96
Animals
Biotin
CD56 Antigen - genetics
CD56 Antigen - metabolism
Cell adhesion
Cell adhesion & migration
Cell adhesion molecules
Cell Line, Tumor
Chlorocebus aethiops
Gene Knockout Techniques
Glioblastoma
Glioblastoma cells
HEK293 Cells
Host-Pathogen Interactions - physiology
Humanities and Social Sciences
Humans
Internalization
multidisciplinary
Neural cell adhesion molecule
Neural Cell Adhesion Molecules - genetics
Neural Cell Adhesion Molecules - metabolism
Proteins
Proteomics
Receptors
Receptors, Virus - metabolism
Science
Science (multidisciplinary)
Spectrometry
Tracks (paths)
Ultraviolet radiation
Vector-borne diseases
Vero Cells
Viral Proteins - metabolism
Virus Attachment
Virus Internalization
Virus Replication - physiology
Viruses
Zika virus
Zika Virus - physiology
Zika Virus Infection - virology
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Abstract The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host cells. ZIKV was labeled on its surface with a chemical probe, which carries a photocrosslinker to covalently link virus-interacting proteins in living cells on UV exposure at different time points, and a biotin tag for subsequent enrichment and mass spectrometric identification of the receptor or other host proteins critical for virus internalization. We identified Neural Cell Adhesion Molecule (NCAM1) as a potential ZIKV receptor and further validated it through overexpression, knockout, and inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG. Collectively, the strategy can serve as a universal tool to map virus entry pathways and uncover key interacting proteins. The mechanism underlying the cellular entry of Zika virus is not fully understood. Here, the authors use a chemically modified virus and time-resolved proteomics to capture interacting host proteins during virus entry and identify NCAM1 as a ZIKV receptor.
AbstractList The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host cells. ZIKV was labeled on its surface with a chemical probe, which carries a photocrosslinker to covalently link virus-interacting proteins in living cells on UV exposure at different time points, and a biotin tag for subsequent enrichment and mass spectrometric identification of the receptor or other host proteins critical for virus internalization. We identified Neural Cell Adhesion Molecule (NCAM1) as a potential ZIKV receptor and further validated it through overexpression, knockout, and inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG. Collectively, the strategy can serve as a universal tool to map virus entry pathways and uncover key interacting proteins.The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host cells. ZIKV was labeled on its surface with a chemical probe, which carries a photocrosslinker to covalently link virus-interacting proteins in living cells on UV exposure at different time points, and a biotin tag for subsequent enrichment and mass spectrometric identification of the receptor or other host proteins critical for virus internalization. We identified Neural Cell Adhesion Molecule (NCAM1) as a potential ZIKV receptor and further validated it through overexpression, knockout, and inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG. Collectively, the strategy can serve as a universal tool to map virus entry pathways and uncover key interacting proteins.
The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host cells. ZIKV was labeled on its surface with a chemical probe, which carries a photocrosslinker to covalently link virus-interacting proteins in living cells on UV exposure at different time points, and a biotin tag for subsequent enrichment and mass spectrometric identification of the receptor or other host proteins critical for virus internalization. We identified Neural Cell Adhesion Molecule (NCAM1) as a potential ZIKV receptor and further validated it through overexpression, knockout, and inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG. Collectively, the strategy can serve as a universal tool to map virus entry pathways and uncover key interacting proteins. The mechanism underlying the cellular entry of Zika virus is not fully understood. Here, the authors use a chemically modified virus and time-resolved proteomics to capture interacting host proteins during virus entry and identify NCAM1 as a ZIKV receptor.
The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host cells. ZIKV was labeled on its surface with a chemical probe, which carries a photocrosslinker to covalently link virus-interacting proteins in living cells on UV exposure at different time points, and a biotin tag for subsequent enrichment and mass spectrometric identification of the receptor or other host proteins critical for virus internalization. We identified Neural Cell Adhesion Molecule (NCAM1) as a potential ZIKV receptor and further validated it through overexpression, knockout, and inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG. Collectively, the strategy can serve as a universal tool to map virus entry pathways and uncover key interacting proteins.
The mechanism underlying the cellular entry of Zika virus is not fully understood. Here, the authors use a chemically modified virus and time-resolved proteomics to capture interacting host proteins during virus entry and identify NCAM1 as a ZIKV receptor.
The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and developing therapeutic strategies. Here, we present a time-resolved chemical proteomic strategy to track the early-stage entry of ZIKV into host cells. ZIKV was labeled on its surface with a chemical probe, which carries a photocrosslinker to covalently link virus-interacting proteins in living cells on UV exposure at different time points, and a biotin tag for subsequent enrichment and mass spectrometric identification of the receptor or other host proteins critical for virus internalization. We identified Neural Cell Adhesion Molecule (NCAM1) as a potential ZIKV receptor and further validated it through overexpression, knockout, and inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG. Collectively, the strategy can serve as a universal tool to map virus entry pathways and uncover key interacting proteins.The mechanism underlying the cellular entry of Zika virus is not fully understood. Here, the authors use a chemically modified virus and time-resolved proteomics to capture interacting host proteins during virus entry and identify NCAM1 as a ZIKV receptor.
ArticleNumber 3896
Author Zhang, Yang
Chen, Zhilu
Kuhn, Richard J.
Srivastava, Mayank
Zhang, Ying
Lu, Haojie
Chen, Jian
Miller, Andrew
Xu, Jianqing
Sirohi, Devika
Andy Tao, W.
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  organization: Department of Chemistry, Purdue University, Department of Biochemistry, Purdue University, Purdue Institute of Inflammation, Immunology and Infectious Disease, Purdue University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32753727$$D View this record in MEDLINE/PubMed
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SSID ssj0000391844
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Snippet The outbreak of Zika virus (ZIKV) in 2016 created worldwide health emergency which demand urgent research efforts on understanding the virus biology and...
The mechanism underlying the cellular entry of Zika virus is not fully understood. Here, the authors use a chemically modified virus and time-resolved...
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pubmedcentral
proquest
pubmed
crossref
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SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 3896
SubjectTerms 631/326/596/2557
631/45/475
631/92/96
82/58
96
Animals
Biotin
CD56 Antigen - genetics
CD56 Antigen - metabolism
Cell adhesion
Cell adhesion & migration
Cell adhesion molecules
Cell Line, Tumor
Chlorocebus aethiops
Gene Knockout Techniques
Glioblastoma
Glioblastoma cells
HEK293 Cells
Host-Pathogen Interactions - physiology
Humanities and Social Sciences
Humans
Internalization
multidisciplinary
Neural cell adhesion molecule
Neural Cell Adhesion Molecules - genetics
Neural Cell Adhesion Molecules - metabolism
Proteins
Proteomics
Receptors
Receptors, Virus - metabolism
Science
Science (multidisciplinary)
Spectrometry
Tracks (paths)
Ultraviolet radiation
Vector-borne diseases
Vero Cells
Viral Proteins - metabolism
Virus Attachment
Virus Internalization
Virus Replication - physiology
Viruses
Zika virus
Zika Virus - physiology
Zika Virus Infection - virology
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Title Chemical proteomics tracks virus entry and uncovers NCAM1 as Zika virus receptor
URI https://link.springer.com/article/10.1038/s41467-020-17638-y
https://www.ncbi.nlm.nih.gov/pubmed/32753727
https://www.proquest.com/docview/2430244875
https://www.proquest.com/docview/2430652925
https://pubmed.ncbi.nlm.nih.gov/PMC7403387
https://doaj.org/article/e083ebec23fd4782a7cf7d04711ee3c2
Volume 11
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