Necroptosis-based CRISPR knockout screen reveals Neuropilin-1 as a critical host factor for early stages of murine cytomegalovirus infection.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
18 08 2020
Historique:
pubmed: 5 8 2020
medline: 7 10 2020
entrez: 5 8 2020
Statut: ppublish

Résumé

Herpesviruses are ubiquitous human pathogens that cause a wide range of health complications. Currently, there is an incomplete understanding of cellular factors that contribute to herpesvirus infection. Here, we report an antiviral necroptosis-based genetic screen to identify novel host cell factors required for infection with the β-herpesvirus murine cytomegalovirus (MCMV). Our genome-wide CRISPR-based screen harnessed the capacity of herpesvirus mutants that trigger antiviral necroptotic cell death upon early viral gene expression. Vascular endothelial growth factor (VEGF) and semaphorin-binding receptor Neuropilin-1 (Nrp-1) emerge as crucial determinants of MCMV infection. We find that elimination of Nrp-1 impairs early viral gene expression and reduces infection rates in endothelial cells, fibroblasts, and macrophages. Furthermore, preincubation of virus with soluble Nrp-1 dramatically inhibits infection by reducing virus attachment. Thus, Nrp-1 is a key determinant of the initial phase of MCMV infection.

Identifiants

pubmed: 32747526
pii: 1921315117
doi: 10.1073/pnas.1921315117
pmc: PMC7443917
doi:

Substances chimiques

Neuropilin-1 144713-63-3

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

20109-20116

Subventions

Organisme : NIDCR NIH HHS
ID : T32 DE014318
Pays : United States
Organisme : NIH HHS
ID : DP5 OD012198
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI141970
Pays : United States
Organisme : NIDCR NIH HHS
ID : F31 DE029395
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI020211
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA054174
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001120
Pays : United States

Déclaration de conflit d'intérêts

The authors declare no competing interest.

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Auteurs

Rebecca K Lane (RK)

Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health at San Antonio, San Antonio, TX 78229.

Hongyan Guo (H)

Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, GA 30303; hguo@gsu.edu wkaiser@inzentx.com.

Amanda D Fisher (AD)

Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health at San Antonio, San Antonio, TX 78229.

Jonathan Diep (J)

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305.

Zhao Lai (Z)

Department of Molecular Medicine, University of Texas Health at San Antonio, San Antonio, TX 78229.
Greehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX 78229.

Yidong Chen (Y)

Greehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX 78229.
Department of Epidemiology and Biostatistics, University of Texas Health at San Antonio, San Antonio, TX 78229.

Jason W Upton (JW)

Department of Biological Sciences, Auburn University, Auburn, AL 36849.

Jan Carette (J)

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305.

Edward S Mocarski (ES)

Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322.

William J Kaiser (WJ)

Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health at San Antonio, San Antonio, TX 78229; hguo@gsu.edu wkaiser@inzentx.com.

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