Title

Expression of SARS coronavirus 1 spike protein from a herpesviral vector induces innate immune signaling and neutralizing antibody responses

UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology; MassBiologics

Publication Date

2021-04-21

Document Type

Article

Disciplines

Amino Acids, Peptides, and Proteins | Immunology of Infectious Disease | Infectious Disease | Virology | Virus Diseases

Abstract

SARS coronavirus 1 (SARS-CoV-1) causes a respiratory infection that can lead to acute respiratory distress characterized by inflammation and high levels of cytokines in the lung tissue. In this study we constructed a herpes simplex virus 1 replication-defective mutant vector expressing SARS-CoV-1 spike protein as a potential vaccine vector and to probe the effects of spike protein on host cells. The spike protein expressed from this vector is functional in that it localizes to the surface of infected cells and induces fusion of ACE2-expressing cells. In immunized mice, the recombinant vector induced antibodies that bind to spike protein in an ELISA assay and that show neutralizing activity. The spike protein expressed from this vector can induce the expression of cytokines in an ACE2-independent, MyD88-dependent process. These results argue that the SARS-CoV-1 spike protein intrinsically activates signaling pathways that induce cytokines and contribute directly to the inflammatory process of SARS.

Keywords

Cytokines, Herpes simplex virus, SARS coronavirus

DOI of Published Version

10.1016/j.virol.2021.04.006

Source

Kurt-Jones EA, Dudek TE, Watanabe D, Mandell L, Che J, Zhou S, Cao L, Greenough T, Babcock GJ, Diaz F, Oh HS, Zhou C, Finberg RW, Knipe DM. Expression of SARS coronavirus 1 spike protein from a herpesviral vector induces innate immune signaling and neutralizing antibody responses. Virology. 2021 Apr 21;559:165-172. doi: 10.1016/j.virol.2021.04.006. Epub ahead of print. PMID: 33930819; PMCID: PMC8058630. Link to article on publisher's site

Journal/Book/Conference Title

Virology

Related Resources

Link to Article in PubMed

PubMed ID

33930819

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