Avian deltacoronaviruses encode fusion-associated small transmembrane proteins that can induce syncytia formation.

Coronavirus Deltacoronavirus FAST protein Fusogen Reovirus Rotavirus Syncytia

Journal

Virology
ISSN: 1096-0341
Titre abrégé: Virology
Pays: United States
ID NLM: 0110674

Informations de publication

Date de publication:
09 Oct 2024
Historique:
received: 16 08 2024
revised: 25 09 2024
accepted: 07 10 2024
medline: 16 10 2024
pubmed: 16 10 2024
entrez: 15 10 2024
Statut: aheadofprint

Résumé

Fusion-associated small transmembrane (FAST) proteins are nonstructural viral proteins that induce cell-cell fusion. FAST proteins, which previously were identified in the genomes of double-stranded RNA viruses, typically contain an acylated N-terminal ectodomain, central transmembrane domain, and C-terminal endodomain with a polybasic region. Using sequence homology and protein motif prediction, we identified accessory proteins in a subset of avian deltacoronaviruses as putative FAST proteins. Transient expression of thrush coronavirus NS7b or common moorhen coronavirus NS7a, but not night heron coronavirus NS7b, induced cell-cell fusion. Syncytia were detected in primate kidney epithelial cells or fibroblasts but not chicken embryo fibroblasts, and addition of an N-terminal FLAG peptide to the proteins ablated fusion activity. These findings suggest that multiple avian deltacoronaviruses, positive-sense RNA viruses, encode nonstructural proteins that can mediate cell-cell fusion and share features with known FAST proteins. Additional studies are needed to understand contributions of these proteins to deltacoronavirus biology.

Identifiants

pubmed: 39406032
pii: S0042-6822(24)00279-4
doi: 10.1016/j.virol.2024.110258
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110258

Informations de copyright

Copyright © 2024 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Kylie Sartalamacchia (K)

Department of Pediatrics, Vanderbilt University Medical Center, 2200 Children's Way, Suite 2404, Nashville, TN, 37232, USA. Electronic address: k.sartalamacchia@vumc.org.

Monique S Porter (MS)

Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Medical Center North, 1161 21st Ave. South, Suite D-2220, Nashville, TN, 37232, USA.

Vanesa Veletanlic (V)

Department of Pediatrics, Vanderbilt University Medical Center, 2200 Children's Way, Suite 2404, Nashville, TN, 37232, USA.

Kristen M Ogden (KM)

Department of Pediatrics, Vanderbilt University Medical Center, 2200 Children's Way, Suite 2404, Nashville, TN, 37232, USA; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Medical Center North, 1161 21st Ave. South, Suite D-2220, Nashville, TN, 37232, USA. Electronic address: kristen.ogden@vumc.org.

Classifications MeSH