PUBLICATION

The Spike protein of SARS-CoV-2 signals via Tlr2 in zebrafish

Authors
Tyrkalska, S.D., Martínez-López, A., Pedoto, A., Candel, S., Cayuela, M.L., Mulero, V.
ID
ZDB-PUB-230102-4
Date
2022
Source
Developmental and comparative immunology   140: 104626 (Journal)
Registered Authors
Mulero, Victor
Keywords
Hematopoiesis, Inflammation, Interleukin-1, Spike protein, TLRs, Zebrafish
MeSH Terms
  • Animals
  • COVID-19*/immunology
  • Myeloid Differentiation Factor 88/genetics
  • SARS-CoV-2
  • Spike Glycoprotein, Coronavirus*
  • Toll-Like Receptor 2*/genetics
  • Zebrafish/genetics
PubMed
36587712 Full text @ Dev. Comp. Immunol.
Abstract
One of the most studied defense mechanisms against invading pathogens, including viruses, are Toll-like receptors (TLRs). Among them, TLR3, TLR7, TLR8 and TLR9 detect different forms of viral nucleic acids in endosomal compartments, whereas TLR2 and TLR4 recognize viral structural and nonstructural proteins outside the cell. Although many different TLRs have been shown to be involved in SARS-CoV-2 infection and detection of different structural proteins, most studies have been performed in vitro and the results obtained are rather contradictory. In this study, we report using the unique advantages of the zebrafish model for in vivo imaging and gene editing that the S1 domain of the Spike protein from the Wuhan strain (S1WT) induced hyperinflammation in zebrafish larvae via a Tlr2/Myd88 signaling pathway and independently of interleukin-1β production. In addition, S1WT also triggered emergency myelopoiesis, but in this case through a Tlr2/Myd88-independent signaling pathway. These results shed light on the mechanisms involved in the fish host responses to viral proteins.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping