Virus-host metabolic interaction: SGIV-induced protein lactylation suppresses viral propagation.

The prevention and cure of Singapore grouper iridovirus (SGIV) was remained a challenging issue, primarily due to our limited understanding of the interaction mechanisms between SGIV and the host. This study investigated the metabolic and protein modification changes in grouper spleen (GS) cells following SGIV infection. SGIV infection induced significant lactate accumulation and up-regulated protein lactylation levels in GS cells at 12 hours post-infection. Transcriptomic analysis revealed that SGIV infection led to host cell metabolic reprogramming, characterized by marked up-regulation of oxidative phosphorylation-related genes alongside dysregulated immune modulation. Proteomic analysis further demonstrated that SGIV infection up-regulated proteins involved in stress-response and immunomodulatory signaling pathways (e.g., AMPK, HIF-1, TGF-β), while proteins associated with fundamental metabolic pathways were generally down-regulated. Lactyl-proteomic analysis showed that SGIV infection induced widespread lactylation modifications on key proteins, including CaM, MEK1/2, ERK1/2, Hsp90, Hsp70, etc., which indicated that lactylation plays a crucial role in systematically reprogramming host cell functions during viral infection. Functional experiments confirmed that exogenous lactate, at concentrations non-cytotoxic to GS cells, significantly inhibited SGIV replication and also exhibited broad-spectrum antibacterial activity. In summary, SGIV infection regulated host immune responses, metabolic adaptation, and signal transduction by remodeling lactate metabolism and inducing protein lactylation, while lactate itself possesses dual biological functions as both an antiviral and an antibacterial agent.

• Publication year

  2026

• Venue

  Fish and Shellfish Immunology

• Publication date

  2026-03-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.fsi.2026.111258PMID 41794158
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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