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Trim2b mediates protection against SVCV infection by degrading NLRP12-like and viral SVCV-N/SVCV-G proteins

ABSTRACT: In the present study, we report the functional characterization of zebrafish trim2b. we show that zebrafish trim2b plays a protective role in the host defense against SVCV infection. During SVCV infection, the in vivo studies revealed that trim2b overexpression led to the decreased virus loads and increased survival rate. Zebrafish trim2b deficiency led to the increased virus loads and decreased survival rate. In addition, Zebrafish trim2b deficiency leads higher numbers of immune related DEGs and signaling pathways enriched during the SVCV infection or uninfection. Among them, NOD-like receptor signaling pathway was significantly enriched. The present study characterized two NLRs degraded by trim2b plays a negative role in the host defense against SVCV infection.

ORGANISM(S): Danio rerio

PROVIDER: GSE232313 | GEO | 2024/04/26

REPOSITORIES: GEO

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Project description:In the last years, the innate immune response has gained importance since evidences indicate that, after an adequate priming protocol, it is possible to obtain some prolonged and enhanced immune response. Nevertheless, several factors, such as timing and method of administration of the immunostimulants need to be carefully considered. An inappropriate protocol can transform the treatments into a double-edged sword for the teleost immune system, resulting in a stressful and immunosuppressive status. In this work, we analyzed the long-term effect of different stimuli (β-glucans, lipopolysaccharide and Polyinosinic:polycytidylic acid) on the transcriptome modulation induced by Spring Viraemia Carp Virus (SVCV) in adult zebrafish (Danio rerio) and on the mortalities caused by this infection. At 35 days post-immunostimulation the transcriptome was found to be highly altered compared to the control fish, and these stimuli also conditioned the response to SVCV challenge, especially in the case of β-glucans. No protection against SVCV was found with any of the stimuli and even non-significant higher mortalities were observed, especially with β-glucans. However, at short-term (a pre-stimulation with β-glucan and infection after 7 days) a slight protection was observed after infection. The transcriptome response in zebrafish kidney at 35 days post-treatment with β-glucans revealed a significant response associated to stress and immunosuppression. The identification of genes differentially expressed before and after the infection seem to indicate a high energy cost of the immunostimulation prolonged in time that could explain the lack of protection against the SVCV. The differential response to stress, alterations in the lipid metabolism, the tryptophan-kynurenine pathway and the interferon-gamma signaling seem to be some of the mechanisms involved in this particular response, which means the end of the trained immunity and the beginning of a stressful status characterized by immunosuppression.

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Trim2b mediates protection against SVCV infection by degrading NLRP12-like and viral SVCV-N/SVCV-G proteins

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