CiATG13 induces autophagy to regulate CiHSP70 to promote GCRV replication.

Identification and analysis of lncRNA50877, which is involved in KRT8-mediated mitochondrial homeostasis and GCRV replication in grass carp (Ctenopharyngodon idella).

It is demonstrated that lncRNA50877 disrupts mitochondrial homeostasis by negatively regulating KRT8 expression, thereby modulating ROS levels, apoptosis, and autophagy; promoting oxidative stress-induced cell injury; and providing favorable conditions for GCRV replication.

Grass Carp Reovirus ( GCRV ): Biology, Immune Responses and Control Strategies

As the world's population grows, aquaculture is becoming a rapidly growing source of protein. Grass carp ( Ctenopharyngodon idella ) is one of the most important aquacultured species in China and has emerged as a significant commercial fish worldwide. However, grass carp reovirus (GCRV) poses a significant threat to grass carp aquaculture. This review covers GCRV biology, phylogeny, pathogenesis, immune response pathways, therapeutic approaches, and future challenges and directions. A comprehensive phylogenetic analysis describes the structure of GCRV, its entry into cells, its molecular architecture, its replication procedures and its interactions with the host, with a particular focus on the pivotal role of Pattern Recognition Receptors (PRRs). The paper explores how PRRs, such as RLRs (RIG‐I and MDA5) and TLRs (TLR3 and TLR19), are essential for identifying GCRV and initiating robust antiviral responses, particularly the interferon pathway. The paper goes on to explain the complex immune evasion tactics employed by GCRV, emphasizing how viral proteins such as VP41, VP4 and VP56 selectively target and interfere with critical components of PRR signaling cascades, such as MAVS‐TBK1 and MITA/STING, thereby reducing host immunity. Various next‐generation vaccines are being developed, including DNA, subunit, VLP and oral/mucosal platforms. These are supported by Chinese herbal and chemical antivirals. According to CRISPR/Cas9, experimental RNAi, PI4KB and SOCS3a/3b are host genes that can be altered to increase grass carp resistance to GCRV. This research offers significant insights into viral cell invasion and strengthens innate and adaptive immunity, enabling safer, more practical and multilayered control in aquaculture.

Thioredoxin 1 inhibits GCRV replication by maintaining redox homeostasis in grass carp (Ctenopharyngodon idella).

Thioredoxin (Trx) is a conserved redox regulatory protein that plays critical roles in maintaining cellular redox homeostasis and immune defense. However, its molecular characteristics and antiviral functions in grass carp (Ctenopharyngodon idella) remain largely unknown. In this study, thioredoxin 1 (trx1) was cloned and functionally characterized. The full-length trx1 cDNA was 834 bp, containing a 324 bp open reading frame encoding a 107-amino-acid protein with the conserved Cys-Gly-Pro-Cys (CGPC) redox-active motif. Phylogenetic and structural analyses demonstrated that Trx1 was highly conserved among vertebrates. The trx1 transcripts were ubiquitously expressed in all tested tissues, with relatively high levels in the spleen and liver, and were significantly induced by lipopolysaccharide (LPS), polyinosinic-polycytidylic acid (poly I:C), and grass carp reovirus (GCRV) infection. Recombinant Trx1 was successfully expressed in Escherichia coli and enhanced bacterial resistance to H2O2-induced oxidative stress. Subcellular localization analysis detected Trx1-GFP signals in the cytoplasm and nucleus of C. idella kidney (CIK) cells, with obvious nuclear enrichment after H2O2 treatment and GCRV infection. Functional analyses demonstrated that trx1 overexpression alleviated oxidative stress, inflammation, and apoptosis, accompanied by reduced GCRV replication, whereas trx1 silencing produced the opposite effects. Collectively, these findings suggest that trx1 acts as an important antiviral regulator that maintains intracellular redox homeostasis and contributes to host protection against GCRV infection by limiting oxidative stress, apoptosis, and excessive inflammatory responses.

MicroRNAome of Spodoptera frugiperda in Response to SfMNPV Infection

RiLinc6978-encoded P6978 interacts with ASR1 to regulate ROS homeostasis.

Tomato (Solanum lycopersicum) fruit ripening is tightly associated with dynamic changes in reactive oxygen species (ROS) homeostasis, yet the underlying regulatory mechanisms remain incompletely understood. Here, we identify a functional protein, P6978, encoded by the long non-coding RNA RiLinc6978, which contains a conserved 333-nucleotides short open reading frame (sORF) with high translational potential. Structural and physicochemical analyses revealed that P6978 is a stable, hydrophilic 110-amino acid basic polypeptide. P6978 predominantly localizes to the nucleus and directly interacts with the abscisic acid/stress-ripening transcription factor ABA stress-ripening 1 (ASR1). Multi-modal interaction assays (in vitro and in vivo) demonstrated that P6978 binding modulates ASR1's transcriptional repression of antioxidant-related genes, thereby coordinately enhancing both enzymatic (such as superoxide dismutase, SOD; catalase, CAT; ascorbate peroxidase, APX; and glutathione reductase, GR) and non-enzymatic (ascorbate, glutathione, carotenoids, polyamines) ROS-scavenging systems during fruit maturation. Integrated transcriptomic and alternative splicing analyses revealed that loss of P6978 perturbs metabolic pathways linked to ROS metabolism, pigment biosynthesis, and stress responses. Our findings establish a previously unrecognized regulatory module in which a lncRNA-derived protein fine-tunes transcription factor output to optimize ROS homeostasis, accelerate tomato fruit ripening, and potentially improve postharvest stress resilience. This work expands the functional scope of plant lncRNAs and provides promising targets for horticultural crop improvement.

Integrated Lipidomic and Transcriptomic Analyses Reveal Stage-Specific Hepatic Lipid Remodeling during GCRV-II Infection in Grass Carp (Ctenopharyngodon idella).

Findings reveal temporally coordinated hepatic lipid metabolic reprogramming during GCRV-II infection and provide a foundation for further studies on how host lipid metabolism contributes to viral replication and pathogenesis.