Time-dependent hepatic immune-metabolic reprogramming in Channa argus under thermal stress: An integrated transcriptomic, biochemical and histological analysis.

Water temperature is a pivotal environmental factor governing fish physiology and health, and disease outbreaks in aquaculture are frequently constrained to specific thermal ranges. In Channa argus, rhabdovirus infections have been reported within a relatively narrow temperature window, yet the underlying host physiological responses remain poorly understood. In this study, transcriptomic, biochemical, and histological approaches were integrated to examine the effects of short-term and prolonged heat stress on host responses. Transcriptomic analysis reveals duration-dependent transcriptional profiles. Heat stress activates signaling pathways such as the Cell cycle and p53 signaling pathway, JAK-STAT signaling pathway, indicating temperature-dependent regulation of immune-related signaling cascades. From a biochemical perspective, acute stress rapidly enhances antioxidant capacity, innate immunity, and energy mobilization, while long-term stress leads to antioxidant depletion. Histologically, prolonged stress induces severe hepatocyte damage, including degeneration and vacuolar necrosis. RT-qPCR analysis reveals that genes such as HSP30, CD40, and anxa2 exhibit temperature-dependent expression characteristics. These findings demonstrate that thermal stress drives a time-dependent transition in C. argus liver from an initial state of defensive activation to a later state of growth arrest, metabolic dysregulation, and immune exhaustion. This study provides a mechanistic link between prolonged thermal exposure and the heightened disease susceptibility observed in aquaculture, underscoring the critical importance of stress duration in thermal management strategies for snakehead fish.