Dynamic Mechanism of Hepatopancreatic Transcriptomic Response in Litopenaeus Vannamei under PirAB Toxin Challenge: A Time-Series Reanalysis Based on Public Databases
Aug 2026· Theoretical and Natural Science· Vol 187, pp. 89-98· 0 citations
TL;DR
A "double-hit" model of PirAB toxin pathogenesis was revealed, suggesting that zinc finger proteins, metallothioneins and other molecules can serve as biomarkers for ultra-early warning, providing new insights into the early diagnosis of AHPND.
Abstract
Acute Hepatopancreatic Necrosis Disease (AHPND) poses a major threat to the shrimp aquaculture industry, and its pathogenic agent is the PirAB toxin. Although it is known to target the hepatopancreas, the early events triggered by toxin attack and their dynamic mechanisms along disease progression remain to be elucidated. In this study, time-series transcriptomic data from public databases (control group and 0.5, 1, 2, 4, 6 hours after toxin treatment) were used to reveal a "double-hit" model of PirAB toxin pathogenesis through K-means clustering and key gene expression analysis. The first hit (0.5 h) was characterized by a sharp downregulation of transcription regulatory factors such as zinc finger proteins, leading to paralyzed transcriptional regulation. The second hit (6 h) manifested as sustained inhibition of metabolic genes and upregulation of apoptosis/degradation genes including matrix metalloproteinases, resulting in functional failure and tissue ulceration. This model identified molecular abnormalities at the very early stage, suggesting that zinc finger proteins, metallothioneins and other molecules can serve as biomarkers for ultra-early warning, providing new insights into the early diagnosis of AHPND.
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