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Acute hepatopancreatic necrosis disease (AHPND), caused by a unique strain of Vibrio parahaemolyticus (Vp (AHPND)), has become the world's most severe debilitating disease in cultured shrimp. Thus far, the pathogenesis of AHPND remains largely unknow. Herein, in Litopenaeus vannamei, we found that a Vp (AHPND) infection significantly increased the expression of lipid droplets (LDs) protein LvPerilipin, as well as promoted the formation of LDs. In addition, the knockdown of LvPerilipin increased the shrimp survival rate in response to the Vp (AHPND) infection, and inhibited the proliferation of Vp (AHPND). Furthermore, we demonstrated that LvPerilipin depletion could increase the production of reactive oxygen species (ROS), which may be responsible for the decreased Vp (AHPND) proliferation. Taken together, our current data for the first time reveal that the shrimp lipid droplets protein Perilipin is involved in the pathogenesis of Vp (AHPND) via promoting LDs accumulation and decreasing ROS production. [ABSTRACT FROM AUTHOR]

• PvMEF2 was upregulated at the late infection stage of WSSV. • PvMEF2 was essential for maintaining WSSV latent infection. • Pv MEF2 was able to faciliate the expression of the viral latency-related genes and enhance hemocytes survival. White spot syndrome virus (WSSV) is a lethal shrimp pathogen that has a latent infection cycle. The latent virus can easily turn into an acute infection when the culture environment changes, leading to widespread shrimp mortality. However, the mechanism of WSSV latent infection is poorly understood. Bioinformatic analysis revealed that the promoters of WSSV latency-related genes (i.e., wsv151 , wsv366 , wsv403 , and wsv427) contained putative myocyte enhancer factor 2 (MEF2) binding sites. This suggested that the transcription factor MEF2 may be involved in WSSV latent infection. To further investigate this, a MEF2 homolog (Pv MEF2) was cloned from Penaeus vannamei and its role in WSSV latent infection was explored. The results showed that knockdown of Pv MEF2 led to an increase in the copy number of WSSV, indicating reactivation of WSSV from a latent infection. It was further demonstrated that suppression of Pv MEF2 significantly decreased expression of the viral latency-related genes in WSSV-latent shrimp, while overexpression of Pv MEF2 in Drosophila S2 cells activated the promoter activity of the viral latency-related gene. Additionally, we demonstrated that silencing of Pv MEF2 was able to upregulate the expression of pro-apoptosis genes, thereby promoting cell apoptosis during latent infection. Collectively, the present data suggest that Pv MEF2 could promote the expression of virus latency-related genes and enhance cell survival to maintain WSSV latent infection. This finding would contribute to a better understanding of the maintenance mechanism of WSSV latent infection. [ABSTRACT FROM AUTHOR]