Hijacking of host Src-PI3K-Akt signaling by WSSV IE1 protein suppresses apoptotic and autophagic defenses to facilitate viral proliferation.

ABSTRACT: The phosphoinositide 3-kinase (PI3K)-Akt pathway is a key signaling cascade regulating diverse cellular processes, including proliferation, survival, autophagy, translation, and metabolism. White spot syndrome virus (WSSV), a major pathogen devastating global crustacean aquaculture, has been demonstrated to exploit the PI3K-Akt pathway to facilitate its proliferation. However, the precise mechanism underlying this viral modulation remained unclear. In this study, we demonstrate that WSSV infection induces activation of the PI3K-Akt pathway during the early infection stage in Penaeus vannamei. Mechanistically, we reveal that the WSSV immediate-early protein IE1 interacts with and activates host Src64B kinase via its Y₁₂₉FTS tyrosine motif. This specific interaction promote

SUBMITTER: Lu K 

PROVIDER: S-EPMC12817958 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature