Saved in:
Bibliographic Details
Main Authors: Lu, Kaiyu, Zhang, Jia, Zhu, Jinghua, Zhao, Yongzhen, Chen, Xiuli, Zhang, Yueling, Yao, Defu
Format: Artículo científico
Language:en
Published: Journal of virology 2026
Subjects:
Online Access:https://pubmed.ncbi.nlm.nih.gov/41400355/
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1868266111380750337
author Lu, Kaiyu
Zhang, Jia
Zhu, Jinghua
Zhao, Yongzhen
Chen, Xiuli
Zhang, Yueling
Yao, Defu
author_facet Lu, Kaiyu
Zhang, Jia
Zhu, Jinghua
Zhao, Yongzhen
Chen, Xiuli
Zhang, Yueling
Yao, Defu
Lu, Kaiyu
Zhang, Jia
Zhu, Jinghua
Zhao, Yongzhen
Chen, Xiuli
Zhang, Yueling
Yao, Defu
collection PubMed - marine biology
contents Hijacking of host Src-PI3K-Akt signaling by WSSV IE1 protein suppresses apoptotic and autophagic defenses to facilitate viral proliferation. Lu, Kaiyu Zhang, Jia Zhu, Jinghua Zhao, Yongzhen Chen, Xiuli Zhang, Yueling Yao, Defu Animals Signal Transduction Proto-Oncogene Proteins c-akt Penaeidae Apoptosis White spot syndrome virus 1 Autophagy Phosphatidylinositol 3-Kinases Host-Pathogen Interactions Virus Replication Immediate-Early Proteins src-Family Kinases 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 . Mechanistically, we reveal that the WSSV immediate-early protein IE1 interacts with and activates host Src64B kinase via its YFTS tyrosine motif. This specific interaction promotes recruitment of the PI3K regulatory subunit alpha (PI3Kp85α), thereby triggering the downstream PI3K-Akt signaling. By activating this pathway, WSSV establishes a favorable environment for its proliferation by suppressing host apoptotic and autophagic defenses. Our findings unveil a previously unknown mechanism of WSSV immune evasion through Src-PI3K-Akt signaling hijacking and identify components of this signaling hub as potential therapeutic targets for anti-WSSV strategies. Viruses usually hijack host signaling pathways to enhance infectivity and evade immune defenses. Understanding these interactions is critical for elucidating viral pathogenesis and developing effective antiviral strategies. Here, we demonstrate that the WSSV immediate-early protein IE1 binds to and activates host Src64B kinase, which in turn recruits PI3Kp85α and activates the PI3K-Akt signaling cascade. Activation of this pathway suppresses apoptosis and autophagy, thereby facilitating viral proliferation. These findings advance our understanding of WSSV pathogenesis and identify the Src-PI3K-Akt signaling as a promising therapeutic target for anti-WSSV intervention.
format Artículo científico
id pubmed_41400355
institution PubMed
language en
publishDate 2026
publisher Journal of virology
record_format pubmed
spellingShingle Hijacking of host Src-PI3K-Akt signaling by WSSV IE1 protein suppresses apoptotic and autophagic defenses to facilitate viral proliferation.
Lu, Kaiyu
Zhang, Jia
Zhu, Jinghua
Zhao, Yongzhen
Chen, Xiuli
Zhang, Yueling
Yao, Defu
Animals
Signal Transduction
Proto-Oncogene Proteins c-akt
Penaeidae
Apoptosis
White spot syndrome virus 1
Autophagy
Phosphatidylinositol 3-Kinases
Host-Pathogen Interactions
Virus Replication
Immediate-Early Proteins
src-Family Kinases
Hijacking of host Src-PI3K-Akt signaling by WSSV IE1 protein suppresses apoptotic and autophagic defenses to facilitate viral proliferation. Lu, Kaiyu Zhang, Jia Zhu, Jinghua Zhao, Yongzhen Chen, Xiuli Zhang, Yueling Yao, Defu Animals Signal Transduction Proto-Oncogene Proteins c-akt Penaeidae Apoptosis White spot syndrome virus 1 Autophagy Phosphatidylinositol 3-Kinases Host-Pathogen Interactions Virus Replication Immediate-Early Proteins src-Family Kinases 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 . Mechanistically, we reveal that the WSSV immediate-early protein IE1 interacts with and activates host Src64B kinase via its YFTS tyrosine motif. This specific interaction promotes recruitment of the PI3K regulatory subunit alpha (PI3Kp85α), thereby triggering the downstream PI3K-Akt signaling. By activating this pathway, WSSV establishes a favorable environment for its proliferation by suppressing host apoptotic and autophagic defenses. Our findings unveil a previously unknown mechanism of WSSV immune evasion through Src-PI3K-Akt signaling hijacking and identify components of this signaling hub as potential therapeutic targets for anti-WSSV strategies. Viruses usually hijack host signaling pathways to enhance infectivity and evade immune defenses. Understanding these interactions is critical for elucidating viral pathogenesis and developing effective antiviral strategies. Here, we demonstrate that the WSSV immediate-early protein IE1 binds to and activates host Src64B kinase, which in turn recruits PI3Kp85α and activates the PI3K-Akt signaling cascade. Activation of this pathway suppresses apoptosis and autophagy, thereby facilitating viral proliferation. These findings advance our understanding of WSSV pathogenesis and identify the Src-PI3K-Akt signaling as a promising therapeutic target for anti-WSSV intervention.
title Hijacking of host Src-PI3K-Akt signaling by WSSV IE1 protein suppresses apoptotic and autophagic defenses to facilitate viral proliferation.
topic Animals
Signal Transduction
Proto-Oncogene Proteins c-akt
Penaeidae
Apoptosis
White spot syndrome virus 1
Autophagy
Phosphatidylinositol 3-Kinases
Host-Pathogen Interactions
Virus Replication
Immediate-Early Proteins
src-Family Kinases
url https://pubmed.ncbi.nlm.nih.gov/41400355/