{
  "id": 9487116,
  "title": "Effect of HSV-1 ICP0 E3 ubiquitin ligase on CIN85 endosomes",
  "url": "https://urgent.news/2026/09/23/effect-of-hsv-1-icp0-e3-ubiquitin-ligase-on-cin85-endosomes",
  "topic": "science",
  "section": "Science",
  "published": "2026-09-23T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.09.21.753399v1?rss=1"
  },
  "original_language": "en",
  "account": "Herpes simplex virus-1 (HSV-1) infects over two-thirds of the global population, leading to illnesses ranging from mild cold sores to severe encephalitis. The virus employs complex mechanisms to evade the host's antiviral defenses. A critical viral protein, immediate early protein ICP0, plays a pivotal role in this evasion process. ICP0 functions as an E3 ubiquitin ligase, essential for initiating the lytic infection and facilitating the reactivation of latent viral genomes. While ICP0's nuclear functions have been extensively studied, its cytoplasmic role remains enigmatic, particularly during late gene expression stages.\n\nOur recent research has revealed that the cytoplasmic localization of ICP0 involves its interaction with CIN85, a scaffolding protein crucial for endocytosis-related processes. This interaction enables the extrusion of host antiviral factors and contributes to viral immunoevasion. In this study, we discovered that the E3 ubiquitin ligase activity of ICP0 is also essential for these cytoplasmic effects. When the RING finger domain of ICP0, which is responsible for its catalytic activity, is disrupted, the number of endosomes containing CIN85 that cannot be exocytosed increases. These endosomes appear to colocalize with autophagosome components but fail to enter the lysosomal degradation pathway. Moreover, mutant viruses unable to exocytose CIN85-rich endosomes produce extracellular vesicles (EVs) with enhanced capacity to activate antiviral responses in host cells.",
  "summary": "Herpes simplex virus-1 (HSV-1) has infected more than 67% of the world population causing diseases that range in severity from benign cold sores to encephalitis. To infect and persist in the host, HSV-1 has evolved sophisticated strategies to counteract antiviral responses. The viral immediate early protein ICP0 (Infected Cells Protein 0) plays a fundamental role in this process. ICP0 is an E3…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}