{
  "id": 9885669,
  "title": "Axonal entry and retrograde transport define HSV-1 latency establishment and reactivation potential in neurons",
  "url": "https://urgent.news/2026/09/25/axonal-entry-and-retrograde-transport-define-hsv-1-latency",
  "topic": "science",
  "section": "Science",
  "published": "2026-09-25T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.09.24.754144v1?rss=1"
  },
  "original_language": "en",
  "account": "Herpes Simplex Virus 1 (HSV-1) establishes lifelong latency in peripheral neurons after initial invasion, but the factors that determine whether it remains latent or becomes productive are not well understood. Current laboratory models do not replicate the natural infection process, as they directly infect neuronal cell bodies while inhibiting the virus with drugs. To address this, researchers developed an axonal infection model that accurately mirrors HSV-1 neuroinvasion and latency formation without using any chemical inhibitors. Primary superior cervical ganglion (SCG) neurons were used to study the effects of different axonal infection doses. It was found that low doses of axonal infection consistently led to latency formation, while higher doses or direct somatic infection resulted in productive replication. Latently infected neurons accumulate a specific viral RNA called latency-associated transcript (LAT) and can be reactivated by either inactivated virus or VP16 protein. However, productive infection during low-dose axonal infection can be triggered when replication-deficient virus enters both neuronal cell bodies and axons. This suggests that delivering the virus to the soma overrides latency establishment. On the other hand, an excess of non-replicative viral particles in axons hinders productive outcomes and future reactivations, indicating a competition for retrograde transport. Overall, these results show that axonal entry and transport are crucial regulatory steps in HSV-1 latency formation and suggest that targeting retrograde trafficking may be a way to prevent the virus from invading the nervous system and causing repeated outbreaks.",
  "summary": "Herpes simplex virus 1 (HSV-1) establishes life-long latency in peripheral neurons following neuroinvasion, yet the early determinants governing latency versus productive infection remain poorly understood. Available in vitro models bypass the physiological route of infection by directly infecting neuronal cell bodies under antiviral suppression. Here, we established a compartmented axonal…",
  "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."
}