Skip to main content

PERSPECTIVE article

Front. Pain Res.
Sec. Neuropathic Pain
Volume 6 - 2025 | doi: 10.3389/fpain.2025.1527106
This article is part of the Research Topic The Challenge: Viral Infections and Initiation of Acute and Persistent Pain Phenotypes View all 3 articles

Virally-Initiated Pain States: Phenotype, Mechanisms, and Future Directions, Editors' Perspective

Provisionally accepted
Sara Dochnal Sara Dochnal 1*Steven Cohen Steven Cohen 2Mark R Hutchinson Mark R Hutchinson 3,4,5Yury I Miller Yury I Miller 6Tony L Yaksh Tony L Yaksh 1
  • 1 Anesthesiology, University of California, San Diego, La Jolla, United States
  • 2 Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States
  • 3 School of Biomedicine, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia
  • 4 Institute for Photonics and Advanced Sensing, Faculty of Sciences, Engineering and Technology, University of Adelaide, Adelaide, South Australia, Australia
  • 5 Davies Research Centre, School of Animal and Veterinary Sciences, Faculty of Sciences, Engineering and Technology, University of Adelaide, Adelaide, South Australia, Australia
  • 6 Medicine, University of California, San Diego, La Jolla, California, United States

The final, formatted version of the article will be published soon.

    The recent SARS-CoV-2 pandemic has underscored the significance of viral infections, affecting billions of lives and costing trillions of dollars globally (1, 2). Even beyond SARS-CoV-2, common infections with viruses like influenza, HIV, and herpesviruses have profound impacts beyond their typical manifestations, often triggering acute and chronic pain syndromes that can be life-altering. These virally induced pain states can arise through direct viral replication within neurons, or indirectly, via immune responses to infection in both the contexts of afferent signaling in the dorsal root ganglion (DRG) or subsequent higher order integration in intracranial systems. Varicella-zoster virus (VZV), influenza virus, and SARS-CoV-2 each provide a unique lens through which to examine the interplay between viral activity and pain. This perspective paper is not meant to be an exhaustive review of virally-induced neuropathic pain states. It seeks to explore curated aspects of the complexities of these pain states, identify research gaps, and suggest solutions using nanoscale molecular understanding and psychoneuroimmunological and biopsychosocial frameworks. Each subheading is accompanied by a list of related issues for study which we think will lead to advances in our understanding of the vexing pain phenotype associated with viral infection.

    Keywords: neuroimmune activation, viral infection, Post-herpetic Neuralgia, Long Covid, influenza, Neurotropic and antiviral therapy

    Received: 12 Nov 2024; Accepted: 10 Jan 2025.

    Copyright: © 2025 Dochnal, Cohen, Hutchinson, Miller and Yaksh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Sara Dochnal, Anesthesiology, University of California, San Diego, La Jolla, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.