Essential contribution of the JAK/STAT pathway to carcinogenesis, lytic infection of herpesviruses and pathogenesis of COVID‑19 (Review)

Mol Med Rep. 2024 Mar;29(3):39. doi: 10.3892/mmr.2024.13163. Epub 2024 Jan 19.

Abstract

The intracellular pathway of Janus kinase/signal transducer and activator of transcription (JAK/STAT) and modification of nucleosome histone marks regulate the expression of proinflammatory mediators, playing an essential role in carcinogenesis, antiviral immunity and the interaction of host proteins with Herpesviral particles. The pathway has also been suggested to play a vital role in the clinical course of the acute infection caused by severe acute respiratory syndrome coronavirus type 2 (SARS‑CoV‑2; known as coronavirus infection‑2019), a novel human coronavirus initially identified in the central Chinese city Wuhan towards the end of 2019, which evolved into a pandemic affecting nearly two million people worldwide. The infection mainly manifests as fever, cough, myalgia and pulmonary involvement, while it also attacks multiple viscera, such as the liver. The pathogenesis is characterized by a cytokine storm, with an overproduction of proinflammatory mediators. Innate and adaptive host immunity against the viral pathogen is exerted by various effectors and is regulated by different signaling pathways notably the JAK/STAT. The elucidation of the underlying mechanism of the regulation of mediating factors expressed in the viral infection would assist diagnosis and antiviral targeting therapy, which will help overcome the infection caused by SARS‑CoV‑2.

Keywords: EBV; JAK/STAT; KSHV; SARS‑CoV‑2; carcinoma; herpesviruses.

Publication types

  • Review

MeSH terms

  • COVID-19*
  • Carcinogenesis
  • Herpesviridae* / metabolism
  • Humans
  • Janus Kinases / metabolism
  • SARS-CoV-2 / metabolism
  • STAT Transcription Factors / metabolism
  • Signal Transduction / physiology

Substances

  • Janus Kinases
  • STAT Transcription Factors

Grants and funding

Funding: No funding was received.