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Journal Article Review Epublish 6 citations

PubMed: 40699645 DOI: 10.3390/cimb47040246

The MAPK Response to Virus Infection Is Modified by Probenecid.

Curr Issues Mol Biol 47(4)

Authors: Les P Jones, David E Martin, Ralph A Tripp

Affiliations

  • Department of Infectious Diseases, University of Georgia, Athens, GA 30605, USA.
  • TrippBio, Inc. Jacksonville, FL 32256, USA.

Abstract

Respiratory viruses such as respiratory syncytial virus (RSV) annually cause respiratory illness, which may result in substantial disease and mortality in susceptible individuals. Viruses exploit host cell machinery for replication, which engages the mitogen-activated protein kinases (MAPK) pathway. The MAPK signaling pathways are triggered by pattern recognition receptors that recognize the pathogen, infection, or external stimuli, leading to the induction and regulation of immunity and inflammation. Probenecid, used to improve renal function by inhibiting the tubular reabsorption of uric acid, has been shown to have therapeutic efficacy in reducing inflammation and blocking viral replication by inhibiting components of the MAPK pathway that preclude virus replication. This review summarizes key molecular cascades in the host response to virus recognition, infection, and replication and how this can be altered by probenecid treatment.

MeSH

Respiratory Syncytial Viruses, Probenecid, Virus Replication, Viruses, Signal Transduction, Therapeutics, Immunity, Innate, Infections, Virus Diseases