SARS-CoV-2 causes senescence in human cells and exacerbates the senescence-associated secretory phenotype through TLR-3
Utkarsh Tripathi, Rayhane Nchioua, Larissa Prata, Yi Zhu, Erin O. Wissler Gerdes, Nino Giorgadze, Tamar Pirtskhalava, Erik Parker, Ailing Xue, Jair Machado Espíndola‐Netto, Steffen Stenger, Paul D. Robbins, Laura J. Niedernhofer, Stephanie Dickinson, David B. Allison, Frank Kirchhoff, Konstantin M. J. Sparrer, Tamar Tchkonia, James L. Kirkland
Abstract
senescent cell burden was higher in patients who died from acute SARS-CoV-2 infection than other causes. Our results suggest that induction of cellular senescence and SASP amplification through TLR-3 contribute to SARS-CoV-2 morbidity, indicating that clinical trials of senolytics and/or SASP/TLR-3 inhibitors for alleviating acute and long-term SARS-CoV-2 sequelae are warranted.
Topics & Concepts
SenescenceBiologyProinflammatory cytokinePhenotypeImmunologyVirologyVirusInflammationCellApoptosisCell biologyGeneGeneticsTelomeres, Telomerase, and SenescenceNeutrophil, Myeloperoxidase and Oxidative MechanismsCytomegalovirus and herpesvirus research