A comprehensive review highlights how chronic infections contribute to cellular senescence and aging by promoting tissue damage through mechanisms like DNA damage, oxidative stress, and chronic inflammation.

The review suggests that treating and eradicating these persistent infections could potentially slow down aging and reduce long-term tissue damage, although more research is needed to confirm causality and develop effective interventions.

Many common chronic infections, such as Epstein-Barr virus, cytomegalovirus, Helicobacter pylori, HIV, E. coli, Mycobacterium tuberculosis, Borrelia burgdorferi, Toxoplasma gondii, Plasmodium, and Trypanosoma cruzi, are widespread and often remain undiagnosed or untreated in the population.

Persistent viral infections like hepatitis C, cytomegalovirus, and HIV can induce cellular senescence by causing DNA damage, cell cycle arrest, and sustained secretion of pro-inflammatory cytokines, which upregulate various senescence markers.

Protozoan parasites such as Toxoplasma gondii, Plasmodium, and Trypanosoma cruzi promote cellular aging by inducing oxidative stress, telomere shortening, and DNA damage, leading to tissue-specific issues like cardiomyopathy and neuroinflammation.