A study by researchers at Baylor College of Medicine (TX, USA), discovered that tuberculosis survivors’ cells had prematurely aged by up to 14 years.
Mycobacterium tuberculosis infected 1.7 billion people worldwide in 2018, according to data from the Centers for Disease Control and Prevention (CDC; GA, USA). The CDC indicated that there were more than 7000 cases of tuberculosis (TB) in the USA in 2020, with a further 13 million people living with latent infections. The disease is present for a median of 3 months before diagnosis, has a treatment mortality rate of 7%, and a 16.9% increase in mortality 2 years after successful therapy, according to a meta-analysis of more than 40,000 cases. Even after successful treatment, survivors are expected to have their lifespans shortened by 7 years.
An epigenetic study by researchers at Baylor College of Medicine, across multiple cohorts and tissue types, revealed regulatory disruptions, particularly in those regulations related to DNA methylation. Network analysis of gene expression data indicated TB-induced expression changes to epigenetic processes, including DNA methylation, across a variety of cohorts. Analysis also confirmed a correlative link between TB and oxidative stress-induced cellular aging, which in turn is associated with damage to cells and DNA. These patterns emerged for both guinea pigs and humans.
Dementia rates were found to be among the lowest in the world in indigenous Bolivian Amazon populations.
“A multi-omic epigenetic clock assay could become part of the standard of care for infectious diseases and further inform increased risk for comorbidities after chronic conditions or environmental exposure,” Cristian Coarfa, the co-corresponding author, proposed. “Now that we know the mechanism, there are some ways that we can target it to slow down and decrease the premature epigenetic aging that is happening in these cells.”
The experiments suggest that certain events, such as intracellular metabolic shifts, could act as the impetus for negative results, including DNA hypermethylation, which is associated with cancer. To further certify this, they suggest a longitudinal study to ascertain how close the links between DNA methylation or premature aging and TB are, and whether these improve after successful treatment.
While the researchers suggest that future studies are needed to validate their results, with a focus on commonly disrupted pathways such as PI3K/AKT or MTOR signaling, the team indicates cellular methylation should be an area of surveillance after severe infection of any kind, including, but not limited to, COVID-19.
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