Malaria infection and telomere length: A review

Abstract

Telomere shortening is a key hallmark of cellular aging, and its association with various infectious diseases is well-documented. However, the role of telomere dynamics in malaria pathogenesis remains underexplored. In addition to its influence, malaria infection not only modulates signals within immune cells but also drives telomere shortening in these cells via diverse mechanisms, potentially leaving long-term imprints on human health. Acute malaria infections initiate rapid telomere degradation, promote accelerated cellular senescence, and suppress telomerase expression with possible partial recovery as the parasite clears during treatment. Conversely, prolonged exposure to Plasmodium infection, prevalent among individuals residing in highly endemic regions like Africa, is often aggravated by coexisting infections, potentially exacerbating malaria pathogenesis, accelerating telomere length shortening, and increasing susceptibility to age-related ailments. Herein, we review recent findings into the effects of malaria on telomere attrition, shedding light on possible mechanisms and key factors contributing to this process. Additionally, we present an overview of how oxidative stress and inflammatory mediators contribute to telomere length shortening in malaria. Furthermore, we discuss the potential of telomere length as a biomarker for malaria severity and treatment outcomes.