Browsing by Author "Afolabi, Israel S."

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Knowledge, practices, and perceptions towards malaria prevention and control among Residents of Canaanland and surrounding areas in Ota, Ogun State, Nigeria: a cross-sectional study
(Frontiers in Tropical Diseases, 2025-10-13) Wakai, Theophilus N.; Fiamitia, Carrin; Kintung, Irrinus; Johngwe, Mac; Chinedu, Shalom; Afolabi, Israel S.
Malaria infection and telomere length: A review
(Microbial Pathogenesis, 2025) Wakai, Theophilus N.; Fiamitia, Carrin; Oba, Emmanuel B.; Chinedu, Shalom N.; Afolabi, Israel S.
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.
Plasmodium telomere maintenance: uncovering the Achilles’ heel for novel antimalarials
(Frontiers in Cellular and Infection Microbiology, 2025-09) Wakai, Theophilus N.; Anzaku, Dorathy O.; Afolabi, Israel S.
This review examines the potential of disrupting telomere maintenance in Plasmodium as a novel antimalarial strategy. Telomeres are repetitive DNA– protein structures located at chromosome termini, where they preserve genome stability and protect against degradation. Telomere maintenance is crucial for rapid growth, genome integrity, and immune evasion in Plasmodium parasites. Unlike humans, Plasmodium maintains continuous telomerase activity and uses unique telomere-binding proteins across its lifecycle. These features drive parasite virulence and antigenic variation. Emerging evidence suggests that Plasmodium telomeres harbor G-quadruplex (G4) DNA structures, which help stabilize telomeres during replication and may be good targets for small molecules to disrupt their function. Additionally, the parasite depends heavily on its telomerase catalytic subunit, PfTERT, for survival. Inhibiting PfTERT has shown promising results in blocking telomere elongation and impairing replication. Targeting this parasite-specific telomere–telomerase axis may offer a strategic means to destabilize chromosomes, weaken immune evasion, and limit parasite survival, making it a promising antimalarial approach. However, researchers must consider the risks of off-target effects in future drug designs. Though current studies are limited and remain inconclusive, we suggest that future research should investigate combining telomere-directed therapies with existing antimalarials to help overcome resistance and improve treatment outcomes. Herein, we review advances in understanding Plasmodium telomere biology, highlighting its distinct structures, critical telomereassociated proteins, and roles in pathogenesis. We further explore how selective targeting could exploit an Achilles’ heel in parasite survival, offering fresh possibilities for next-generation, parasite-specific malaria therapies.