Title : Virulence factors and genetic diversity of Trypanosoma cruzi: Implications for pathogenesis mechanisms
Abstract:
Introduction: The genetic diversity of Trypanosoma cruzi, classified into different DTUs, has a major influence on the pathogenic mechanisms of Chagas disease. This variability accounts for differences in the expression of virulence factors such as trans-sialidases and mucins, affecting the parasite-host interaction and contributing to the wide clinical heterogeneity observed among strains and infected populations.
Objective: To investigate how the virulence factors and genetic diversity of Trypanosoma cruzi influence the pathogenic mechanisms of Chagas disease, highlighting the main molecules involved, the differences among DTUs, and the implications for the clinical variability observed.
Methodology: A bibliographic review was conducted using databases such as PubMed, SciELO, and Google Scholar, focusing on publications from 2019 to 2024 and using descriptors related to the genetic diversity and virulence factors of Trypanosoma cruzi. Published studies addressing the modulation of pathogenesis and the clinical heterogeneity of Chagas disease were included. Studies that did not focus on virulence or genetic diversity of Trypanosoma cruzi were excluded.
Results: In Brazil, the parasite’s genetic diversity is distributed among different DTUs (TcI to TcVI and TcBat). This variability is associated with different clinical manifestations of Chagas disease. Strains with higher expression of virulence factors such as trans-sialidases, mucins, MASPs, and cruzipain show greater capacity for cell invasion and immune evasion, promoting chronic infections. The geographic distribution of DTUs influences transmission cycles: TcI predominates in wild regions and is often related to outbreaks of oral transmission, while TcII, TcV, and TcVI are more associated with human infection in central areas of Brazil. The diversity of vectors and reservoirs including triatomines, marsupials, bats, and rodents contributes to the maintenance and spread of the parasite, reinforcing the epidemiological complexity of the disease in the country.
Conclusion: The genetic heterogeneity of Trypanosoma cruzi and the expression of its virulence factors, combined with the diversity of vectors and reservoirs, explain the clinical variability of Chagas disease and its transmission dynamics. Understanding these factors is essential for improving strategies for diagnosis, surveillance, and control.
