The description of the genus Leishmania as the causative agent of leishmaniasis occurred in the modern age. However, evolutionary studies suggest that the origin of Leishmania can be traced back to the Mesozoic era. Subsequently, during its evolutionary process, it achieved worldwide dispersion predating the breakup of the Gondwana supercontinent. It is assumed that this parasite evolved from monoxenic Trypanosomatidae. Phylogenetic studies locate dixenous Leishmania in a well-supported clade, in the recently named subfamily Leishmaniinae, which also includes monoxenous trypanosomatids. Virus-like particles have been reported in many species of this family. To date, several Leishmania species have been reported to be infected by Leishmania RNA virus (LRV) and Leishbunyavirus (LBV). Since the first descriptions of LRVs decades ago, differences in their genomic structures have been highlighted, leading to the designation of LRV1 in L. (Viannia) species and LRV2 in L. (Leishmania) species. There are strong indications that viruses that infect Leishmania spp. have the ability to enhance parasitic survival in humans as well as in experimental infections, through highly complex and specialized mechanisms. Phylogenetic analyses of these viruses have shown that their genomic differences correlate with the parasite species infected, suggesting a coevolutionary process. Herein, we will explore what has been described in the literature regarding the relationship between Leishmania and endosymbiotic Leishmania viruses and what is known about this association that could contribute to discussions about the worldwide dispersion of Leishmania.

Leishmania parasites present astonishing adaptative abilities that represent a matter of life or death within disparate environments during the heteroxenous parasite life cycle. From an evolutionary perspective, organisms develop methods of overcoming such challenges. Strategies that extend beyond the genetic diversity have been discussed and include variability between parasite cells during the infections of their hosts. The occurrence of Leishmania subpopulation fluctuations with variable structural genomic contents demonstrates that a single strain might shelter the variability required to overcome inconsistent environments. Such intrastrain variability provides parasites with an extraordinary ability to adapt and thus survive and propagate. However, different perspectives on this evolution have been proposed. Strains or species living in the same environment can cooperate but also compete. These interactions might increase the replication rate of some parasites but cause the loss of more aggressive competitors for others. Adaptive responses to intra- and interspecific competition can evolve as a fixed strategy (replication is adapted to the average genetic complexity of infections) or an optional strategy (replication varies according to the genetic complexity of the current infection). This review highlights the complexity of interspecies and intrastrain interactions among Leishmania parasites as well as the different factors that influence this interplay.

Leishmania parasites present astonishing adaptative abilities that represent a matter of life or death within disparate environments during the heteroxenous parasite life cycle. From an evolutionary perspective, organisms develop methods of overcoming such challenges. Strategies that extend beyond the genetic diversity have been discussed and include variability between parasite cells during the infections of their hosts. The occurrence of Leishmania subpopulation fluctuations with variable structural genomic contents demonstrates that a single strain might shelter the variability required to overcome inconsistent environments. Such intrastrain variability provides parasites with an extraordinary ability to adapt and thus survive and propagate. However, different perspectives on this evolution have been proposed. Strains or species living in the same environment can cooperate but also compete. These interactions might increase the replication rate of some parasites but cause the loss of more aggressive competitors for others. Adaptive responses to intra- and interspecific competition can evolve as a fixed strategy (replication is adapted to the average genetic complexity of infections) or an optional strategy (replication varies according to the genetic complexity of the current infection). This review highlights the complexity of interspecies and intrastrain interactions among Leishmania parasites as well as the different factors that influence this interplay.

Background: The co-circulation of Leishmania ( Leishmania ) infantum strains carrying a naturally occurring 12 kb genomic deletion (DEL) and the wild-type (NonDEL) parasites in the Americas raises important challenges for epidemiological surveillance, molecular diagnostics, and the interpretation of infection dynamics in visceral leishmaniasis (VL). In this study, we aimed to develop and apply a robust molecular approach to discriminate and quantify DEL and NonDEL genotypes and to assess their distribution, frequency, and patterns of co-infection across endemic regions. Methods: We established a qPCR-based genotyping strategy combining a constitutive genomic target, present in all Leishmania (L.) infantum strains, with a NonDEL-specific target, enabling simultaneous genotype discrimination and parasite quantification. Results: After validation using cultured parasites, the assay was applied to a large and diverse panel of strains isolates from humans and dogs preserved in a biobank, as well as clinical samples from dogs, cats, coatis, and sand flies across South and Central America. DEL parasites predominated (69.8%) and showed a wide geographic distribution in both strains and clinical samples, indicating their major contribution to transmission cycles. No significant association was observed between host type (human vs. canine) and genotype frequency. Notably, mixed-genotype infections were frequently detected, revealing within-host complexity not captured by conventional diagnostic methods. Quantification based on the constitutive target strongly correlated with kDNA-based parasite load estimates, supporting its simultaneous use for genotyping and quantification of L. ( L. ) infantum variants directly from clinical material. Conclusions: This approach thus provides new insights into parasite population structure and infection dynamics and supports improved molecular surveillance and interpretation of diagnostic and epidemiological data in VL.