Going ballistic: Leishmania nuclear subversion of host cell plasticity

Intracellular parasites have evolved intricate strategies to subvert host cell functions for their own survival. These strategies are particularly damaging to the host if the infection involves immune cells, as illustrated by protozoan parasites of the genus Leishmania that thrive inside mononuclear phagocytic cells, causing devastating immunopathologies. While the impact of Leishmania infection on host cell phenotype and functions has been well documented, the regulatory mechanisms underlying host cell subversion were only recently investigated. Here we summarize the current knowledge on how Leishmania infection affects host nuclear activities and propose thought-provoking new concepts on the reciprocal relationship between epigenetic and transcriptional regulation in host cell phenotypic plasticity, its potential subversion by the intracellular parasite, and its relevance for host-directed therapy.

Automated summary

Intracellular parasites have evolved complex strategies to disrupt host cell functions and ensure their own survival. Leishmania parasites, in particular, cause severe immunopathologies by thriving inside immune cells. While the impact of Leishmania infection on host cell phenotype and functions has been studied, the regulatory mechanisms underlying host cell subversion were only recently investigated.