Cytotoxic CD4 T lymphocytes are abundantly generated in T. cruzi-infected mice, predominantly infiltrate infected hearts, depend on T-cell intrinsic IL-18R/MyD88 signaling for expansion and their blood frequency correlates with the severity of chronic myocarditis in patients with Chagas disease.

Precise genome editing by homology-directed repair occurs more efficiently with a chromatin donor template than with a naked DNA donor template.

Dsup, a unique protein found only in tardigrades, is a nucleosome-binding protein that protects DNA from damage by hydroxyl radicals, such as those generated by ionizing radiation or oxidants.

Intracellular amastigotes of the Chagas disease agent Trypanosoma cruzi can spontaneously enter an extended state of replicative dormancy, during which time they are resistant to drug treatment both in vitro and in vivo.

Predators may amplify multiple-host parasite spreading in systems with multiple transmission routes.

Development of a robust Th1 response to infection against an intracellular parasite requires T-cell intrinsic MyD88 signaling, mostly through the upstream IL-18 receptor, for the induction of genes involved in proliferation, cytokine production and migration.

A minimal subset of two to three residues in cyclic nucleotide binding (CNB) domains controls nucleoside vs. cyclic nucleotide specificity, repurposing PKA of certain pathogens for novel nucleoside signaling pathways or sensing.

While flooding events may drive spillover transmission of Leptospira spp. through dispersal of the bacteria at low elevations, at higher elevations environmental risk is more localised and directly driven by the distribution of local rat reservoir populations.

Structurally divergent bacterial-like mechanosensitive channels control multiple cellular functions in protozoan parasites.

A vastly improved PCR-based approach provides a long-sought test of cure and parasite load monitoring tool for Chagas disease.