Beyond cuts and scrapes: plasmin in malaria and other vector-borne diseases

Plasmodium and other vector-borne pathogens have evolved mechanisms to hijack the mammalian fibrinolytic system to facilitate infection of the human host and the invertebrate vector. Plasmin, the effector protease of fibrinolysis, maintains homeostasis in the blood vasculature by degrading the fibrin that forms blood clots. Plasmin also degrades proteins from extracellular matrices, the complement system, and immunoglobulins. Here, we review some of the mechanisms by which vector-borne pathogens interact with components of the fibrinolytic system and co-opt its functions to facilitate transmission and infection in the host and the vector. Further, we discuss innovative strategies beyond conventional therapeutics that could be developed to target the interaction of vector-borne pathogens with the fibrinolytic proteins and prevent their transmission.

Automated summary

Plasmodium and other vector-borne pathogens have evolved mechanisms to exploit the mammalian fibrinolytic system for infection and transmission. Plasmin plays a crucial role in maintaining vascular homeostasis and degrading proteins. Understanding these mechanisms can help develop innovative strategies to prevent pathogen transmission.