I had always assumed that EDN's purpose was to attack the nervous systems of helminths and similar multicellular parasitic organisms, given the function of eosinophils. The enzyme was named due to its ability to induce a neurotoxic syndrome called the Gordon phenomenon when injected into nervous tissue. However, it is a cytotoxic ribonuclease with strong antiviral activity, which doesn't make it seem much like a neurotoxin. I'm not sure if the fact that it is a neurotoxin is biologically relevant or not.
To this day, the mechanism of EDN's neurotoxicity remains mostly a mystery. For instance, it is not at all clear whether EDN exerts direct toxicity to Purkinje cells, or whether cell loss is the result of an indirect activation of another cell type, resulting in the release of a cytotoxic mediator. Sorrentino and colleagues  demonstrated that iodoacetate-inactivation of the ribonucleolytic activity of EDN eliminated its neurotoxic activity in the rabbit model. However, the neurotoxic activity is shared with the related RNase A ribonuclease ECP , and the very distantly related, and ribonucleolytically weak bullfrog ribonuclease, onconase , but it is not shared by the more closely related, and highly enyzmatically active human pancreatic RNase .
Unlike the other EDGPs, EDN is a poor cationic toxin with limited toxicity for helminth parasites and mammalian cells at high concentrations (50, 56). However, as a ribonuclease, it is considerably more effective against single-stranded RNA viruses (51).
Does EDN function against helminths' nervous systems, or is it primarily an antiviral enzyme that just happens to have neurotoxic properties when injected intrathecally into rabbits? Is it even capable of reaching the nervous system of these parasites when nearby eosinophils degranulate?