Therapeutic interventions in sepsis models, such as administration of ethyl pyruvate (74) , an agent that limits HMGB1 release in vitro, or administration of an anti-HMGB1 antibody (75) , save a significant proportion of mice, implicating the inhibition of HMGB1 release or activity as a therapeutic target during immune pathology. As previously mentioned, glycyrrhizin protects influenza virus (H2N2)-infected mice from fatality (33) potentially via its ability to bind to, and inactivate, HMGB1 (34) . Therefore it would be important to establish whether or not therapeutic intervention with any of the agents discussed here reverse the fatality of severe influenza in animal models via effects on HMGB1 and/or other aspects of the host response.