Timothy C. Barnett

Abstract The pathogenesis of acute rheumatic fever (ARF) is poorly understood, limiting the development of immune-modulating therapies to treat disease and prevent progressive heart damage. Here, participants with definite ARF were compared to other severe acute paediatric conditions and matched healthy controls by profiling circulating immune molecules and cells to inform disease mechanisms and potential druggable pathways.

Introduction Streptococcus pyogenes (Group A Streptococci; GAS) is a versatile human pathogen that causes infections of multiple organ systems (Efstratiou and Lamagni, 2022), with pharyngitis (or “strep throat”) being the most common infection that results in up to 600 million episodes worldwide every year (Carapetis et al., 2005; Tan et al., 2014).

Abstract The re-emergence of scarlet fever poses a new global public health threat. The capacity of North-East Asian serotype M12 (emm12) Streptococcus pyogenes (group A Streptococcus, GAS) to cause scarlet fever has been linked epidemiologically to the presence of novel prophages, including prophage ΦHKU.vir encoding the secreted superantigens SSA and SpeC and the DNase Spd1. Here, we report the molecular characterization of ΦHKU.vir-encoded exotoxins.