Opportunistic infection of individuals on immunosuppressive therapy are a major problem for patient outcome, despite current prophylactic strategies. While the ability to prevent infection with well-characterized pathogens has improved, infection by less-known microbes have been on the rise. One such example is the increasing occurrence of mucormycosis, a life-threatening infection caused by Mucorales fungi. A defining characteristic of Mucorales is the ability to invade host cells via interaction with glucose-regulated protein 78 (GRP78) on the surface of endothelial cell.
In this issue of the Journal of Clinical Investigation, Ashraf Ibrahim and colleagues at the University of California, Los Angeles identified spore coat protein homologues (CotH) on the surface of Mucorales fungi as the ligand for GRP78 and that gene encoding these proteins are unique to Mucorales. Furthermore, loss of CotH in the Mucorales fungi Rhizopus oryzae decreased invasion and virulence.
In a companion commentary, J. Andrew Alspaugh of Duke University discusses the potential of targeting CotH proteins for prevention and treatment of mucormycosis.
TITLE: CotH3 mediates fungal invasion of host cells during mucormycosis
ACCOMPANYING COMMENTARY TITLE: Hostile takeover: fungal protein promotes host cell invasion