IL10 and respiratory failure: The syndrome has an unknown pathophysiology but is thought to occur secondary to active HHV-8 replication and associated extensive interleukin (IL) production, specifically IL-6 and IL-10 [8]. Immune system overactivation leads to a cytokine storm, hypotension, systemic inflammation, and respiratory failure [8, 18], as seen in our patient who experienced rapidly progressive acute hypoxic respiratory failure.