Abstract
ABSTRACT
Hantavirus pulmonary syndrome (HPS) carries a case fatality rate of 35%–40% and has no approved pharmacologic treatment. Its pathophysiology is rooted in the plasma compartment: cytokines, viral antigens, immune complexes, and platelet‐binding glycoproteins circulate as drivers of immunopathologic endothelial injury, noncardiogenic pulmonary edema, and cardiogenic depression. Therapeutic plasma exchange (TPE) achieves bulk clearance of plasma‐borne mediators and is established by the American Society for Apheresis (ASFA) for numerous indications that share an analogous mechanistic rationale. This commentary argues that the immunopathology of HPS maps onto the therapeutic targets of TPE, that any intervention would need to be timed to the early cardiopulmonary phase, and that the coagulopathic dimension of the disease provides a mechanistic argument for incorporating plasma into the replacement strategy. We deliberately situate this rationale against the uneven record of TPE in diseases of comparable pathophysiology, in which the intervention has been effective in some settings and without demonstrable benefit in others. The recent Andes virus outbreak aboard the cruise ship MV Hondius, which produced a multinational cluster of severe cardiopulmonary cases, prompted us, as transfusion medicine and apheresis physicians, to articulate this hypothesis. We emphasize that these arguments are mechanistic and hypothesis‐generating rather than evidence‐based: no clinical data yet support TPE in HPS, and systematic outcome reporting, ideally through a multicenter case series, would be required before any conclusion about efficacy could be drawn.