Viral hemorrhagic fever caused by hantaviruses is an emerging infectious
disease for which suitable treatments are not available. In order to improve
this situation a better understanding of hantaviral pathogenesis is urgently
required. Hantaviruses infect endothelial cell layers in vitro without causing
any cytopathogenic effect and without increasing permeability. This implies
that the mechanisms underlying vascular hyperpermeability in hantavirus-
associated disease are more complex and that immune mechanisms play an
important role. In this review we highlight the latest developments in
hantavirus-induced immunopathogenesis. A possible contribution of neutrophils
has been neglected so far. For this reason, we place special emphasis on the
pathogenic role of neutrophils in disrupting the endothelial barrier
