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Abstract

Over the past few decades understanding and recognition of hantavirus infection has greatly improved worldwide, but both, the amplitude and the magnitude of hantavirus outbreaks have been increasing. Very recently, several novel hantaviruses with unknown pathogenic potential have been identified in a variety of insectivore hosts. With new hosts also new geographical distribution of hantaviruses has been discovered and several new species were found also in Africa. Hantavirus infection in humans can result in two clinical syndromes: HFRS or HCPS caused by Old World or New World hantaviruses, respectively. The clinical presentation of HFRS varies from subclinical, mild, and moderate to severe, depending in part on the causative agent of the disease. In general, HFRS caused by HTNV, AMRV, and DOBV are more severe with mortality rates from 5 to 15%, while SEOV causes moderate and PUUV and SAAV cause mild form of disease with mortality rates below 1%. The central phenomena behind the pathogenesis of both HFRS and HCPS are increased vascular permeability and acute thrombocytopenia. The pathogenesis is likely to be a complex multifactorial process that includes contributions from immune responses, platelet dysfunction and the deregulation of endothelial cell barrier functions. Also a genetic predisposition, related to HLA type, seems to be important for the severity of the disease. Since there is no effective treatment or vaccine, approved for the use in the USA and Europe, the public awareness and precaution measures are the only way of minimizing the risk of hantavirus disease.

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