Pathogenesis of Puumala and other hantavirus infections

M Kanerva, J Mustonen, A Vaheri - Reviews in medical virology, 1998 - Wiley Online Library
M Kanerva, J Mustonen, A Vaheri
Reviews in medical virology, 1998Wiley Online Library
Hantaviruses are rodent/insectivore‐borne negative‐stranded RNA viruses which belong to
the Bunyaviridae family. They do not cause any symptomatic disease in their adult carrier
rodents, but in humans they are aetiologic agents of haemorrhagic fever with renal
syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), both associated with a
significant mortality. In cell culture hantaviruses do not cause cytopathic effects and the
mechanisms of disease in man are not well understood. Increased capillary permeability is a …
Abstract
Hantaviruses are rodent/insectivore‐borne negative‐stranded RNA viruses which belong to the Bunyaviridae family. They do not cause any symptomatic disease in their adult carrier rodents, but in humans they are aetiologic agents of haemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), both associated with a significant mortality. In cell culture hantaviruses do not cause cytopathic effects and the mechanisms of disease in man are not well understood. Increased capillary permeability is a central phenomenon in the pathogenesis of hantavirus infections. Although the viruses have in vivo a predilection for endothelial cells, it is presumed that inflammatory mediators of the host immune response play a significant role in the capillary leak that may produce abrupt hypotension and shock in severely ill patients. Mediators released by activated macrophages including NO and TNF‐α are considered important. The pathogenesis of renal failure in HFRS also awaits to be resolved. This review summarises what is known about these phenomena and discusses also the molecular basis of the putative virulence factors of hantaviruses. Finally, the genetic predisposition and HLA association with severe Puumala virus infection will be discussed. © 1998 John Wiley & Sons, Ltd.
Wiley Online Library