Citation

Marty AM, Jahrling PB, Geisbert TW. Clin. Lab. Med. 2006; 26(2): 345-86, viii.

Affiliation

Battelle Memorial Institute, Suite 601, 1550 Crystal Drive, Arlington, VA 22202-4172, USA. martya@battelle.org

Copyright

(Copyright © 2006, Elsevier Publishing)

DOI

10.1016/j.cll.2006.05.001

PMID

16815457

Abstract

A taxonomically diverse set of single-stranded ribonucleic acid(ssRNA) viruses from four diverse viral families Arenaviridae,Bunyaviridae, Filoviridae, and Flaviviridae cause an acute systemic febrile syndrome called viral hemorrhagic fever (VHF). The syndrome produces combinations of prostration, malaise, increased vascular permeability, and coagulation maladies. In severe illness,VHF may include generalized bleeding but the bleeding does not typically constitute a life-threatening loss of blood volume. To a certain extent, it is a sign of damage to the vascular endothelium and is an indicator of disease severity in specific target organs. Although the viruses that cause hemorrhagic fever (HF) can productively replicate in endothelial cells, much of the disease pathology including impairment to the vascular system is thought to result primarily from the release of a variety of mediators from virus-infected cells, such as monocytes and macrophages that subsequently alter vascular function and trigger the coagulation disorders that epitomize these infections. While significant progress has been made over the last several years in dissecting out the molecular biology and pathogenesis of the HF viruses, there are currently no vaccines or drugs licensed available for most of the VHFs.

Language: en