Abstract
Two species of Ebola virus were discovered in 1976 during simultaneous outbreaks of viral hemorrhagic fever in southern Sudan ( Sudan ebolavirus ) and northern Zaire ( Zaire ebolavirus ). Subsequently, two additional species, Reston ebolavirus and Côte d ’ Ivoire ebolavirus , were identified in 1989 and 1994, respectively. Sudan and Zaire ebolavirus, which are endemic in Central Africa, cause a severe hemorrhagic fever in human and nonhuman primates, similar to the related Marburg virus, with person-to-person transmission being the main route of infection among humans. The reservoir of this presumptive zoonosis has not been convincingly identified, but bats are considered a putative reservoir for at least Zaire ebolavirus. In general terms, the disease is associated with fluid distribution problems, hypotension, and coagulation disorders, all of which contribute to the development of fulminant shock. Viral replication, in conjunction with immune system and vascular dysregulation, are important pathogenic factors. Currently, a licensed treatment or vaccine is not available, but promising experimental therapeutic strategies and vaccine platforms have been developed. Ebola viruses are filamentous, nonsegmented, negative-stranded RNA viruses with a life cycle most similar to that of rhabdoviruses. Four structural proteins are involved in virus transcription/replication and three in particle maturation/budding. The role of the viral proteins in pathogenesis is still poorly understood, but might be deciphered with the help of recently developed reverse genetics systems.
Published Version
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