ABSTRACT
Simian hemorrhagic fever (SHF) is lethal for macaques. Based on clinical presentation and serological diagnosis, all reported SHF outbreaks were thought to be caused by different strains of the same virus, simian hemorrhagic fever virus (SHFV; Arteriviridae). Here we show that the SHF outbreaks in Sukhumi in 1964 and in Alamogordo in 1989 were caused not by SHFV but by two novel divergent arteriviruses. Our results indicate that multiple divergent simian arteriviruses can cause SHF.
Subject(s)
Arterivirus Infections/veterinary , Arterivirus/isolation & purification , Hemorrhagic Fevers, Viral/veterinary , Macaca/virology , Primate Diseases/virology , Amino Acid Sequence , Animals , Arterivirus/classification , Arterivirus/genetics , Arterivirus/physiology , Arterivirus Infections/history , Arterivirus Infections/virology , Evolution, Molecular , Hemorrhagic Fevers, Viral/history , Hemorrhagic Fevers, Viral/virology , History, 20th Century , Humans , Molecular Sequence Data , Phylogeny , Primate Diseases/history , Sequence Homology, Amino Acid , Viral Proteins/chemistry , Viral Proteins/geneticsABSTRACT
The Neanderthals were a Eurasian human species of the genus Homo that disappeared approximately 30,000 years ago. The cause or causes of their extinction continues to intrigue specialists and non-specialists alike. Here a contributory role for Transmissible Spongiform Encephalopathies (TSEs) is suggested. TSEs could have infected Neanderthal groups as a result of general cannibalistic activity and brain tissue consumption in particular. Further infection could then have taken place through continued cannibalistic activity or via shared used of infected stone tools. A modern human hunter-gatherer proxy has been developed and applied as a hypothetical model to the Neanderthals. This hypothesis suggests that the impact of TSEs on the Neanderthals could have been dramatic and have played a large part in contributing to the processes of Neanderthal extinction.
