AbstractRift Valley fever (RVF) is a re-emerging zoonotic disease responsible for major losses in livestock production, with negative impact on the livelihoods of both commercial and resource-poor farmers in sub-Sahara African countries. The disease remains a threat in countries where its mosquito vectors thrives. Outbreaks of RVF usually follow weather conditions which favour increase in mosquito populations. Such outbreaks are usually cyclical, occurring every 10-15 years.Recent outbreaks of the disease in South Africa have occurred unpredictably and with increased frequency. In 2008 outbreaks were reported in Mpumalanga, Limpopo and Gauteng provinces, followed by a 2009 outbreak in KwaZulu-Natal, Mpumalanga and Northern Cape provinces and in 2010 in the Eastern Cape, Northern Cape, Western Cape, North West, Free State and Mpumalanga provinces. By August 2010, 232 confirmed infections had been reported in humans, with 26 confirmed deaths.To investigate the evolutionary dynamics of RVF viruses (RVFVs) circulating in South Africa, we undertook complete genome sequence analysis of isolates from animals at discrete foci of the 2008-2010 outbreaks. The genome sequences of these viruses were compared with viruses from earlier outbreaks in South Africa and in other countries. The data indicates that one 2009 and all the 2008 isolates from South Africa and Madagascar (M49/08) cluster in Lineage C or Kenya-1. The remaining of the 2009 and 2010 isolates cluster within Lineage H, except isolate M259_RSA_09, a probable segment M reassortant.Author summaryA single RVF virus serotype exists, yet differences in virulence and pathogenicity of the virus have been observed. This necessitates the need for detailed genetic characterization of various isolates of the virus. The RVF virus isolates that caused the 2008-2010 disease outbreaks in South Africa were most probably reassortants. Reassortment results from exchange of portions of the genome, particularly those of segment M. Although clear association between RVFV genotype and phenotype has not been established, various amino acid substitutions have been implicated in the phenotype. Viruses with amino acid substitutions from glycine to glutamic acid at position 277 of segment M have been shown to be more virulent in mice in comparison to viruses with glycine at the same position. Phylogenetic analysis indicated the viruses responsible for the 2008-2010 RVF outbreaks in South Africa were not introduced from outside the country, but mutated in time and caused the outbreaks when environmental conditions became favourable.
Characterization of the Golgi Retention Motif of Rift Valley Fever Virus GN Glycoprotein
