Molecular biology of rift valley Fever virus

Abstract

Rift Valley fever virus (RVFV) causes large outbreaks of acute febrile and often fatal illness among humans and domesticated animals in sub-saharan Africa and the Arabian peninsula. RVFV is a member of the family Bunyaviridae, genus Phlebovirus. Like all members of this large virus family, it contains a three-segmented genome of negative/ambisense strand RNA, packaged into viral nucleocapsid protein, and enveloped by a lipid bilayer containing two viral glycoproteins. During the past years, there was an increased interest in RVFV epidemiology, molecular biology, and virulence mechanisms. Here, we will try to provide an overview over the basic features of this significant pathogen, and review the latest developments in this highly active research field.

Keywords: Rift Valley fever; interferon antagonism.; non-structural proteins; reverse genetics.

Fig. (1)

Genome and expression strategies of RVFV. (A) Schematic representation of the three genomic segments L (large), M (medium) and S (small) and the proteins encoded on them. (B) The mRNA transcribed from the M segment contains five in-frame start codons which gove rise to the 78kDa and the 14 kDa proteins, as well as some minor products [13]. Scissor indicate host cell protease sites for cleavage of the polyproteins.

Fig. (2)

RVFV NSs forms a filamentous structure in the nucleus. Confocal microscopy picture showing a section of a L929 cell nucleus infected by ZH548 and stained with the DNA intercalating dye ToPro3 (red), with anti-NSs antibodies (green) and merge. The cellular DNA is predominantly excluded from the filament (from Mansuroglu et al., J. Virol. in press).