Aetiology
Rift Valley fever virus (RVFV) is a single-stranded RNA virus of the Bunyavirales order in the Phenuiviridae family (genus Phlebovirus) and is related to hantavirus and Crimean-Congo haemorrhagic fever virus. Transmission to humans is either via infected vector bites or contact with the blood, body fluid, or tissues of infected livestock. Several mosquito species, including Aedes, Culex, and Mansonia species, are competent vectors.[7][8] Outbreaks are linked to times of excessive rainfall or flooding as mosquitoes bloom and amplify RVFV.[21][22][23][24][25][26] Aerosol transmission and infection has occurred in the laboratory environment and transmission via this mechanism has been linked to severe disease in humans. Human-to-human transmission has not been documented and therefore the human-animal-environment interface is critical for pathogen persistence.[27]
[Figure caption and citation for the preceding image starts]: Rift Valley fever virus ecology showing enzootic and epizootic cyclesCenters for Disease Control; used with permission [Citation ends].
Pathophysiology
The Rift Valley fever virus (RVFV) has an outer lipid envelope with 2 glycoproteins (Gn and Gc). These glycoproteins mediate entry into the host cell and are linked to virulence. These are therefore an important candidate for vaccine and other antiviral strategies (such as the use of virus-like particles). The virus also has 2 non-structural proteins: NSm and NSs. The role of NSm is still unclear; however, NSs has been shown to be an interferon antagonist, hence reducing the host antiviral response.
The incubation period of RVFV is 2 to 6 days. Infection can manifest as several different disease syndromes, although most people are asymptomatic or have a mild generalised illness only.[8]
Severe manifestations of RVF can be defined as febrile illness with one or more of the following progressive symptoms: retinitis, encephalitis, or haemorrhagic diathesis with hepatitis during epidemics.[8][28] RVFV also leads to miscarriage in approximately one half of infected pregnant women in endemic areas.[3] The reasons some individuals develop severe disease or complications are unknown and the subject of ongoing research. Previous studies suggest that genetic polymorphisms may enhance an individual’s risk of developing severe RVF disease, and that specific single nucleotide polymorphisms may be directly linked to severe symptom presentation.[29] Other studies suggest advanced age, contact with animal abortus, and occupation involving slaughtering or butchering livestock may increase risk of severe disease.[28] Further research is necessary to determine the mechanisms and pathogenesis associated with severe RVF disease.
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