Rift Valley fever

Rift Valley fever is an acute viral zoonosis affecting livestock and humans, caused by the Rift Valley fever virus, a member of the Phlebovirus genus within the class Bunyaviricetes. The disease varies widely in severity: most human infections are mild or asymptomatic, while a small proportion progress to severe complications, including haemorrhagic fever, meningoencephalitis and ocular disease. In livestock, especially sheep, goats, cattle and camels, infection can result in high mortality among young animals and near-universal abortion rates during epizootics. Outbreaks occur predominantly in sub-Saharan Africa and the Arabian Peninsula and are closely associated with periods of unusually heavy rainfall that promote mosquito population surges.

Signs and Symptoms

In humans, clinical presentation ranges from asymptomatic infection to severe multisystem disease. The majority of symptomatic cases involve an influenza-like illness with fever, myalgia, headache, generalised weakness and hepatic abnormalities. These symptoms typically last between two and seven days, and most individuals recover fully.
Approximately two per cent of cases progress to more severe forms. Haemorrhagic disease may arise within the first few days, accompanied by jaundice, bleeding tendencies and liver dysfunction, and carries a high fatality risk. Neurological involvement results in meningoencephalitis, manifesting as severe headache, confusion and, occasionally, long-term neurological deficits. Ocular complications include retinitis with potential visual loss, often appearing several weeks after the initial infection. Overall human case fatality is estimated at around one per cent.
In livestock, disease severity is markedly greater. Rift Valley fever epizootics are frequently heralded by a wave of unexplained abortions, especially in sheep and goats. Young animals may exhibit fever, lethargy, anorexia, diarrhoea, respiratory disease and sudden death. Mortality rates in newborn animals are high, and fetal loss in pregnant animals approaches 100 per cent during outbreaks.

Cause and Virology

The Rift Valley fever virus is an enveloped, negative-sense single-stranded RNA virus. Its genome consists of three segments—designated L, M and S—encoding six major proteins. The L segment codes for the viral polymerase, while the M segment encodes two envelope glycoproteins, GN and GC, essential for host-cell entry. The S segment is ambisense and encodes the nucleocapsid protein and the non-structural proteins NSs and NSm.
The GC glycoprotein contains a class II membrane fusion architecture similar to that of flaviviruses and alphaviruses, indicating possible evolutionary links among these viral groups. NSs is a principal virulence factor and suppresses the host antiviral response by inhibiting interferon signalling. It achieves this through interactions that disrupt transcription factor assembly, binding to proteins such as SAP30 to impede histone acetylation and interfering with protein kinase R pathways. NSs also forms filamentous structures within the nucleus that can alter chromosome structure and undermine normal antiviral functions.

Transmission

The virus is transmitted to humans and livestock primarily through mosquito vectors. Several Aedes and Culex species act as competent vectors, including Aedes vexans, Aedes caspius, Aedes ochraceus, Culex tritaeniorhynchus, Culex pipiens and others. Vertical transmission in mosquito eggs enables the virus to persist in dry conditions for prolonged periods; subsequent rainfall triggers hatching and potential amplification of the virus.
Humans are most commonly infected through direct contact with the blood, tissues or bodily fluids of infected animals, particularly during slaughtering or veterinary procedures. Additional risks include inhaling aerosols generated during the handling of infected carcasses or consuming raw milk. Person-to-person transmission has not been demonstrated.
Reservoir hosts may include bats, with viral isolation recorded from species such as the Peters’s dwarf epauletted fruit bat and the Aba roundleaf bat, suggesting possible ecological maintenance of the virus outside mosquito populations.

Pathogenesis

Pathogenesis is intimately tied to the virus’s capacity to suppress innate immunity. NSs-mediated inhibition of interferon production allows the virus to replicate extensively within hepatic cells, leading to acute liver injury. In severe cases, widespread vascular leakage, coagulopathy and multi-organ involvement contribute to haemorrhagic manifestations. Neurological disease likely arises from direct viral invasion or inflammatory responses within the central nervous system.

Diagnosis

Definitive diagnosis depends on the detection of viral RNA, antigens or antibodies in blood or tissues. Laboratory methods include viral isolation, nucleic acid amplification tests, enzyme-linked immunosorbent assays for IgM antibodies and cell culture systems. Rapid diagnostic tools such as Immunoline, developed by the Kenya Medical Research Institute, have accelerated case identification in endemic regions.

Prevention

Preventive measures focus on reducing exposure to infected animals and controlling mosquito vectors. Protective clothing, gloves and face shields are recommended for individuals working with livestock in endemic areas. The use of bed nets, mosquito repellents and vector-control programmes such as larviciding help reduce human infections.
Animal vaccination is a core strategy for preventing outbreaks, though vaccination must occur before viral circulation begins. Killed veterinary vaccines require multiple doses and are less suitable for large-scale use. Live vaccines, such as MP-12 and clone 13, offer single-dose immunity but may carry risks of birth defects in some species. Recombinant and genetically engineered vaccines, including those lacking NSs and NSm proteins, show promise in experimental settings.
No human vaccine is widely available, though experimental candidates have been administered to high-risk laboratory personnel.
Restricting livestock movement during outbreaks and enhancing environmental and disease surveillance can reduce epidemic spread.

Epidemiology

Rift Valley fever occurs primarily across sub-Saharan Africa, with occasional incursions into the Arabian Peninsula. Outbreaks are strongly correlated with climatic anomalies linked to the El Niño–Southern Oscillation, during which increased rainfall fosters vegetation growth and the expansion of mosquito populations.
The ability of the virus to remain dormant in mosquito eggs for extended periods enables sudden explosive outbreaks following heavy rains or flooding. Geographic hotspots reflect the intersection of susceptible livestock populations, suitable mosquito habitats and climatic triggers.