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PubMed2026

Spatiotemporal patterns of Rift Valley fever virus in Africa: a retrospective genomic epidemiology and phylodynamic modelling study.

BACKGROUND: Rift Valley fever virus (RVFV) is a mosquito-borne zoonotic pathogen causing outbreaks in humans and ruminants across Africa and the Arabian Peninsula. Originally restricted to the Great Rift Valley, RVFV has expanded geographically, prompting its classification by WHO as a pathogen of pandemic potential. We investigated the evolutionary and spatial dynamics of RVFV across Africa. METHODS: We used genomic data generated at the International Livestock Research Institute Nairobi genomic laboratory (BioProject PRJNA1106221) and combined with publicly available datasets retrieved from the National Center for Biotechnology (NCBI) GenBank nucleotide database. In retrieving RVFV genome sequences from the NCBI GenBank, we applied the search terms "Rift Valley fever virus segment L AND 6404[SLEN]", "Rift Valley fever virus segment M AND 3885[SLEN]", and "Rift Valley fever virus segment S AND 1520:1690[SLEN]" for L (Large), M (Medium), and S (Small) segments, respectively. For sequences without additional spatiotemporal information, we searched PubMed to extract the associated sequence metadata. We performed molecular clock analysis, phylogenetic inference, phylodynamic modelling (continuous phylogeographic reconstruction), and landscape phylogeography on the three RVFV genome segments (L, M, and S). We aimed to assess evolutionary rates, dispersal patterns, and environmental drivers. Focus was placed on lineage C, the most widely distributed variant. FINDINGS: The global dataset used in this study consisted of large (n=236), medium (n=237), and small (n=247), which were further filtered to exclude potential reassortants and vaccine strains. Genome sequences retrieved from NCBI GenBank database comprised large (n=180), medium (n=184), and small (n=202). The genome sequences from retrospective human and livestock isolates comprised large (n=56), medium (n=53), and small (n=45) collected in Burundi (2018), Kenya (2007, 2018, 2019, 2021, and 2022), and Rwanda (2018 and 2022). Our dataset revealed that RVFV exhibited low overall genetic diversity. Lineage C, however, showed evidence of active evolution, with substitution rates ranging from 3·58 × 10-4 to 9·76 × 10-4 substitutions per site per year. This lineage probably originated in Zimbabwe in the mid-1970s and has since expanded across eastern and southern Africa. Phylogeographic reconstructions revealed rapid spread, with diffusion coefficients exceeding 50 000 km2 per year. INTERPRETATION: Lineage C appears capable of establishing endemic transmission in new regions, with ongoing diversification observed during interepidemic periods. These observations reinforce the value of continuous genomic surveillance, particularly during cryptic transmission phases when adaptive mutations might emerge. Although further evidence is needed, observed trends in climate variability and land-use change point to the potential benefit of targeted surveillance in settings that could be at increased risk, including urban centres and wetlands. FUNDING: This work was supported by the German Federal Ministry for Economic Cooperation and Development, the Rockefeller Foundation, and the Africa Centres for Disease Control and Prevention.

Rift Valley fever virus↗

PubMed1979

Clinical, virological and serological response of the West African dwarf sheep to experimental infection with different strains of Rift Valley fever virus.

West African dwarf sheep were inoculated with three different strains of Rift Valley fever virus (RVFV). Using infective mouse serum as the source of virus classical RVFV disease characterised by sudden onset, a sharp but transient febrile response, viraemia, abortions and the development of specific RVFV antibodies in surviving animals was observed. The severity of clinical response was, however, dependent on the strain of virus used, with animals inoculated with Smithburn's neuroadapted strain showing a milder response than those inoculated with either the Nigerian or Lunyo strain. The inoculation of sheep with RVFV infective mouse brain material of the three different strains resulted in a mild febrile response with low level viraemia. Immune sera from sheep inoculated with both the Nigerian and Smithburn's neurotropic strains did not neutralise the Lunyo virus strain in a mouse intracerebral neutralisation test; the reverse, however, was not the case. The findings indicate that the West African dwarf sheep is highly susceptible to RVFV infection and that previous reports of only a mild clinical response following inoculation with the Nigerian strain were due to infective mouse brain rather than infective mouse serum.

Animals↗

PubMed1979

Pathogenicity of different strains of Rift Valley fever virus in Swiss albino mice.

Laboratory mice were inoculated with 3 different strains of Rift Valley fever virus (RVFV): namely, the prototype, the Nigerian, and the Lunyo variant strains of RVFV. Animals were inoculated with either infective mouse brain or serum by the i.c. or i.p. route and organs of inoculated animals examined for virus content and histopathological changes. Animals inoculated with either the classical or the Nigerian encephalitis only, to a ditropism involving mild lesions in the brain and liver or the typically severe RVFV hepatitis. The type of lesion shown was dependent on the source of inoculum and the route of inoculation. On the other hand, animals inoculated by the i.c. route with the infective brain material of the Lunyo variant virus showed a mild encephalitis, while the use of the i.p. route or infective blood source of the Lunyo virus resulted in the development of typical RVFV hepatitis. Typical intranuclear eosinophilic inclusion bodies were found in both the brain and liver of animals inoculated with the Lunyo variant virus. These inclusion bodies were found only in the livers of mice inoculated with the infective blood material of either the prototype or the Nigerian strain. There was no correlation between the virus titres in the different organs and the severity of histopathological lesions.

Animals↗

PubMed2025

Altered histone modifications in Aedes aegypti following Rift Valley fever virus exposure.

When arthropod-borne viruses (arboviruses) are delivered to vector mosquitoes in an infectious bloodmeal, viral components interact with host proteins to hijack cells and initiate replication. The extent to which arbovirus infection alters mosquito host transcriptional and genomic regulatory processes is currently unknown. We hypothesized that histone modifications would be altered in mosquitoes exposed to Rift Valley fever virus (RVFV MP12, Phlebovirus riftense, family Phleboviridae). We interrogated transcriptome and chromatin landscapes in Aedes aegypti midguts by performing Cleavage Under Targets and Release Using Nuclease (CUT&RUN), using H3K27ac and H3K9me3 marks. Altered H3K27ac marks were identified following RVFV MP12 exposure, as well as upon bloodfeeding alone. It took several days for differential H3K27ac marks to be associated with differentially expressed genes (DEGs) in RVFV-exposed midguts. H3K27ac peaks showed progressive depletion as infection progressed. Gene set enrichment analysis revealed that immune response transcripts were enriched at 1 and 3 dpf (days post-feeding) but depleted by 7 dpf. Hedgehog/Gli (glioma-associated oncogene homolog) signaling pathway transcripts were depleted, indicating possible viral manipulation of cellular polarization. Moreover, at 7 dpf, 7 of 102 DEGs were proximal to differentially acetylated sites in a pattern expected to favor viral propagation. However, one transcript coding for an antiviral effector (LysM-TLDc domain protein) showed significant depletion of both H3K9me3 and H3K27ac marks. Analysis of midguts after a non-infectious bloodmeal versus sugar-fed controls revealed global changes to H3K27ac and H3K9me3 marks during and following the period of bloodmeal digestion. Differential H3K27ac marks were proximal to one quarter of all DEGs at 1 dpf, consistent with an important role of H3K27ac in bloodmeal digestion. These results demonstrate that H3K27ac and H3K9me3 patterns are altered upon virus exposure in a complex interplay that favors viral replication but is also countered by host responses to limit replication.

ChIP-Seq↗

PubMed2025

Use of Rift Valley Fever Virus Expressing NanoLuc Luciferase for the Assessment of Neutralizing Antibodies and Antivirals.

Rift Valley fever (RVF) is an arboviral zoonotic disease affecting many African countries with the potential to spread to other geographical areas. In this chapter we describe the use of a replication-competent recombinant (r)RVFV expressing NanoLuc Luciferase (Nluc) for in vitro studies. The determination of parameters such as neutralizing antibodies in serum samples, or the antiviral activity of drugs is usually carried out using standard assays based on the assessment of cytopathic effect on cell cultures. The use of a virus encoding a traceable reporter protein allows to correlate the presence or absence of infection with the detection of the product in the infected cultures, thus tracking the level of RVFV infection in an objective, quantitative manner. In addition to this quantitative measurement of results, our protocol offers two other advantages, such as a shorter time to read, given that 48 h post-infection the production of the reporter protein is enough to give an accurate result, and the use of an attenuated virus, which reduces the risk of exposure.

Rift Valley fever virus↗