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PubMed1984

Detection of human immunoglobulins G and M antibodies to Rift Valley fever virus by enzyme-linked immunosorbent assay.

Rift Valley fever virus (RVFV) is an important human and animal pathogen in Africa and has been responsible for infections in travelers. Because of the aerosol infectivity and risk of dissemination of the virus, a need exists for simple, safe, serological tests for diagnosis. An enzyme-linked immunosorbent assay (ELISA) was developed to detect RVFV-specific immunoglobulins (immunoglobulin G [IgG] and IgM). In the test, a betapropiolactone-inactivated, sucrose-acetone-extracted, suckling mouse liver RVFV antigen was captured by mouse RVFV antibodies adsorbed to polystyrene plates. The test sample (human serum) was then added, and the binding of specific antibodies was indicated by alkaline phosphatase-conjugated swine anti-human IgG or IgM. A mu-capture IgM ELISA was also developed by using polystyrene plates coated with goat anti-human IgM incubated successively with serum sample, RVFV antigen, and indicator antibodies. The ELISA for RVFV-specific IgG proved to be more sensitive than hemagglutination inhibition or complement fixation tests and almost as sensitive as the plaque reduction neutralization test in detecting specific antibodies in human sera after vaccination. The two ELISA IgM tests could detect specific IgM antibodies during the first 6 weeks after RVFV vaccination. Three injections of inactivated vaccine were given on days 0, 6 to 8, and 32 to 34. ELISA IgM values for sera obtained on days 6 to 8 were negative or in the lower range of significance, on days 32 to 34 they were strongly positive, and on days 42 to 52 they were waning. Later sera were negative. The plague reduction neutralization test was negative on days 6 to 8 but rose progressively in later samples. These findings suggest that the three doses of RVFV vaccine induce a prolonged primary antibody response. The ELISA IgM could become an important tool for early diagnosis in acute human infection. A number of African sera, some of which were positive for RVFV by plaque reduction neutralization test, were also tested by ELISA IgG. There was good agreement between both tests.

Animals↗

PubMed1986

A possible route for the introduction of Rift Valley fever virus into Egypt during 1977.

Rift Valley fever (RVF), which was enzootic in Sudan in 1976 and epidemic in Egypt in 1977-78, may have been introduced into Egypt from Sudan via sheep transported along Lake Nasser. A hypothesis is presented which describes sheep transport from holding areas in north-central Sudan, where RVF was epizootic, to live animal markets in southern Egypt. Travel time from north-central Sudan to the Aswan area was less than 5 days, approximating the incubation period of RVF virus in sheep. Reintroduction of RVF or other diseases from Sudan into Egypt will be facilitated by the construction of new roads linking the two countries.

Animals↗

PubMed1988

Morphology and development of Rift Valley fever virus in Vero cell cultures.

Rift Valley fever virus (RVFV) grown in vero cell cultures has a completed replication cycle within 13 hours. The first signs are the appearance of intranuclear fibrillar rods, followed by aggregations of precursor viral material in host cell cytoplasm and viral nucleocapsids budding into vacuoles associated with the Golgi apparati. Mature particles, liberated by the disintegration of vero cells, contained ribosomelike structures within the nucleocapsid, which was surrounded by a typical unit membrane through which were inserted some 350-375 surface spikes whose inner ends were incorporated into the nucleocapsid structure. In the negatively stained material, the overall diameter of the virion was 90-110 nm; the spikes were 10-18 nm in length and 5 nm in diameter.

Animals↗

PubMed2002

Bidirectional infection and release of Rift Valley fever virus in polarized epithelial cells.

Rift Valley Fever (RVF) virus is an arbovirus and is responsible for large outbreaks of disease predominantly in sub-Saharan Africa. However, several aspects of RVF virus transmission, such as high viremia, multiple vector species, and broad host range, result in a pathogen with high likelihood of geographic spread. RVF virus infection in humans and livestock is characterized by broad dissemination of RVF virus antigens throughout the body. We sought insight into the high pathogenicity and broad tropism of this virus through a characterization of its interaction with polarized epithelial cells. Our results indicate that infection and release of RVF virus in polarized epithelial cells occurs at both apical and basolateral membranes and hence is bidirectional. Furthermore, our results indicate that RVF virus causes disruptions in both the microfilament and the microtubule networks. These disruptions may provide a mechanism for bidirectional release of RVF virions.

Actin Cytoskeleton↗

PubMed1988

Genetic variation among geographic isolates of Rift Valley fever virus.

The genetic variation of Rift Valley fever virus (RVFV) was estimated by sequencing a portion of the M segment RNA of 22 isolates from a variety of host species collected over 34 years in 6 African countries. The M segment RNA of the Egyptian isolate, ZH501, which has been molecularly cloned and sequenced, was used as a reference for these comparisons. Specific gene regions, responsible for antigenic determinants presumed to play a role in protection against disease, were emphasized in these investigations. Comparative sequence data revealed that most isolates were very similar to ZH501 at both the nucleic acid and deduced amino acid sequence levels. Nucleic acid sequence variation range was 0-4.5%. Amino acid sequence variation range was 0-2.4%. We identified specific amino acid coding changes which may be involved in virus neutralization and may contribute to the virulence characteristics of RVFV.

Amino Acid Sequence↗

PubMed1997

Variability of the NS(S) protein among Rift Valley fever virus isolates.

Eighteen strains of Rift Valley fever (RVF) virus collected over a period of 38 years and isolated from diverse localities in Africa and from various hosts (human, animal and arthropod) were investigated by RT-PCR followed by sequencing of the NS(S) protein coding region. This region was chosen to analyse variability because, in contrast to the N protein, the NS(S) protein differs in various phleboviruses and there exists an RVF virus (clone 13) in which 70% of the NS(S) ORF is deleted, suggesting that this sequence is under a weak selective pressure. Sequence data indicated that percentage divergence among isolates ranged from 0 to 9.6% at the nucleotide level and from 0 to 9.5% at the amino acid level. Phylogenetic analysis based on the NS(S) gene revealed two major lineages: Egyptian and sub-Saharan. This led to the establishment of the relatedness between strains and insights into the NS(S) protein, the function of which is still undetermined. Alignment of the deduced amino acid sequences indicated that the cysteine residues are conserved, as are several motifs representing potential phosphorylation sites.

Animals↗

PubMed2002

Characterization of the Golgi retention motif of Rift Valley fever virus G(N) glycoprotein.

As Rift Valley fever (RVF) virus, and probably all members of the family Bunyaviridae, matures in the Golgi apparatus, the targeting of the virus glycoproteins to the Golgi apparatus plays a pivotal role in the virus replication cycle. No consensus Golgi localization motif appears to be shared among the glycoproteins of these viruses. The viruses of the family Bunyaviridae synthesize their glycoproteins, G(N) and G(C), as a polyprotein. The Golgi localization signal of RVF virus has been shown to reside within the G(N) protein by use of a plasmid-based transient expression system to synthesize individual G(N) and G(C) proteins. While the distribution of individually expressed G(N) significantly overlaps with cellular Golgi proteins such as beta-COP and GS-28, G(C) expressed in the absence of G(N) localizes to the endoplasmic reticulum. Further analysis of expressed G(N) truncated proteins and green fluorescent protein/G(N) chimeric proteins demonstrated that the RVF virus Golgi localization signal mapped to a 48-amino-acid region of G(N) encompassing the 20-amino-acid transmembrane domain and the adjacent 28 amino acids of the cytosolic tail.

Amino Acid Motifs↗

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↗

PubMed1992

[Serological survey of Rift Valley fever in sheep on the Ivory Coast].

A serological survey of Rift Valley fever was carried out in sheep in Côte-d'Ivoire. Thousand and fifty one seras collected between 1988 and 1990 in the South of the country were tested for IgG and IgM by ELISA with two objectives: determining the incidence of the Rift Valley fever and analysing the role of this virus in reproductive failure and abortion. The incidence rate was 6.85%. No difference was found between the three different geographic areas nor between the three years of the survey. Antibody prevalence increased significantly with age. The Rift Valley fever must be considered as enzootic in Côte-d'Ivoire. A significant relationship was found between positivity and abortion in ewes. Thus, the economic impact of Rift Valley fever has to be studied. The presence of antibodies in young animals aged from 6 months to 1 year, showed a recent activity of the virus; a permanent epidemio-surveillance of the Rift Valley fever in Côte-d'Ivoire is needed, because of the potential risk for human population in contact with the animals.

Animals↗

PubMed1980

Rift Valley fever in humans in South Africa.

During an epizootic of Rift Valley fever in South Africa in 1974/1975, mainly affecting sheep and cattle, a large number of human cases occurred. The majority of the patients, mostly farmers, farm labourers and veterinary surgeons, acquired the infection while handling the carcasses of animals which had died of Rift Valley fever. Some gave no history of contact with infected animals and it is presumed that they were infected by mosquitoes. Complications were common. Retinitis clinically associated with defective vision occurred in about 20% of patients investigated. In others, meningo-encephalitis developed; 1 patient died and the brain showed perivascular cuffing and round-cell infiltration. In 110 cases the diagnosis was confirmed in the laboratory, in 17 by isolation of the virus and in 93 by the finding of an antibody response in serological tests. In 3 fatal cases the virus was isolated from the liver, and in a further 4 fatal cases in which virus isolation was not attempted, there was clinical and epidemiological evidence of the diagnosis; in each case a haemorrhagic state associated with hepatitis had developed. In 1978, follow-up studies showed that immune rates among residents on affected farms varied from 10% in children to 17,1% in adult males, with an overall immunity rate of 14,5%.

Adult↗

PubMed1979

[Rift Valley Fever, a Veterinary and Medical Problem (author's transl)].

Rift Valley fever probably occurred in East and South Africa for many years, where it occasionally caused sever epizootics among sheep and to a less extent in cattle and goats. Particularly newborn animals fall victims to the disease, whereas the majority of pregnant ewes and cows abort. In recent years, the disease spread to the Sudan and reached the Nile delta in 1977, where it not only caused an epizootic but also an epidemic among the population, resulting in approximately 18,000 cases and nearly 600 deaths. During the summer of 1978, the disease was observed again so that the virus must have overwintered in the newly infested area. The disease in animals and subsequently in man, displaying four different clinical forms, is discussed. The limited knowledge of the pathogenesis and epidemiology is stressed particular attention being paid to the Egyptian epizootic and epidemic. Because of inadequate knowledge of the clinical features, pathogenesis and other data, the disease among cattle was not detected until from five to six months after it had broken out. The spread of Rift Valley fever to the north-eastern part of Africa forms a potential threat of dissemination of the virus to neighbouring countries, situated on the two adjacent continents of Asia and Europe, and it is a real one. International travel and movement of goods and animals as well as the political situation in that area involves the danger of the Rift Valley fever virus also being transferred to new areas and becoming established there.

Africa, Eastern↗

PubMed1992

Patterns of Rift Valley fever activity in Zambia.

An hypothesis that there was an annual emergence of Rift Valley fever virus in Zambia, during or after the seasonal rains, was examined with the aid of sentinel cattle. Serum samples taken during 1974 and 1978 showed evidence of epizootic Rift Valley fever in Zambia, with more than 80% positive. A sentinel herd exposed from 1982 to 1986 showed that some Rift Valley fever occurred each year. This was usually at a low level, with 3-8% of the susceptible cattle seroconverting. In 1985-6 more than 20% of the animals seroconverted, and this greater activity was associated with vegetational changes--which could be detected by remote-sensing satellite imagery--which have also been associated with greater virus activity in Kenya.

Animals↗

PubMed1990

[Evaluation of indicators of health in the area of Trarza during the epidemic of Rift Valley fever in 1987].

Randomized epidemiological studies conducted inside the Rift Valley fever epidemic area permitted an estimate of the different epidemiological rates. For the town of Rosso, the total number of infected persons was estimated at 9,320, the total number of symptomatic diseases at 1,013 and the number of deaths at 47. The minimal number of deaths for the area which had access to the hospital was 232. The immunity rate in the town was 34.89% after the epidemic. The ELISA test was used to test human and animal IgG and IgM antibodies. Human samples were collected using the "confetti" technique. After the epizootic the incidence was 36.9% and the immunity was 70.06% for animals sampled in the town.

Animals↗

PubMed1981

Respiratory infectivity of a recently isolated Egyptian strain of Rift Valley fever virus.

The respiratory infectivity of a strain of Rift Valley fever virus isolated in Egypt (strain ZH-501) was compared with that of one isolate from Uganda (Entebbe strain) and two isolates from South Africa (strains SA-51 and SA-75). Studies were performed with ICR mice which were infected by exposure to infectious aerosols composed of particles with a mass median diameter of 0.96 micrometer. The respiratory median lethal doses for ZH-501, Entebbe, SA-51, and SA-75 were 2.2, 1.9, 2.6, and 1.9 log10 plaque-forming units, respectively. Although these values are statistically different, the biological implications of such differences seem unimportant. In an additional study of pathogenesis, a single group of mice was infected with 3.1 log10 plaque-forming units of ZH-501, and tissues were assayed sequentially through 96 h postinfection. Between 6 and 30 h, demonstration of an increasing virus concentration only in the lungs indicated that initial replication occurred there; however, determination of histopathological changes did not reveal evidence of pneumonia. Virus was isolated from the liver by 48 h, and the ultimate outcome of infection was a fulminating and fatal hepatic necrosis.

Aerosols↗

PubMed1982

The susceptibility of Culicoides variipennis Coq. (Diptera: Ceratopogonidae) to laboratory infection with Rift Valley fever virus.

The vector potential of Culicoides variipennis for Rift Valley fever virus (RVFV) was investigated. Insects from a colony maintained at the Animal Virus Research Institute, Pirbright, were fed through a membrane on a mixture of mouse blood and RVFV (virus concentration of blood meal 7 X 95 log10 MLD50ml). Engorged insects were maintained at 25 degrees C +/- 1 degrees C. Samples of insects were tested at daily intervals to determine their virus content. Four of the five females tested immediately after feeding contained virus. The mean virus concentration of these infected flies was 2 X 7 log10MLD50. The virus concentration per fly decreased to 0 by day 2 post infection. On day 3, a virus concentration of 2 X 4 log10 MLD50 per fly was recorded from a pool of 17 flies but between day 4 and day 12 when the experiment terminated no virus was detected in any of the 135 females tested. Because of the pathogenic nature of RVFV, this work was carried out under the stringent security regulations at the PHLS Centre for Applied Microbiology and Research, Porton Down. The problems arising from experiments requiring the handling and infection of insects under such conditions are described.

Animals↗

PubMed2006

Protective immune responses induced by different recombinant vaccine regimes to Rift Valley fever.

The glycoprotein (GP) and nucleocapsid (NC) genes of Rift Valley fever virus (RVFV) were expressed in different expression systems and were evaluated for their ability to protect mice from virulent challenge using a prime-boost regime. Mice vaccinated with a lumpy skin disease virus-vectored recombinant vaccine (rLSDV-RVFV) expressing the two RVFV glycoproteins (G1 and G2) developed neutralising antibodies and were fully protected when challenged, as were those vaccinated with a crude extract of truncated G2 glycoprotein (tG2). By contrast mice vaccinated with a DNA vaccine expressing G1 and G2 did not sero-convert with only 20% of them surviving challenge. Mice vaccinated with the DNA vaccine and boosted with rLSDV-RVFV also failed to sero-convert but 40% survived challenge. Surprisingly, although none of the mice immunised with the purified NC protein sero-converted, 60% of them survived virulent challenge. The rLSDV-RVFV construct was then further evaluated in sheep for its dual protective abilities against RVFV and sheeppox virus (SPV). Vaccinated sheep sero-converted for both viruses and were protected against RVFV challenge, however, neither the immunised or negative control animals showed any significant reactions to the virulent SPV challenge.

Animals↗

PubMed1987

Pathogenesis of Rift Valley fever virus (RVFV) in inbred rats.

The pathogenesis of Rift Valley fever in adult rats from 3 inbred strains (LEW, MAXX, WF) was investigated. WF rats all died by day 2 postinoculation with viral tissue titers reaching 9 log10 PFU/g. LEW and MAXX rats were resistant to liver disease, but fatal necrotising encephalitis developed in 16 and 44% of the rats, respectively. Detection of serum neutralising antibody on day 3 coincided with clearance of virus from serum and liver, although infectious virus was detected in spleen homogenates as late as day 19 postinfection. Viral titers in LEW and MAXX rats did not exceed 4.5 log10 PFU/g. Cyclophosphamide immunosuppression of LEW rats led to death 5-9 days postinfection; early patterns of viral replication were not affected, but continued growth in the liver resulted in fatal hepatitis. These animals could be protected by passive antibody therapy administered on days 2-5 postinfection to mimic the serum neutralising antibody pattern seen in unmanipulated infected LEW rats. Thus, RVF virus replication and spread is rapid in the WF rats tissues, whereas in LEW and MAXX rats viral growth is less due to an intrinsic mechanism which allows sufficient time for an immune response to terminate infection. A slightly diminished immune response may lead to the development of encephalitis more frequently in MAXX than LEW rats. These rat strains should be useful in elucidating those mechanisms of resistance which limit RVFV-induced hepatitis and encephalitis.

Animals↗

PubMed2002

Genetic analysis of viruses associated with emergence of Rift Valley fever in Saudi Arabia and Yemen, 2000-01.

The first confirmed Rift Valley fever outbreak outside Africa was reported in September 2000, in the Arabian Peninsula. As of February 2001, a total of 884 hospitalized patients were identified in Saudi Arabia, with 124 deaths. In Yemen, 1,087 cases were estimated to have occurred, with 121 deaths. Laboratory diagnosis of Rift Valley fever virus (RVFV) infections included virus genetic detection and characterization of clinical specimens by reverse transcription-polymerase chain reaction, in addition to serologic tests and virus isolation. Genetic analysis of selected regions of virus S, M, and L RNA genome segments indicated little genetic variation among the viruses associated with disease. The Saudi Arabia and Yemen viruses were almost identical to those associated with earlier RVF epidemics in East Africa. Analysis of S, M, and L RNA genome segment sequence differences showed similar phylogenetic relationships among these viruses, indicating that genetic reassortment did not play an important role in the emergence of this virus in the Arabian Peninsula. These results are consistent with the recent introduction of RVFV into the Arabian Peninsula from East Africa.

Antigens, Viral↗