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PubMedDate not supplied

Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted.

Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.

Animals↗
PubMed1979

An epidemic of Rift Valley fever in Egypt. 1. Diagnosis of Rift Valley fever in man.

Rift Valley fever (RVF) virus was isolated from 53 of 56 sera collected from patients with a clinical picture of dengue-like illness during the peak of the epidemic of RVF in Egypt in the autumn of 1977. RVF virus was also isolated from the throat washings of two patients and the faeces of four, all of whom were positive for virus isolation from the serum. All the isolates were identified by the complement fixation (CF) test. Serological diagnosis of RVF, using paired sera from 16 patients, was made by both the haemagglutination-inhibition (HI) and CF tests. HI antibodies were demonstrated in all the acute sera, whereas CF antibodies, which seem to appear later, were detected in only seven acute and twelve convalescent sera. A longer period than the 12 days in this study must be allowed to elapse between the taking of the paired sera for a definite serological diagnosis to be obtained, especially when CF antibodies are taken into account.

Adult↗
PubMed1989

Ingestion of immune bloodmeals and infection of Aedes fowleri, Aedes mcintoshi, and Culex pipiens with Rift Valley fever virus.

Rift Valley fever (RVF) virus infection, dissemination, and transmission rates were determined for Aedes fowleri, Aedes mcintoshi and Culex pipiens 7 or 10 days after sequentially feeding to repletion on RVF virus immune hamsters and RVF viremic hamsters, or after feeding on a mixture of RVF virus immune sheep serum and RVF viremic hamster blood through a pledget. No significant differences in infection or dissemination rates were detected among Ae. fowleri and Cx. pipiens feeding to repletion on immune hamsters before or after feeding to repletion on a viremic hamster. Similarly, no significant differences in infection, dissemination, or transmission rates were observed among Ae. fowleri and Cx. pipiens feeding to repletion on immune hamsters or nonimmune (control) hamsters 0 or 24 hr after inoculation with RVF virus. Infection rates were significantly higher for Ae. fowleri (56/66, 85%) and Cx. pipiens (123/148, 83%) fed only on viremic hamsters than for those interrupted to complete feeding on an immune hamster (Ae. fowleri [24/49, 59%], Cx. pipiens [66/131, 50%]) or a nonimmune hamster (Ae. fowleri [32/51, 63%], Cx. pipiens [69/127, 54%]). However, no significant differences were detected in infection, dissemination, or transmission rates among Ae. fowleri, Ae. mcintoshi or Cx. pipiens fed on a viremic hamster and interrupted to complete feeding on an immune vs. a nonimmune hamster. Results from interrupted feeding experiments were significantly different from pledget feeding experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Aedes↗
PubMed1988

Viral determinants of virulence for Rift Valley fever (RVF) in rats.

Rift Valley fever viral strains or variants (RVFV) were compared with respect to (a) virulence for Wistar-Furth rats; (b) in vitro sensitivity to rat and human interferon; (c) ability to form plaques in primary hepatocyte cultures from genetically resistant or susceptible rat strains, and (d) replicative potential in continuous rat cell lines. Egyptian strains were highly virulent for Wistar-Furth rats; relatively resistant to rat interferon-alpha/beta; capable of producing plaques in primary hepatocyte monolayers; and, in general, replicated more rapidly than the low-virulent, sub-Saharan strains. Virtually all strains from sub-Saharan Africa were sensitive to rat interferon and did not form plaques in rat hepatocyte monolayers. An exception was the 2269/74 strain from Zimbabwe, which had characteristics of the Egyptian strains including increased virulence for Wistar-Furth rats. The relative virulence of RVFV strains for rats did not correlate with interferon sensitivity when human recombinant interferon-alpha was tested on A-549 cells. Thus, several in vitro phenotypic characteristics of RVFV strains tend to correlate with virulence for Wistar-Furth rats and with geographical origin of the viral strains.

Animals↗
PubMed1975

Observations on the epidemiology of Rift Valley fever in Kenya.

The epizootic range of Rift Valley fever in Kenya is defined from the results of virus isolations during epizootics, and form an extensive serological survey of cattle which were exposed during an epizootic. A study of the sera from a wide range of wild bovidae sampled immediately after the epizootic, showed that they did not act as reservoir or amplifying hosts for RVF. Virus isolation attempts from a variety of rodents proved negative. Rift Valley fever did not persist between epizootics by producing symptomless abortions in cattle in areas within its epizootic range. A sentinel herd sampled annually after an epizootic in 1968 revealed not one single seroconversion from 1969 to 1974. Certain forest and forest edge situations were postulated as enzootic for Rift Valley fever, and a small percentage of seroconversions were detected in cattle in these areas, born four years after the last epizootic. This has been the only evidence for the persistence of the virus in Kenya since 1968, and may be a part of the interepizootic maintenance cycle for Rift Valley fever in Kenya, which otherwise remains unknown.

Abortion, Veterinary↗
PubMed1987

Differentiation of a human monocytic cell line associated with increased production of Rift Valley fever virus by infected cells.

Rift Valley fever (RVF) virus is a cause of significant human and animal disease in many parts of Africa. In some cases, it causes a hemorrhagic fever, which is frequently fatal. Prior studies have shown that RVF virus productively infects peritoneal macrophages from susceptible rat strains. The U937 human monocytic cell line was used to determine the effect of monocytic cell differentiation on the degree of viral production by cell cultures infected with RVF virus. Differentiation of U937 cells to more mature monocytic cells by phorbol ester resulted in production of 10 times more infectious virions in comparison with undifferentiated cells. These studies imply that monocytic cell differentiation increases permissiveness for RVF virus production.

Bunyaviridae↗
PubMedDate not supplied

Hemostatic derangement produced by Rift Valley fever virus in rhesus monkeys.

Rift Valley fever (RVF) is an important cause of disease in animals and humans in sub-Saharan Africa. In a small percentage of human cases, the disease is complicated by hemorrhage, which often is associated with a fatal outcome. Inoculation of rhesus monkeys with the Zagazig Hospital strain of RVF virus produced a clinical picture similar to illness in humans. Ten of 17 monkeys developed clinical evidence of hemostatic impairment. When coagulation tests were performed, this group of monkeys had significant abnormalities, including evidence for disseminated intravascular coagulation. These abnormalities were much less pronounced in the remaining seven monkeys-whose only sign of illness was transient fever-and, in general, they paralleled the level of viremia and the degree of elevation in levels of serum hepatic enzymes. Autopsy of the three monkeys with severe disease revealed hepatic necrosis.

Animals↗
PubMed1991

Impact of stressful conditions on the survival of Culex pipiens exposed to Rift Valley fever virus.

Several groups of Rift Valley fever (RVF) virus-exposed and unexposed Culex pipiens were allowed differential access to a carbohydrate food source and their survival monitored. When stressed by deprivation of a carbohydrate source, mean survival times of RVF virus-exposed mosquitoes were consistently higher than those of unexposed mosquitoes in each of the carbohydrate-deficient experiments. These differences were statistically significant when mosquitoes were provided 5% sucrose for 24 hours. Mosquitoes that were provided access to a carbohydrate source for 24 h after a bloodmeal and then were denied access survived significantly longer than did those mosquitoes denied access, regardless of their exposure to RVF virus. When not stressed, RVF virus-exposed individuals had slightly higher daily survival rates than did unexposed individuals.

Animals↗
PubMed1977

An inactivated rift valley fever vaccine.

The immunising potency of an inactivated Rift Valley fever (RVF) vaccine prepared from RVF virus infected mouse brain and RVF infected cell culture was studied in cattle and sheep. Different doses and adjuvants were compared. In laboratory trials both cattle and sheep developed neutralising antibodies against virulent RVF virus and in cattle antibodies were still detectable 9 months after immunisation. Although the immunity produced was inadequate to prevent viraemia after challenge, evidence of protection against clinical RVF was obtained. Field trials in sheep showed that vaccination induced a good immunity in pregnant ewes.

Animals↗
PubMed1991

Ability of a mutagenized virus variant to protect young lambs from Rift Valley fever.

A live attenuated vaccine virus variant of Rift Valley fever (RVF) virus was developed by passaging a human isolate in tissue culture under the influence of the mutagen 5-fluorouracil. This virus variant (MV P12) has been assessed in this study as to its suitability as a vaccine, by testing its pathogenicity in young lambs and measuring its ability to induce a protective immune response. Even high doses of the vaccine virus failed to induce any of the clinical or histopathologic changes associated with classical RVF virus infection. Although the vaccine induced mild pyrexia when given in high doses, viremia was not induced. Neutralizing antibody and a protective immune response was elicited with even low doses of vaccine virus. These data, along with data of other workers on the lack of abortigenicity of this virus variant, indicate that the MV P12 variant of RVF virus is an excellent candidate for a safe and effective vaccine against RVF.

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↗
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↗
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↗
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↗