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Results for “Rift Valley Fever”

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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↗

PubMed1999

Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya.

All known Rift Valley fever virus outbreaks in East Africa from 1950 to May 1998, and probably earlier, followed periods of abnormally high rainfall. Analysis of this record and Pacific and Indian Ocean sea surface temperature anomalies, coupled with satellite normalized difference vegetation index data, shows that prediction of Rift Valley fever outbreaks may be made up to 5 months in advance of outbreaks in East Africa. Concurrent near-real-time monitoring with satellite normalized difference vegetation data may identify actual affected areas.

Animals↗

PubMed1984

Protein synthesis in Rift Valley fever virus-infected cells.

Rift Valley fever virus-induced protein synthesis was examined by polyacrylamide gel electrophoresis and fluorography. Five virus-induced polypeptides were detected, the nucleocapsid protein N, the nucleus-associated nonstructural protein NS1, the glycoproteins G1 and G2, and a protein of molecular weight 80K. The N, G1, G2, and 80K proteins were present in virion preparations. Sequential studies showed that NS1 accumulated in the nucleus as soon as it was formed and readily associated with nuclei partitioned from noninfected cells. The G1 and G2 proteins labelled with [3H]glucosamine and [3H]mannose. NS1 was shown to be the only virus-induced protein which was phosphorylated.

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↗

PubMed1982

Reduced pathogenicity associated with a small plaque variant of the Egyptian strain of Rift Valley fever virus (ZH501).

Variants of Rift Valley fever virus producing plaques in CER cells of four different sizes are described. A plaque-forming unit (PFU) variant forming minute plaques was isolated and purified. Virus derived from this variant was not pathogenic to adult Swiss albino mice by the intraperitoneal (i.p.) route and was less pathogenic than the parent strain (ZH501) to adult Sprague Dawley rats by i.p. route, but produced typical severe liver necrosis in adult Syrian hamsters with intranuclear and intracytoplasmic eosinophilic inclusions. Antigen and antiserum to the minute variant prepared in mice reciprocally cross-reacted with antisera and antigens of the original strain (ZH501) in the complement fixation test. Plaque size of the minute variant remained constant after serial passages in cell culture and in suckling mouse brain. When the minute plaque variant was passaged i.p. in hamsters, virus which formed large plaques in CER cells was recovered from the hamster sera.

Animals↗

PubMed2001

Climate-disease connections: Rift Valley Fever in Kenya.

All known Rift Valley fever(RVF) outbreaks in Kenya from 1950 to 1998 followed periods of abnormally high rainfall. On an interannual scale, periods of above normal rainfall in East Africa are associated with the warm phase of the El Niño/Southern Oscillation (ENSO) phenomenon. Anomalous rainfall floods mosquito-breeding habitats called dambos, which contain transovarially infected mosquito eggs. The eggs hatch Aedes mosquitoes that transmit the RVF virus preferentially to livestock and to humans as well. Analysis of historical data on RVF outbreaks and indicators of ENSO (including Pacific and Indian Ocean sea surface temperatures and the Southern Oscillation Index) indicates that more than three quarters of the RVF outbreaks have occurred during warm ENSO event periods. Mapping of ecological conditions using satellite normalized difference vegetation index (NDVI) data show that areas where outbreaks have occurred during the satellite recording period (1981-1998) show anomalous positive departures in vegetation greenness, an indicator of above-normal precipitation. This is particularly observed in arid areas of East Africa, which are predominantly impacted by this disease. These results indicate a close association between interannual climate variability and RVF outbreaks in Kenya.

Aedes↗

PubMed1999

Host feeding of mosquitoes (Diptera: Culicidae) associated with the recurrence of Rift Valley fever in Egypt.

In 1993, Rift Valley fever (RVF) virus reappeared in Egypt. We determined the prevalence and feeding patterns of mosquitoes in 5 villages where the virus was active. Of 10 species recovered, Aedes caspius (Pallas), Culex pipiens L., Cx. antennatus (Becker), and Cx. perexiguus Theobald constituted 99% of > 35,000 mosquitoes captured in dry ice-baited CDC light traps. Ae. caspius was most prevalent, except at Nag' El Hagar where it was replaced by Cx. perexiguus. Cx. pipiens ranked 2nd, except at Nag' El Ghuneimiya, where it was replaced by Cx. antennatus. Most blood meals analyzed by an enzyme-linked immunosorbent assay reacted to > or = 1 antiserum. Cx. pipiens was mainly anthropophagic, and therefore may have been the main vector of RVF virus among humans. Ae. caspius feeds were chiefly from humans, bovines, and equines. Cx. antennatus and Cx. perexiguus fed generally on bovines. Mixed blood meals from humans and RVF virus susceptible animals were identified in the predominant mosquitoes. Prevalence and host selection, as well as predicted probability for a blood meal being interrupted, indicated that Ae. caspius may have served as a bridge vector between humans and bovines in 4 of the villages. Cx. perexiguus may have played this role at Nag' El Hagar. Because potential vectors are abundant, susceptible domestic animals are associated closely with humans, and surveillance of imported livestock is not systematic, we conclude that RVF virus sporadically will recur in Egypt.

Aedes↗

PubMed2001

Genetic evidence for an interferon-antagonistic function of rift valley fever virus nonstructural protein NSs.

Rift Valley fever virus (RVFV), a phlebovirus of the family Bunyaviridae, is a major public health threat in Egypt and sub-Saharan Africa. The viral and host cellular factors that contribute to RVFV virulence and pathogenicity are still poorly understood. All pathogenic RVFV strains direct the synthesis of a nonstructural phosphoprotein (NSs) that is encoded by the smallest (S) segment of the tripartite genome and has an undefined accessory function. In this report, we show that MP12 and clone 13, two attenuated RVFV strains with mutations in the NSs gene, were highly virulent in IFNAR(-/-) mice lacking the alpha/beta interferon (IFN-alpha/beta) receptor but remained attenuated in IFN-gamma receptor-deficient mice. Both attenuated strains proved to be excellent inducers of early IFN-alpha/beta production. In contrast, the virulent strain ZH548 failed to induce detectable amounts of IFN-alpha/beta and replicated extensively in both IFN-competent and IFN-deficient mice. Clone 13 has a defective NSs gene with a large in-frame deletion. This defect in the NSs gene results in expression of a truncated protein which is rapidly degraded. To investigate whether the presence of the wild-type NSs gene correlated with inhibition of IFN-alpha/beta production, we infected susceptible IFNAR(-/-) mice with S gene reassortant viruses. When the S segment of ZH548 was replaced by that of clone 13, the resulting reassortants became strong IFN inducers. When the defective S segment of clone 13 was exchanged with the wild-type S segment of ZH548, the reassortant virus lost the capacity to stimulate IFN-alpha/beta production. These results demonstrate that the ability of RVFV to inhibit IFN-alpha/beta production correlates with viral virulence and suggest that the accessory protein NSs is an IFN antagonist.

Animals↗

PubMed1999

An epizootic of Rift Valley fever in Egypt in 1997.

An epizootic of Rift Valley fever (RVF) occurred in Egypt between April and August 1997. The signs among infected cattle and sheep were high fever, icterus, bloody diarrhoea and abortion. Aborted sheep foetuses and sera from the affected herds were collected in the Aswan and Assiut Provinces, Upper Egypt, for virological and serological examination. A cytopathic effect was detected in Vero cell cultures 48 h after inoculation with the foetal liver and spleen suspensions. The same suspensions caused paralysis and mortalities two to three days post intracerebral injection in mice. The isolated virus was identified using an agar gel precipitation test (AGPT) and a direct fluorescent antibody technique. Serological examination revealed that all tested sheep (57) and cattle (93) gave positive results to serological tests, using a complement fixation (CF), serum neutralisation (SN) and indirect immunofluorescence assay; while only 48 (84.2%) out of 57 sheep sera and 69 (74.2%) out of 93 cattle sera gave positive results using an AGPT. Titration of the serum samples indicated that SN is more sensitive than CF. Importation of infected ruminants, especially camels from the Sudan, is the principal source of infection. Aswan, the nearest Egyptian province to the Sudan, is the focus of RVF virus infection in Egypt. As a result of high insect populations, the epizootics of RVF have usually occurred during the summer in Egypt. Reoccurrence of epizootics from time to time indicates failure of the applied RVF vaccination programme in Egypt.

Abortion, Veterinary↗

PubMed2001

Single-tube and nested reverse transcriptase-polymerase chain reaction for detection of Rift Valley fever virus in human and animal sera.

Rift Valley fever (RVF) is an anthropozoonosis caused by a Phlebovirus (Bunyaviridae family) that has re-emerged recently in East and West Africa in 1997-1998. This emphasizes the need for early and rapid detection of the virus and an efficient surveillance system. To this goal, a single tube or a nested reverse transcriptase-polymerase chain reaction (RT-PCR) method focusing on the NSs coding region of the S segment was developed and used to detect the RVF virus (RVFV) genome, resulting respectively in the synthesis of 810 and 662 bp DNA amplimers. The assay was specific for RVFV and did not amplify any other phleboviruses known to circulate in sub-Saharan Africa. When serial dilutions of RVFV were artificially mixed with human normal serum, the minimal detection limits were 50 and 0.5 plaque forming units respectively using the simple and the nested RT-PCR. The RT-PCR method was efficient for the detection of RVFV RNA in the blood from experimentally RVFV-infected mice and lamb and the nested RT-PCR was found more sensitive than the virus isolation method. Additionally, this detection method was applied successfully for the diagnosis of human cases during the 1998 Mauritanian outbreak.

Animals↗

PubMedDate not supplied

New vectors of Rift Valley fever in West Africa.

After an outbreak of Rift Valley fever in Southern Mauritania in 1987, entomologic studies were conducted in a bordering region in Sénégal from 1991 to 1996 to identify the sylvatic vectors of Rift Valley fever virus. The virus was isolated from the floodwater mosquitoes Aedes vexans and Ae. ochraceus. In 1974 and 1983, the virus had been isolated from Ae. dalzieli. Although these vectors differ from the main vectors in East and South Africa, they use the same type of breeding sites and also feed on cattle and sheep. Although enzootic vectors have now been identified in West Africa, the factors causing outbreaks remain unclear.

Aedes↗

PubMed2000

Resistance to Rift Valley fever virus in Rattus norvegicus: genetic variability within certain 'inbred' strains.

Rift Valley fever virus (RVFV) is the causative agent of Rift Valley fever, a widespread disease of domestic animals and humans in sub-Saharan Africa. Laboratory rats have frequently been used as an animal model for studying the pathogenesis of Rift Valley fever. It is shown here that Lewis rats (LEW/mol) are susceptible to infection with RVFV, whereas Wistar-Furth (WF/mol) rats are resistant to RVFV infection. LEW/mol rats developed acute hepatitis and died after infection with RVFV strain ZH548, whereas WF/mol rats survived the infection. Cross-breeding of resistant WF/mol rats with susceptible LEW/mol rats demonstrated that resistance is segregated as a single dominant gene. Primary hepatocytes but not glial cells from WF/mol rats showed the resistant phenotype in cell culture, indicating that resistance was cell type-specific. Moreover, when cultured hepatocytes were stimulated with interferon (IFN) type I there was no indication of a regulatory role of IFN in the RVFV-resistance gene expression in WF/mol rats. Interestingly, previous reports have shown that LEW rats from a different breeding stock (LEW/mai) are resistant to RVFV infections, whereas WF/mai rats are susceptible. Thus, inbred rat strains seem to differ in virus susceptibility depending on their breeding histories. A better genetic characterization of inbred rat strains and a revision in nomenclature is needed to improve animal experimentation in the future.

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↗

PubMed1984

Replication of Rift Valley fever virus in the sand fly Lutzomyia longipalpis.

Rift Valley fever virus was shown to replicate in Lutzomyia longipalpis after intrathoracic inoculation. Viral titers peaked at approximately 4 days postinoculation [mean titer = 10(4.0) plaque forming units (PFU)] and remained relatively constant through day 7. A minimum of 6 of 326 sand flies transmitted virus by bite to susceptible hamsters after 5-9 days of extrinsic incubation. Viral titers of sand flies exposed per os declined steadily through day 9. None of 378 flies that had ingested approximately 10(4.0) PFU of virus transmitted virus when refed on susceptible hamsters.

Animals↗

PubMed1980

Ocular disease resulting from infection with Rift Valley fever virus.

The demonstration of serological conversion to Rift Valley fever (RVF) virus in paired acute and convalescent sera established RVF as the cause of two cases of retinitis seen during the 1977 RVF epidemic in Egypt. Colour photography of the retina revealed macular, paramacular and extramacular exudate-like lesions with associated haemorrage and oedema. One patient has not recovered central vision during a six-month convalescence. An ongoing study of a larger group of RVF patients with ocular disease revealed that the findings presented for these two cases represented the types of lesions most frequently encountered during the epidemic.

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↗

PubMed1980

Evaluation of a formalin-inactivated Rift Valley fever vaccine in sheep.

A formalin-inactivated Rift Valley fever (RVF) vaccine prepared in cell culture for human use was immunogenic in sheep. Vaccine was administered as a single dose of diluted (1:5) or undiluted vaccine with or without an adjuvant. Serum-neutralizing antibodies induced by RVF vaccine persisted for at least 7 months. Seven of 11 vaccinated sheep with prechallenge plaque-reduction neutralization (PRN80) antibody titers of less than or equal to 10 were protected against challenge exposure with 10(6) plaque-forming units of Zagazig 501 strain of RVF virus. Challenge exposure induced abortion in 2 of 2 pregnant sheep. Five sheep with PRN80 titers greater than or equal 1:20 were protected from detectable viremia after challenge exposure. Additionally, 5 of 6 lambs (3 months old) were protected (by maternal antibodies) against challenge exposure. Challenge control sheep developed clinical disease and detectable viremia after exposure. Virus was isolated from saliva of 1 challenge control sheep and virus was transmitted by contact exposure to 1 of 4 seronegative contact-control sheep. Immunization of sheep with formalin-inactivated RVF vaccine induced a priming effect against RVF viral antigens. Challenge exposure with RVF virus resulted in significantly higher neutralizing titers in vaccinated sheep than in nonvaccinated sheep.

Animals↗