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A serosurvey of Rift Valley Fever virus infection conducted among 557 sheep and 643 goats from Niger in 1986 points out that 2.8% of the 1,200 animals tested had RVF virus reacting antibodies. The circulation of the virus is demonstrated, as well for another phlebovirus related to RVF virus, the strain Arumowot.
A retrospective study was undertaken to examine domestic ruminant sera for Rift Valley fever (RVF) virus antibodies. The sera were collected between 1992 and 1995 from cattle, sheep and goats from various locations in Saudi Arabia. The standard capture enzyme-linked immunosorbent assay system was employed to detect specific RVF antibodies in the animals and the results indicated an absence of RVF antibodies. This finding confirms the assumption that Saudi Arabia was free from RVF up until at least 1995 and most probably before the 2000 epidemic. The finding also confirms that RVF was not endemic in Saudi Arabia.
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.
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OBJECTIVE: To examine safety and efficacy of a mutagen attenuated Rift Valley fever virus (RVFV) vaccine (RVF MP-12) in cattle. ANIMALS: 38 pregnant cows, 14 steers, and 10 lactating dairy cows. PROCEDURE: Pregnant cows in their third, fifth, or eighth month of gestation were vaccinated (1 ml of RVF MP-12 containing 5 log10 plaque-forming units [PFU] of virus) and were monitored daily through parturition for signs of disease, viremia, and immunologic response. Additionally, 10 vaccinated pregnant cows were challenge inoculated with virulent RVFV at post-vaccination day (PVD) 30 and were monitored daily for untoward effects. Ten unvaccinated pregnant cows also were challenge inoculated with virulent RVFV and served as challenge controls. Vaccinated lactating dairy cows were monitored for viremia and virus shedding in the milk through PVD 14. Yearling steers were vaccinated to assess their immunologic response to various doses of vaccine and were challenge inoculated with virulent RVFV at PVD 28 to assess protection. RESULTS: 10 of 38 (26.3%) cows vaccinated during pregnancy developed transient postvaccination viremia titer > or = 2.5 log10 PFU/ml of serum. All vaccinated cows delivered live, healthy calves that were RVFV seronegative at birth, but which quickly acquired colostral antibodies. Vaccinated cows and their fetuses were protected when challenge exposed with virulent RVFV at PVD 30, whereas unvaccinated pregnant cows inoculated with RVFV became febrile and viremic, and aborted. Vaccine virus was unsuccessfully sought from milk of lactating dairy cows after vaccination, suggesting that shedding of vaccine virus through milk should not be a concern. Steers, inoculated with tenfold escalating vaccine doses, beginning with 1.0 log10 PFU, were protected against virulent RVFV challenge exposure. CONCLUSIONS: RVF MP-12 may be safe and efficacious for use in pregnant or lactating bovids, and a minimal dose of vaccine may provide suitable protection against viremia.
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The importance of rainfall for the development of Aedes vexans arabiensis populations, one of the potential vectors of Rift Valley Fever in West Africa, was demonstrated in a two-year follow-up study conducted in the Ferlo region of Senegal. In 2003, the rainy season began with heavy rains and, as a result, temporary ponds, the breeding places for mosquitoes, were flooded at their maximum level immediately. In such conditions, Aedes vexans arabiensis populations are abundant at the very beginning of the season, when the majority of eggs in quiescence are flooded. Females, hatching from eggs laid the year before, quickly lay eggs on the pond's wet soil, which will undergo dormancy as the water level goes down. Rainless periods longer than seven days, the time needed for embryogenesis, followed by significant rainfall, will result in the hatching of very large numbers of new eggs. Thus, several generations of adults may exist during the same rainy season. Because of potential vertical transmission of Rift Valley Fever virus in Aedes species, viral transmission and disease risk can appear as early as the beginning of the rainy season and if late rains occur, at the end of the season. This dynamic maximizes the virus' chance to persist from one year to another, thus facilitating endemisation of Rift Valley Fever in areas where Aedes vexans arabiensis exists.
In the early summer of 1993, an outbreak of Rift Valley fever (RVF) was reported among both humans and animals in Aswan Governorate, Upper Egypt. To determine whether RVF infection had spread to the Nile delta region of the country, we carried out a cross-sectional survey of 1181 occupationally exposed abattoir workers (97% male; age 10-72 years) in 15 governorates of Egypt in November 1993. The overall prevalence of anti-RVF virus IgM antibody was 2% (range: 0% (7 governorates) to 10%). The highest prevalences were in Ismailia (10%) and Sharqîya (8%) Governorates. None of the seropositive subjects reported having experienced an episode of fever in the 2 months prior to the study. The prevalence of antibody was significantly higher (P < 0.05) among workers employed in high-risk jobs such as cutting animals' throats (relative risk (RR = 2.24)) and handling animal parts (RR = 2.37). The findings suggest that abattoir workers represent a useful sentinel population for surveillance of RVF.
Eosinophilic intranuclear filaments described previously in Rift Valley Fever infected cells, were shown to fluoresce specifically in an indirect technique with antiserum to the virus. Actinomycin D failed to suppress development of the filaments or replication of the virus.
Several cell cultures and animals were compared for their relative sensitivity as primary isolation systems for Rift Valley fever virus (RVFV) and to determine if virulence characteristics of the isolates were altered in these systems. Eleven human sera from known cases of Rift Valley fever (RVF) were obtained from the 1987 epidemic in Mauritania and served as the source of virus for these studies. Sera were inoculated directly into cell cultures (Vero, C6/36 and DBS-FRhL-2) and animals (ICR suckling mice, Lak:LVG(SYR) hamsters and WF rats) concurrently. The cell lines provided a quick method to propagate, quantitate and identify these specimens without prior adaption. The isolates were highly virulent for suckling mice and hamsters, but not for WF rats, even after cell culture passage, which indicated that the Mauritanian isolates more closely resembled those strains from sub-Saharan Africa than those from the 1977-78 Egyptian epidemic.
Rhesus monkeys inoculated with Rift Valley fever (RVF) virus provide a model in which serial observations of serum viral antigen and antibodies can be made. In 9 non-fatal and 3 fatal infections, either antigen or IgM enzyme-linked immunosorbent assay (ELISA) antibodies were detected in every serum sample during the acute phase. Furthermore, viral nucleic acid could be detected by filter hybridization in most samples taken on days 1 to 3. Circulation of significant quantities of viral RNA provides an additional approach to the diagnosis and study of RVF.
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Rift Valley fever (RVF) virus belongs to the Bunyaviridae family of segmented negative-strand RNA viruses and causes mosquito-borne disease in sub-Saharan Africa. We report the development of a T7 RNA polymerase-driven plasmid-based genetic system for the virulent Egyptian isolate, ZH501. We have used this system to rescue a virus that has a 387 nucleotide deletion on the genomic M segment that eliminates the coding region for two non-structural proteins known as NSm. This virus, DeltaNSm rZH501, is indistinguishable from the parental ZH501 strain with respect to expression of structural proteins and growth in cultured mammalian cells.
After the Rift valley fever (RVF) epidemic of 1987 in the Senegal River Basin, RVF surveillance based on serosurveys has been conducted for 10 years. Serum samples were obtained from 1336 persons and from sheep and goats in selected areas, and these were tested for IgG/IgM RVF antibodies by ELISA. After a period of regular decrease in RVF prevalence in domestic animals until 1993, an epizootic was observed in all herds in 1994-95 with increases in IgM levels and abortions. During the same period, no human cases or RVF IgM were detected. The RVF IgG prevalence significantly correlated with date of birth: children born after 1987 have a low prevalence (5%) in clear contrast to the older population (25.3%) in Podor district. A retrospective analysis of rainfall and RVF prevalence in small domestic animals over the last 10 years showed that the re-emergence correlated with heavy rainfall. A general analysis of the risk of re-emergence and the efficiency of this RVF surveillance system are presented.
The wild-type ZH501 strain of Rift Valley fever (RVF) virus and two small-plaque strains (T1 and T46) derived from it were characterized by plaque size, pathogenicity for hamsters and ability to replicate in Vero cells. Additionally, a mutagenized, attenuated, large-plaque, vaccine-candidate strain of RVF virus (ZH548-M12) was also studied. Infections with either the ZH501 or T46 strain were uniformly fatal to hamsters. In contrast, nearly all hamsters infected with either the T1 or ZH548-M12 strains survived and were immune to challenge with 10(5) LD50 of the ZH501 strain. Both of these attenuated strains failed to replicate in Vero cells maintained at 41 degrees C, whereas the more virulent strains (ZH501 and T46) replicated at this temperature. The low virulence and ability to induce protection against lethal RVF virus challenge that is associated with the T1 and ZH548-M12 strains make them potential vaccine candidates.
To investigate past infection in and transmission of Rift Valley fever (RVF) virus to humans within an endemic focus, we undertook a retrospective cohort study of the seminomadic Peul people living in sub-Saharan northcentral Senegal. Residents of the rural settlement of Yonofere five years of age or older were studied during February-May 1989. Anti-RVF virus IgG was found in blood samples of 22.3% of 273 persons who responded to a standard questionnaire; none had IgM antibodies. Seropositivity was similar for males (25.4%) and females (21.1%), increased markedly with age for both sexes, and varied considerably among compounds (groups of huts) (0-37.5%). Risk factors for past RVF virus infection were nursing sick people, assisting animals during abortions/births, and treating sick animals. In all age groups, odds ratios (ORs) for RVF viral antibody among females who reported treating sick animals were three to six times greater than for those who did not. The ORs for males who reported assisting with animal births/abortions and nursing sick people were approximately five times those for males who did not. Serologic prevalence of RVF viral antibody among sheep averaged 30.1% overall (0.8% IgM), but varied among compounds (0-66.7%) in a manner different from that of humans. The seasonal abundance and relative density of potential mosquito vectors were estimated by monthly samples captured in Centers for Disease Control and Prevention-type traps. Mosquito abundance varied seasonally with rainfall (> 90% captures during four months). Species diversity was large (28 spp.), dominated by Aedes and Culex. Rift Valley fever virus was not isolated from 142 pools of 2,956 unengorged mosquitoes tested, although three other arboviruses were found. Results indicate that RVF is endemic in this region, people are at considerable risk of infection, and that a heretofore unrecognized mode of human infection under nonepizootic conditions may be transmission via contact with infected animals or humans.
A double-antibody (sandwich) enzyme-linked immunosorbent assay (ELISA) was adapted to detect Rift Valley fever virus antigen. Antibodies were purified from hyperimmune mouse and rabbit sera by affinity chromatography, using CNBr-activated Sepharose 4B coupled to a beta-propiolactone-inactivated sucrose-acetone-extracted suckling mouse liver antigen. In the assay, antigen was captured by mouse antibody adsorbed to polystyrene plates and then detected by reacting sequentially with rabbit anti-Rift Valley fever virus antibody and swine anti-rabbit immunoglobulin G conjugated to alkaline phosphatase. ELISA proved to be useful in measuring viral antigen in different animal systems. However, great variation was found in the amount of antigen per PFU encountered in different circumstances. The ELISA system was optimized using supernatant fluids from infected Vero cell cultures and had a sensitivity of 10(5) PFU/ml. Hamsters develop progressive viremia, much as seen in susceptible domestic animals, such as lambs; ELISA could reliably detect 10(6) PFU/ml of viremic hamster serum. Rhesus monkeys with Rift Valley fever infection were positive by ELISA even when viremias were only 5 X 10(3) PFU/ml. ELISA also proved to be useful in measuring viral antigen in infected mosquitoes.
Rift Valley fever (RVF) virus is a mosquito-borne RNA virus responsible for large explosive outbreaks of acute febrile disease in humans and livestock in Africa with significant mortality and economic impact. The successful high-throughput generation of the complete genome sequence was achieved for 33 diverse RVF virus strains collected from throughout Africa and Saudi Arabia from 1944 to 2000, including strains differing in pathogenicity in disease models. While several distinct virus genetic lineages were determined, which approximately correlate with geographic origin, multiple exceptions indicative of long-distance virus movement have been found. Virus strains isolated within an epidemic (e.g., Mauritania, 1987, or Egypt, 1977 to 1978) exhibit little diversity, while those in enzootic settings (e.g., 1970s Zimbabwe) can be highly diverse. In addition, the large Saudi Arabian RVF outbreak in 2000 appears to have involved virus introduction from East Africa, based on the close ancestral relationship of a 1998 East African virus. Virus genetic diversity was low (approximately 5%) and primarily involved accumulation of mutations at an average of 2.9 x 10(-4) substitutions/site/year, although some evidence of RNA segment reassortment was found. Bayesian analysis of current RVF virus genetic diversity places the most recent common ancestor of these viruses in the late 1800s, the colonial period in Africa, a time of dramatic changes in agricultural practices and introduction of nonindigenous livestock breeds. In addition to insights into the evolution and ecology of RVF virus, these genomic data also provide a foundation for the design of molecular detection assays and prototype vaccines useful in combating this important disease.