Search

Rift Valley fever (RVF), a mosquito-borne transboundary zoonosis, was first confirmed in Rwanda's livestock in 2012 and since then sporadic cases have been reported almost every year. In 2018, the country experienced its first large outbreak, which was followed by a second one in 2022. To determine the circulating virus lineages and their ancestral origin, two genome sequences from the 2018 outbreak, and thirty-six, forty-one, and thirty-eight sequences of small (S), medium (M), and large (L) genome segments, respectively, from the 2022 outbreak were generated. All of the samples from the 2022 outbreak were collected from slaughterhouses. Both maximum likelihood and Bayesian-based phylogenetic analyses were performed. The findings showed that RVF viruses belonging to a single lineage, C, were circulating during the two outbreaks, and shared a recent common ancestor with RVF viruses isolated in Uganda between 2016 and 2019, and were also linked to the 2006/2007 largest East Africa RVF outbreak reported in Kenya, Tanzania, and Somalia. Alongside the wild-type viruses, genetic evidence of the RVFV Clone 13 vaccine strain was found in slaughterhouse animals, demonstrating a possible occupational risk of exposure with unknown outcome for people working in meat-related industry. These results provide additional evidence of the ongoing wide spread of RVFV lineage C in Africa and emphasize the need for an effective national and international One Health-based collaborative approach in responding to RVF emergencies.

Rift Valley fever (RVF) is a re-emerging vector-borne zoonosis with a high public health and veterinary impact. In West Africa, many lineages were previously detected, but since 2020, lineage H from South Africa has been the main cause of the outbreaks. In this study, clinical samples collected through national surveillance were screened for RVF virus (RVFV) acute infection by RT-PCR and IgM ELISA tests. Sequencing, genome mapping and in vitro phenotypic characterization in mammal cells were performed on RT-PCR positive samples in comparison with other epidemic lineages (G and C). Four RVFV human cases were detected in Senegal and the sequence analyses revealed that the strains belonged to lineage H. The in vitro kinetics and genome mapping showed different replication efficiency profiles for the tested RVFV lineages and non-conservative mutations, which were more common to lineage G or specific to lineage H. Our findings showed the re-emergence of lineage H in Senegal in 2022, its high viral replication efficiency in vitro and support the findings that genetic diversity affects viral replication. This study gives new insights into the biological properties of lineage H and calls for deeper studies to better assess its potential to cause a future threat in Senegal.

In 2018, a large outbreak of Rift Valley fever (RVF)-like illness in cattle in Rwanda and surrounding countries was reported. From this outbreak, sera samples from 157 cows and 28 goats suspected to be cases of RVF were tested to confirm or determine the etiology of the disease. Specifically, the hypothesis that orthobunyaviruses-Bunyamwera virus (BUNV), Batai virus (BATV), and Ngari virus (NRIV)-were co-circulating and contributed to RVF-like disease was tested. Using reverse transcriptase-polymerase chain reaction (RT-PCR), RVFV RNA was detected in approximately 30% of acutely ill animals, but in all cases of hemorrhagic disease. Seven cows with experienced abortion had positive amplification and visualization by gel electrophoresis of all three segments of either BUNV or BATV, and three of these were suggested to be coinfected with BUNV and BATV. On sequencing, five of these seven cows were conclusively positive for BUNV. However, in several other animals, sequencing was successful for some but not all segments of targeted viruses BUNV and BATV. In addition, there was evidence of RVFV-orthobunyavirus coinfection, through RT-PCR/gel electrophoresis and subsequent Sanger sequencing. In no cases were we able to definitely identify the specific coinfecting viral species. This is the first time evidence for orthobunyavirus circulation has been molecularly confirmed in Rwanda. Furthermore, RT-PCR results suggest that BUNV and BATV may coinfect cattle and that RVFV-infected animals may be coinfected with other orthobunyaviruses. Finally, we confirm that BUNV and, perhaps, other orthobunyaviruses were co-circulating with RVFV and contributed to the burden of disease attributed to RVFV in Rwanda.

Rift Valley fever (RVF) is a mosquito-borne viral zoonosis that was first discovered in Kenya in 1930 and is now endemic throughout multiple African countries and the Arabian Peninsula. RVF virus primarily infects domestic livestock (sheep, goats, cattle) causing high rates of neonatal mortality and abortion, with human infection resulting in a wide variety of clinical outcomes, ranging from self-limiting febrile illness to life-threatening haemorrhagic diatheses, and miscarriage in pregnant women. Since its discovery, RVF has caused many outbreaks in Africa and the Arabian Peninsula with major impacts on human and animal health. However, options for the control of RVF outbreaks are limited by the lack of licensed human vaccines or therapeutics. For this reason, RVF is prioritized by the World Health Organization for urgent research and development of countermeasures for the prevention and control of future outbreaks. In this review, we highlight the current understanding of RVF, including its epidemiology, pathogenesis, clinical manifestations and status of vaccine development.

Rift Valley fever phlebovirus (RVFV) is a mosquito-transmitted pathogen endemic to sub-Saharan Africa and the Arabian Peninsula. RVFV is a threat to both animal and human health and has costly economic consequences mainly related to livestock production and trade. Competent hosts and vectors for RVFV are widespread, existing outside of endemic countries including the USA. Thus, the possibility of RVFV spreading to the USA or other countries worldwide is of significant concern. RVFV (genus Phlebovirus) is comprised of an enveloped virion containing a three-segmented, negative-stranded RNA genome that is able to undergo genetic reassortment. Reassortment has the potential to produce viruses that are more pathogenic, easily transmissible, and that have wider vector or host range. This is especially concerning because of the wide use of live attenuated vaccine strains throughout endemic countries. This review focuses on the molecular aspects of RVFV, genetic diversity of RVFV strains, and RVFV reassortment.

Phylogenetic analysis of Rift Valley fever virus partial genomic sequences from a patient infected in South Africa in May 2018 suggests reemergence of an endemic lineage different from that of the epidemic in South Africa during 2010-2011. Surveillance during interepidemic periods should be intensified to better predict future epidemics.

Rift Valley fever phlebovirus (RVFV), the causative agent of an emerging zoonotic disease in Africa and Arabia, can infect a variety of species, predominantly ruminants, camelids, and humans. While clinical symptoms are mostly absent in adult ruminants and camelids, RVFV infection may lead to a serious, sometimes fatal disease in humans. Virus transmissions between individuals and between species mainly occur through mosquito bites, but direct or even indirect contact with infectious materials may also result in infection. Although the main reservoir of the virus is not yet identified, small mammals such as rodents and bats may act as amplifying hosts. We therefore inoculated Rousettus aegyptiacus fruit bats that are abundant in northern Africa with the vaccine strain MP-12, in order to elucidate the general competence of this species for virus propagation and transmission. We were able to detect the RVFV genome in the spleen of each of these animals, and re-isolated the virus from the spleen and liver of some animals. Moreover, we were able to identify the Gc RVFV surface antigen in mild subacute multifocal necrotizing hepatic lesions of one bat which was sacrificed 7 days post exposure. These findings demonstrate that Ro u settus aegyptiacus fruit bats can propagate RVFV., Competing Interests: The authors declare no conflicts of interest.

Rift Valley fever (RVF), caused by an arthropod borne Phlebovirus in the family Bunyaviridae, is a haemorrhagic disease that affects ruminants and humans. Due to the zoonotic nature of the virus, a biosafety level 3 laboratory is required for isolation of the virus. Fresh and frozen samples are the preferred sample type for isolation and acquisition of sequence data. However, these samples are scarce in addition to posing a health risk to laboratory personnel. Archived formalin-fixed, paraffin-embedded (FFPE) tissue samples are safe and readily available, however FFPE derived RNA is in most cases degraded and cross-linked in peptide bonds and it is unknown whether the sample type would be suitable as reference material for retrospective phylogenetic studies. A RT-PCR assay targeting a 490 nt portion of the structural G N glycoprotein encoding gene of the RVFV M-segment was applied to total RNA extracted from archived RVFV positive FFPE samples. Several attempts to obtain target amplicons were unsuccessful. FFPE samples were then analysed using next generation sequencing (NGS), i.e. Truseq ® (Illumina) and sequenced on the Miseq ® genome analyser (Illumina). Using reference mapping, gapped virus sequence data of varying degrees of shallow depth was aligned to a reference sequence. However, the NGS did not yield long enough contigs that consistently covered the same genome regions in all samples to allow phylogenetic analysis., (Copyright © 2017 Elsevier B.V. All rights reserved.)

We report the first imported case of Rift Valley fever (RVF) in China. The patient returned from Angola, a non-epidemic country, with an infection of a new reassortant from different lineages of Rift Valley fever viruses (RVFVs). The patient developed multiorgan dysfunction and gradually recovered with continuous renal replacement therapy and a short regimen of methylprednisolone treatment. The disordered cytokines and chemokines in the plasma of the patient revealed hypercytokinemia, but the levels of protective cytokines were low upon admission and fluctuated as the disease improved. Whole-genome sequencing and phylogenetic analysis revealed that the imported strain was a reassortant comprising the L and M genes from lineage E and the S gene from lineage A. This case highlights that RVFV had undergone genetic reassortment, which could potentially alter its biological properties, cause large outbreaks and pose a serious threat to global public health as well as the livestock breeding industry.

Rift Valley Fever is an acute zoonotic viral disease caused by Rift Valley Fever virus (RVFV) that affects ruminants and humans in Sub-Saharan Africa and the Arabian Peninsula. We used phylogenetic analyses to understand the demographic history of RVFV populations, using sequence data from the three minigenomic segments of the virus. We used phylogeographic approaches to infer RVFV historical movement patterns across its geographic range, and to reconstruct transitions among host species. Results revealed broad circulation of the virus in East Africa, with many lineages originating in Kenya. Arrival of RVFV in Madagascar resulted from three major waves of virus introduction: the first from Zimbabwe, and the second and third from Kenya. The two major outbreaks in Egypt since 1977 possibly resulted from a long-distance introduction from Zimbabwe during the 1970s, and a single introduction took RVFV from Kenya to Saudi Arabia. Movement of the virus between Kenya and Sudan, and CAR and Zimbabwe, was in both directions. Viral populations in West Africa appear to have resulted from a single introduction from Central African Republic. The overall picture of RVFV history is thus one of considerable mobility, and dynamic evolution and biogeography, emphasizing its invasive potential, potentially more broadly than its current distributional limits., Competing Interests: The authors have declared that no competing interests exist.

In early 2014, abortions and death of ruminants were reported on farms in Maputo and Gaza Provinces, Mozambique. Serologic analysis and quantitative and conventional reverse transcription PCR confirmed the presence of Rift Valley fever virus. The viruses belonged to lineage C, which is prevalent among Rift Valley fever viruses in southern Africa.

Rift Valley fever virus (RVFV), a Category A pathogen and select agent, is the causative agent of Rift Valley fever. To date, no fully licensed vaccine is available in the U.S. for human or animal use and effective antiviral drugs have not been identified. The RVFV MP12 strain is conditionally licensed for use for veterinary purposes in the U.S. which was excluded from the select agent rule of Health and Human Services and the U.S. Department of Agriculture. The MP12 vaccine strain is commonly used in BSL-2 laboratories that is generally not virulent in mice. To establish a small animal model that can be used in a BSL-2 facility for antiviral drug development, we investigated susceptibility of six mouse strains (129S6/SvEv, STAT-1 KO, 129S1/SvlmJ, C57BL/6J, NZW/LacJ, BALB/c) to the MP12 virus infection via an intranasal inoculation route. Severe weight loss, obvious clinical and neurologic signs, and 50% mortality was observed in the STAT-1 KO mice, whereas the other 5 mouse strains did not display obvious and/or severe disease. Virus replication and histopathological lesions were detected in brain and liver of MP12-infected STAT-1 KO mice that developed the acute-onset hepatitis and delayed-onset encephalitis. In conclusion, the STAT-1 KO mouse strain is susceptible to MP12 virus infection, indicating that it can be used to investigate RVFV antivirals in a BSL-2 environment., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Rift Valley fever is a mosquito-borne zoonotic disease that affects both ruminants and humans. The nonstructural (NS) protein, which is a major virulence factor for Rift Valley fever virus (RVFV), is encoded on the S-segment. Through the cullin 1-Skp1-Fbox E3 ligase complex, the NSs protein promotes the degradation of at least two host proteins, the TFIIH p62 and the PKR proteins. NSs protein bridges the Fbox protein with subsequent substrates, and facilitates the transfer of ubiquitin. The SAP30-YY1 complex also bridges the NSs protein with chromatin DNA, affecting cohesion and segregation of chromatin DNA as well as the activation of interferon-β promoter. The presence of NSs filaments in the nucleus induces DNA damage responses and causes cell-cycle arrest, p53 activation, and apoptosis. Despite the fact that NSs proteins have poor amino acid similarity among bunyaviruses, the strategy utilized to hijack host cells are similar. This review will provide and summarize an update of recent findings pertaining to the biological functions of the NSs protein of RVFV as well as the differences from those of other bunyaviruses.

Rift Valley fever virus (RVFV) is a mosquito-borne pathogen that affects domesticated ruminants and occasionally humans. Classical RVF vaccines are based on formalin-inactivated virus or the live-attenuated Smithburn strain. The inactivated vaccine is highly safe but requires multiple administrations and yearly re-vaccinations. Although the Smithburn vaccine provides solid protection after a single vaccination, this vaccine is not safe for pregnant animals. An alternative live-attenuated vaccine, named Clone 13, carries a large natural deletion in the NSs gene which encodes the major virulence factor of the virus. The Clone 13 vaccine was previously shown to be safe for young lambs and calves. Moreover, a study in pregnant ewes suggested that the vaccine could also be applied safely during gestation. To anticipate on a possible future incursion of RVFV in Europe, we have evaluated the safety of Clone 13 for young lambs and pregnant ewes. In line with the guidelines from the World Organisation for Animal health (Office International des Epizooties, OIE) and regulations of the European Pharmacopeia (EP), these studies were performed with an overdose. Our studies with lambs showed that Clone 13 dissemination within vaccinated animals is very limited. Moreover, the Clone 13 vaccine virus was not shed nor spread to in-contact sentinels and did not revert to virulence upon animal-to-animal passage. Importantly, a large experiment with pregnant ewes demonstrated that the Clone 13 virus is able to spread to the fetus, resulting in malformations and stillbirths. Altogether, our results suggest that Clone 13 can be applied safely in lambs, but that caution should be taken when Clone 13 is used in pregnant animals, particularly during the first trimester of gestation.

Rift valley fever (RVF) is a mosquito-borne disease of domestic and wild ruminants caused by RVF virus (RVFV), a phlebovirus (Bunyaviridae). RVF is widespread in Sub-Saharan Africa. In September of 2010, an RVF outbreak occurred in northern Mauritania involving mass abortions in small ruminants and camels (Camelus dromedarius) and at least 63 human clinical cases, including 13 deaths. In camels, serological prevalence was 27.5-38.5% (95% confidence interval, n=279). For the first time, clinical signs other than abortions were reported in this species, including hemorrhagic septicemia and severe respiratory distress in animals. We assessed the presence of RVFV in camel sera sampled during this outbreak and generated whole-genome sequences of RVFV to determine the possible origin of this RVFV strain. Phylogenetic analyses suggested a shared ancestor between the Mauritania 2010 strain and strains from Zimbabwe (2269, 763, and 2373), Kenya (155_57 and 56IB8), South Africa (Kakamas, SA75 and SA51VanWyck), Uganda (Entebbe), and other strains linked to the 1987 outbreak of RVF in Mauritania (OS1, OS3, OS8, and OS9).

After a period of heavy rainfall, an outbreak of Rift Valley fever occurred in southern Mauritania during September-November 2012. A total of 41 human cases were confirmed, including 13 deaths, and 12 Rift Valley fever virus strains were isolated. Moudjeria and Temchecket Departments were the most affected areas.

A Rift Valley fever (RVF) outbreak in humans and animals occurred in Mauritania in 2010. Thirty cases of RVF in humans and 3 deaths were identified. RVFV isolates were recovered from humans, camels, sheep, goats, and Culex antennatus mosquitoes. Phylogenetic analysis of isolates indicated a virus origin from western Africa.

During May-July 2010 in Namibia, outbreaks of Rift Valley fever were reported to the National Veterinary Service. Analysis of animal specimens confirmed virus circulation on 7 farms. Molecular characterization showed that all outbreaks were caused by a strain of Rift Valley fever virus closely related to virus strains responsible for outbreaks in South Africa during 2009-2010.

Rift Valley fever virus strain MP-12 was generated by serial plaque passages of parental strain ZH548 12 times in MRC-5 cells in the presence of a chemical mutagen, 5-fluorouracil. As a result, MP-12 encoded 4, 9, and 10 mutations in the S, M, and L segments, respectively. Among them, mutations in the M and L segments were responsible for attenuation, while the MP-12 S segment still encoded a virulent phenotype. We performed high-throughput sequencing of MP-12 vaccine, ZH548, and recombinant MP-12 (rMP-12) viruses. We found that rMP-12 contains very low numbers of viral subpopulations, while MP-12 and ZH548 contain 2 to 4 times more viral genetic subpopulations than rMP-12. MP-12 genetic subpopulations did not encode the ZH548 sequence at the 23 MP-12 consensus mutations. On the other hand, 4 and 2 mutations in M and L segments of MP-12 were found in ZH548 subpopulations. Thus, those 6 mutations were no longer MP-12-specific mutations. ZH548 encoded several unique mutations compared to other Egyptian strains, i.e., strains ZH501, ZH1776, and ZS6365. ZH548 subpopulations shared nucleotides at the mutation site common with those in the Egyptian strains, while MP-12 subpopulations did not share those nucleotides. Thus, MP-12 retains unique genetic subpopulations and has no evidence of reversion to the ZH548 sequence in the subpopulations. This study provides the first information regarding the genetic subpopulations of RVFV and shows the genetic stability of the MP-12 vaccine manufactured in MRC-5 cells.

Rift Valley Fever (RVF) virus (Family Bunyaviridae) is an arthropod-borne RNA virus that infects primarily domestic ruminants and occasionally humans. RVF epizootics are characterized by numerous abortions and mortality among young animals. In humans, the illness is usually characterized by a mild self-limited febrile illness, which could progress to more serious complications. RVF virus is widespread and endemic in many regions of Africa. In Western Africa, several outbreaks have been reported since 1987 when the first major one occurred at the frontier of Senegal and Mauritania. Aiming to evaluate the spreading and molecular epidemiology in these countries, RVFV isolates from 1944 to 2008 obtained from 18 localities in Senegal and Mauritania and 15 other countries were investigated. Our results suggest that a more intense viral activity possibly took place during the last century compared to the recent past and that at least 5 introductions of RVFV took place in Senegal and Mauritania from distant African regions. Moreover, Barkedji in Senegal was possibly a hub associated with the three distinct entries of RVFV in West Africa.

Phylogenetic relationships were examined for 198 Rift Valley fever virus isolates and 5 derived strains obtained from various sources in Saudi Arabia and 16 countries in Africa during a 67-year period (1944-2010). A maximum-likelihood tree prepared with sequence data for a 490-nt section of the Gn glycoprotein gene showed that 95 unique sequences sorted into 15 lineages. A 2010 isolate from a patient in South Africa potentially exposed to co-infection with live animal vaccine and wild virus was a reassortant. The potential influence of large-scale use of live animal vaccine on evolution of Rift Valley fever virus is discussed.

Rift Valley fever virus (RVFV), a mosquito-borne phlebovirus, has been detected in Madagascar since 1979, with occasional outbreaks. In 2008 to 2009, a large RVFV outbreak was detected in Malagasy livestock and humans during two successive rainy seasons. To determine whether cases were due to enzootic maintenance of the virus within Madagascar or to importation from the East African mainland, nine RVFV whole genomic sequences were generated for viruses from the 1991 and 2008 Malagasy outbreaks. Bayesian coalescent analyses of available whole S, M, and L segment sequences were used to estimate the time to the most recent common ancestor for the RVFVs. The 1979 Madagascar isolate shared a common ancestor with strains on the mainland around 1972. The 1991 Madagascar isolates were in a clade distinct from that of the 1979 isolate and shared a common ancestor around 1987. Finally, the 2008 Madagascar viruses were embedded within a large clade of RVFVs from the 2006-2007 outbreak in East Africa and shared a common ancestor around 2003 to 2004. These results suggest that the most recent Madagascar outbreak was caused by a virus likely arriving in the country some time between 2003 and 2008 and that this outbreak may be an extension of the 2006-2007 East African outbreak. Clustering of the Malagasy sequences into subclades indicates that the viruses have continued to evolve during their short-term circulation within the country. These data are consistent with the notion that RVFV outbreaks in Madagascar result not from emergence from enzootic cycles within the country but from recurrent virus introductions from the East African mainland.

The increasing interest in Rift Valley fever virus (RVFV) and its potential impact on naive animal populations deserve revisiting experimental reproduction of RVFV infection, particularly in those animal breeds for which no data about their susceptibility to RVFV infection have ever been recorded. In this study we show the susceptibility of 9-10 weeks old European sheep (Ripollesa breed) to RVFV infection, showing a mild, subacute form of disease. Four different viral isolates efficiently replicated in vivo after subcutaneous experimental inoculation, and consistent viral loads in blood and virus shedding (variable in length depending on the RVFV isolate used) were detected, showing horizontal transmission to a noninfected, sentinel lamb. RVFV infection caused transient pyrexia in adult lambs and no other clinical symptoms were observed, with the exception of corneal opacity ("blue eye") found in 3 out of 16 subcutaneously inoculated sheep. In conclusion, adult sheep from this European breed are readily infected with RVFV without apparent clinical manifestations.

Rift Valley fever (RVF) virus historically has caused widespread and extensive outbreaks of severe human and livestock disease throughout Africa, Madagascar, and the Arabian Peninsula. Following unusually heavy rainfall during the late autumn of 2006, reports of human and animal illness consistent with RVF virus infection emerged across semiarid regions of the Garissa District of northeastern Kenya and southern Somalia. Following initial RVF virus laboratory confirmation, a high-throughput RVF diagnostic facility was established at the Kenyan Central Veterinary Laboratories in Kabete, Kenya, to support the real-time identification of infected livestock and to facilitate outbreak response and control activities. A total of 3,250 specimens from a variety of animal species, including domesticated livestock (cattle, sheep, goats, and camels) and wildlife collected from a total of 55 of 71 Kenyan administrative districts, were tested by molecular and serologic assays. Evidence of RVF infection was found in 9.2% of animals tested and across 23 districts of Kenya, reflecting the large number of affected livestock and the geographic extent of the outbreak. The complete S, M, and/or L genome segment sequence was obtained from a total of 31 RVF virus specimens spanning the entire known outbreak period (December-May) and geographic areas affected by RVF virus activity. Extensive genomic analyses demonstrated the concurrent circulation of multiple virus lineages, gene segment reassortment, and the common ancestry of the 2006/2007 outbreak viruses with those from the 1997-1998 east African RVF outbreak. Evidence of recent increases in genomic diversity and effective population size 2 to 4 years prior to the 2006-2007 outbreak also was found, indicating ongoing RVF virus activity and evolution during the interepizootic/epidemic period. These findings have implications for further studies of basic RVF virus ecology and the design of future surveillance/diagnostic activities, and they highlight the critical need for safe and effective vaccines and antiviral compounds to combat this significant veterinary and public health threat.

In October 2003, 9 human cases of hemorrhagic fever were reported in 3 provinces of Mauritania, West Africa. Test results showed acute Rift Valley fever virus (RVFV) infection, and a field investigation found recent circulation of RVFV with a prevalence rate of 25.5% (25/98) and 4 deaths among the 25 laboratory-confirmed case-patients. Immunoglobulin M against RVFV was found in 46% (25/54) of domestic animals. RVFV was also isolated from the mosquito species Culex poicilipes. Genetic comparison of virion segments indicated little variation among the strains isolated. However, phylogenetic studies clearly demonstrated that these strains belonged to the East-Central African lineage for all segments. To our knowledge, this is the first time viruses of this lineage have been observed in an outbreak in West Africa. Whether these strains were introduced or are endemic in West Africa remains to be determined.

A great body of data on the fauna and ecology of wild mammals and their participation in the circulation of arboviruses were collected when the ecology of the latter of the Republic of Guinea was studied in 1978 to 1989. A hundred and eighteen species belonging to 10 orders were identified. Over 2,000 biological specimens were virologically and serologically examined. Six arboviruses were isolated. These included Dugbe virus (from the hussar monkey Cercopithecus (Erythrocebus patas) and 5 viruses from chiropters: Rift valley fever, from Micropteropus pusillus, Miniopterus schreibersi, and Hipposideros caffer, Saboya, Fomede, and Ank 6909 from Nycteris gambiensis and Kolenter from Hipposideros sp. Fomede, Kolente, and Ank 6909 viruses turned out to be new species for science. Rodents were found to have viral antigens of Lass fever (Mastomys natalensis, Tatera valida kempi and Rattus rattus), Dugbe and Chikungunya fevers (M. natalensis) and West Nile fever (Mus sp.). A serological survey of mammals revealed that the latter had antibodies to 12 arboviruses. Thus, the mammals of Guinea participate in the circulation of 18 arboviruses, 13 of them are pathogenic for man.

Rift Valley fever is considered to be one of the most important viral zoonoses in Africa. In 2000, the Rift valley fever virus spread to the Arabian Peninsula and caused two simultaneous outbreaks in Yemen and Saudi Arabia. It is transmitted to ruminants and to humans by mosquitoes. The viral agent is an arbovirus, which belongs to the Phlebovirus genus in the Bunyaviridae family. This family of viruses comprises more than 300 members grouped into five genera: Orthobunyavirus, Phlebovirus, Hantavirus, Nairovirus, and Tospovirus. Several members of the Bunyaviridae family are responsible for fatal hemorrhagic fevers: Rift Valley fever virus (Phlebovirus), Crimean-Congo hemorrhagic fever virus (Nairovirus), Hantaan, Sin Nombre and related viruses (Hantavirus), and recently Garissa, now identified as Ngari virus (Orthobunyavirus). Here are reviewed recent advances in Rift Valley fever virus, its epidemiology, molecular biology and focus on recent data on the interactions between viral and cellular proteins, which help to understand the molecular mechanisms utilized by the virus to circumvent the host cellular response.

Rift Valley fever (RVF) is an arthropod-borne viral disease of ruminants, camels and humans. It is also a significant zoonosis which may be encountered as an uncomplicated influenza-like illness, but may also present as a haemorrhagic disease with liver involvement; there may also be ocular or neurological lesions. In animals, RVF may be inapparent in non-pregnant adults, but outbreaks are characterised by the onset of abortions and high neonatal mortality. Jaundice hepatitis and death are seen in older animals. Outbreaks of RVF are associated with persistent heavy rainfall with sustained flooding and the appearance of large numbers of mosquitoes, the main vector. Localised heavy rainfall is seldom sufficient to create conditions for an outbreak; the simultaneous emergence of large numbers of first generation transovarially infected mosquitoes is also required. After virus amplification in vertebrates, mosquitoes act as secondary vectors to sustain the epidemic.

An outbreak of Rift Valley fever in the Kingdom of Saudi Arabia and Yemen in 2000 was the first recognized occurrence of the illness outside of Africa and Madagascar. An assessment of potential mosquito vectors in the region yielded an isolate from Aedes vexans arabiensis, most closely related to strains from Madagascar (1991) and Kenya (1997).

Between February and April 1991, unusual numbers of bovine abortion around Antananarivo (central highlands, Madagascar) were reported by official veterinary services. Rift Valley fever (RVF) virus isolations were made from sixteen aborted foetuses and one dead calf in different foci. Using monoclonal antibodies, the isolated viruses were found to be different from the 1979 RVF strains isolated in Madagascar from mosquitoes and human laboratory infection, and closer to African RVF strains. In a bovine population--previously characterized by a negative or very low RVF antibody prevalence--a high prevalence of IgM antibodies (264/994: 26.5% positive) was revealed; the IgM prevalence in recently aborting females varied from 40 to 91%. Among 994 human sera tested by IgG-IFA (immunofluorescent antibody assay) and IgM ELISA, 8.2% and 4.5%, respectively, proved positive. A total of 11,371 mosquitoes (61% Culex antennatus) were collected in the epizootic areas and tested without any virus isolation. Extensive studies were conducted to determine the geographical extension and the impact of this epidemic on the highly susceptible livestock and human populations.

Electron microscopic examination of a negatively stained suspension of Zinga virus showed particles 90-100 nm in diameter, enveloped with spikes 12-20 nm in length and 5 nm in diameter. Further identification of the virus by immune electron microscopy showed the reactivity of human Rift Valley fever virus-positive serum with Zinga virus. Results of this study are in agreement with earlier reports that Zinga virus is a strain of Rift Valley fever virus.

During 1984 and 1985, six Rift Valley Fever virus strains (RVF) were isolated in Central African Republic, among them five from human samples. Three strains were isolated in 1985 at the end of the rainy season, from sera of patients dead with severe jaundice with haemorrhagic syndrome, what could evoke a little outbreak. At this occasion, these RVF strains and the other strains of phleboviruses previously isolated in CAR, were antigenically compared by Immuno-fluorescent assay (IFA) and Complement Fixation Test (CF), using mice immuno ascitic fluids prepared against each strain. A lot of cross reactions were noted between the different strains, but all the RVF strains seem to have the same antigenic outline.

Virological investigations of bats performed in the territory of Republic of Guinea permitted for the first time to isolate from the bats Micropteropus pusillus and Hipposideros abae two strains which were identified as R. V. F. V. Serological investigation revealed specific antibodies to R. V. F. V. among natives in 3.3% and among domestic animals in 6.8%. It is supposed that bats are reservoir of this virus. They can transmit agent of R. V. F. by means of mosquitoes or by being part of the native diet.