Reassortment and distinct evolutionary dynamics of Rift Valley Fever virus genomic segments
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Abstract Rift Valley Fever virus (RVFV) is a member of Bunyaviridae family that causes a febrile disease affecting mainly ruminants and occasionally humans in Africa, with symptoms that range from mid to severe. RVFV has a tri-segmented ssRNA genome that permits reassortment and could generate more virulent strains. In this study, we reveal the importance of reassortment for RVFV evolution using viral gene genealogy inference and phylodynamics. We uncovered seven events of reassortment that originated RVFV lineages with discordant origins among segments. Moreover, we also found that despite similar selection regimens, the three segments have distinct evolutionary dynamics; the longer segment L evolves at a significant lower rate. Episodes of discordance between population size estimates per segment also coincided with reassortment dating. Our results show that RVFV segments are decoupled enough to have distinct demographic histories and to evolve under different molecular rates.Keywords:
Reassortment
Viral phylodynamics
Phlebovirus
Rift Valley Fever
Evolutionary Dynamics
Balancing selection
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Journal Article Serological evidence in sheep suggesting phlebovirus circulation in a Rift Valley fever enzootic area in Burkina Faso Get access J.P. Gonzalez, J.P. Gonzalez ∗ 1Institut Français de Recherche Scientifique pour le Développement en Coopération, B. P. 1386, Dakar, Sénégal ∗Address for correspondence: Dr J. P. Gonzalez, Laboratory of Epidemiology and Public Health, School of Medicine, P.O. Box 3333, New Haven, CT 06510, USA. Search for other works by this author on: Oxford Academic PubMed Google Scholar B. Le Guenno, B. Le Guenno 2Institut Pasteur, B. P. 220, Dakar, Sénégal Search for other works by this author on: Oxford Academic PubMed Google Scholar M.J.R. Some, M.J.R. Some 3Ecole Inter-Etats des Sciences et Médecine Vétérinaires, Dakar, Sénégal Search for other works by this author on: Oxford Academic PubMed Google Scholar J.A. Akakpo J.A. Akakpo 3Ecole Inter-Etats des Sciences et Médecine Vétérinaires, Dakar, Sénégal Search for other works by this author on: Oxford Academic PubMed Google Scholar Transactions of The Royal Society of Tropical Medicine and Hygiene, Volume 86, Issue 6, November-December 1992, Pages 680–682, https://doi.org/10.1016/0035-9203(92)90190-N Published: 01 November 1992 Article history Received: 23 August 1991 Revision received: 10 March 1992 Accepted: 10 April 1992 Published: 01 November 1992
Rift Valley Fever
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Rift Valley Fever
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Rift Valley fever (RVF), an emerging mosquito-borne zoonotic infectious viral disease caused by the RVF virus (RVFV) (Bunyaviridae: Phlebovirus), presents significant threats to global public health and agriculture in Africa and the Middle East. RVFV is listed as a select agent with significant potential for international spread and use in bioterrorism. RVFV has caused large, devastating periodic epizootics and epidemics in Africa over the past ∼60 years, with severe economic and nutritional impacts on humans from illness and livestock loss. In the past 15 years alone, RVFV caused tens of thousands of human cases, hundreds of human deaths, and more than 100,000 domestic animal deaths. Cattle, sheep, goats, and camels are particularly susceptible to RVF and serve as amplifying hosts for the virus. This review highlights recent research on RVF, focusing on vectors and their ecology, transmission dynamics, and use of environmental and climate data to predict disease outbreaks. Important directions for future research are also discussed.
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Phlebovirus
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Rift Valley fever (RVF) virus is an arbovirus in the Bunyaviridae family that, from phylogenetic analysis, appears to have first emerged in the mid-19th century and was only identified at the begininning of the 1930s in the Rift Valley region of Kenya. Despite being an arbovirus with a relatively simple but temporally and geographically stable genome, this zoonotic virus has already demonstrated a real capacity for emerging in new territories, as exemplified by the outbreaks in Egypt (1977), Western Africa (1988) and the Arabian Peninsula (2000), or for re-emerging after long periods of silence as observed very recently in Kenya and South Africa. The presence of competent vectors in countries previously free of RVF, the high viral titres in viraemic animals and the global changes in climate, travel and trade all contribute to make this virus a threat that must not be neglected as the consequences of RVF are dramatic, both for human and animal health. In this review, we present the latest advances in RVF virus research. In spite of this renewed interest, aspects of the epidemiology of RVF virus are still not fully understood and safe, effective vaccines are still not freely available for protecting humans and livestock against the dramatic consequences of this virus.
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Within the Phlebovirus serogroup, Rift Valley fever (RVF) virus is endemo-enzootic in the African sahelian zone. Recently an RVF epizootic in West Africa prompted a serosurvey in the major sheep and cattle raising areas. Because of the close antigenic relationship between the phleboviruses it appeared of interest to evaluate the prevalence of the other phleboviruses also. In 1987, 482 sheep serum samples were collected in 2 different ecological zones of Burkina Faso and tested for the presence of phlebovirus antibodies. A sensitive but non-specific immunofluorescent antibody test and a specific enzyme-linked immunosorbent assay (elisa) were used, with the following African phlebovirus antigens: Rift Valley fever (RVF), Arumowot, Gabek Forest, Gordil, Saint Floris and Odrenisrou. A total of 15.8% of the sera sampled had anti-RVF antibody in the elisa. RVF virus appeared to be more active in drier areas such as the sahelian region, known to be an enzootic area for the disease. Antibodies to other phleboviruses were found in 11·8% of the samples, independent of RVF virus activity. It is asumed that sheep can be infected by different phleboviruses.
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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.
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Adult golden hamsters inoculated subcutaneously with either of two sandfly fever group viruses, Punta Toro and Gabek Forest (Phlebovirus, Bunyaviridae), developed a fulminating fatal illness characterized by hepatic and splenic necrosis and interstitial pneumonitis. Most animals died within three days after infection; this was accompanied by high levels of viremia. Necropsy and histopathologic examination of the infected animals revealed pathologic changes involving multiple organs that resembled those described in Rift Valley fever. These two hamster-phlebovirus systems may serve as alternative animal models for Rift Valley fever and should be useful in studying the pathogenesis of severe phlebovirus infection and for testing potential therapeutic agents.
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Rift Valley Fever (RVF) is a disease caused by the Rift Valley Fever virus (RVFV), which is member of the Bunyaviridae family, Phlebovirus genus. RVF a viral zoonosis that primarily affects animals but can also infect humans. This one affects mainly domestic ruminants, causing large epizootics, with high rates of lethality in young animals and abortions in infected females. The virus was first identified in 1931 during an investigation into an epidemic among sheep on a farm in the Rift Valley of Kenya.
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