Bunyaviridae

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Ramon Flick - One of the best experts on this subject based on the ideXlab platform.

  • Rift Valley fever virus.
    Current Molecular Medicine, 2005
    Co-Authors: Ramon Flick, Michele Bouloy
    Abstract:

    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.

  • reverse genetics system for uukuniemi virus Bunyaviridae rna polymerase i catalyzed expression of chimeric viral rnas
    Journal of Virology, 2001
    Co-Authors: Ramon Flick, Ralf F Pettersson
    Abstract:

    The procedures developed during the 1990s to genetically manipulate the genomes of negative-strand viruses and to rescue infectious viruses entirely from cloned cDNAs, commonly referred to as reverse genetics, have revolutionized the analyses of viral gene expression and the dissection of cis-acting regulatory sequences important for replication and transcription. They have also paved the road for engineering these viruses for vaccine and gene therapy purposes (6, 36). The ability to rescue infectious viruses from cloned cDNAs has by now been well established for nonsegmented, negative-strand viruses (Mononegavirales), such as members of the Rhabdoviridae (22, 41, 48) and Paramyxoviridae (1, 5, 18, 19, 35) families. The development of similar protocols for manipulating the genomes and creating viruses from cloned cDNAs of segmented, negative-strand viruses, i.e., members of the Orthomyxoviridae, Bunyaviridae, and Arenaviridae families, have turned out to be much more difficult. Although the ability to manipulate RNA segments of influenza A viruses was developed more than a decade ago (10, 25), it was not until last year that the first reports on the rescue of infectious influenza A virus entirely from cloned cDNAs were published (15, 20, 31, 32). Members of the Bunyaviridae family, which comprises more than 300 viruses (28) grouped into the five genera Bunyavirus, Hantavirus, Nairovirus, Phlebovirus, and Tospovirus, are enveloped viruses with a tripartite, single-stranded RNA genome of negative polarity. The L segment encodes the RNA-dependent RNA polymerase (L), the M segment encodes the two spike proteins (G1 and G2) and in some viruses a nonstructural protein (NSm), while the S segment encodes the nucleoprotein (N) and in some viruses a nonstructural protein (NSs) (8, 40). Initiation of transcription of the viral mRNAs is primed by short sequences derived from the 5′ end of host mRNAs (2, 40, 43). This cap-snatching mechanism is reminiscent of that first described for influenza virus (21), with the important difference that cap snatching occurs in the cytoplasm of Bunyaviridae-infected cells, as opposed to the nucleus in influenza virus-infected cells. This is due to the fact that Bunyaviridae members replicate exclusively in the cytoplasm. As is the case for all negative-strand RNA viruses, the templates for L polymerase-catalyzed replication and transcription of Bunyaviridae members are the ribonucleoproteins (RNPs) consisting of the full-length positive- or negative-strand RNA segments associated with the N protein. To date, methods to study the role of cis-acting sequences at the 5′ and 3′ termini of viral RNA (vRNA) segments have been developed for Bunyamwera (BUN) virus (Bunyavirus) (7) and Rift Valley fever (RVF) virus (Phlebovirus) (24, 34), using the now classical T7-vaccinia virus (T7-VV) system (16) to express a chloramphenicol acetyltransferase (CAT) reporter cDNA flanked by 5′ and 3′ vRNA ends. An important step was taken when Bridgen and Elliott in 1996 (4) were able to rescue infectious BUN virus entirely from cloned cDNAs, although the procedure was cumbersome and the efficiency of generating infectious virus was rather low. To look for an alternative approach for developing a reverse genetics system for Bunyaviridae, we have turned to the RNA polymerase I (pol I) expression system, which was recently successfully used to rescue infectious influenza virus (15, 31, 32). This system, originally developed by Hobom and coworkers (30, 49), has been used to study cis-acting sequences important for transcription and replication (14) and to develop a procedure for indirect selection of recombinant influenza viruses (12). An ambisense strategy to further simplify the procedure was recently reported (20). In the pol I system, cDNAs coding for viral RNA segments, or reporter genes flanked by viral sequences, are cloned between the RNA pol I promoter and terminator to generate transcripts that have correct 5′ and 3′ ends without modifications such as a cap structure and a poly(A) tail (12, 49). In the case of influenza virus, these pol I transcripts are then replicated and transcribed in the nucleus by the necessary viral proteins. Following transport of the RNPs to the cytoplasm, infectious particles are assembled by budding at the plasma membrane. We have adopted the pol I system to express reporter genes flanked by the 5′ and 3′ noncoding sequences of the M RNA segment of Uukuniemi (UUK) virus, a member of the Phlebovirus genus (28). We have previously characterized extensively the molecular and cell biology of UUK virus. Full-length cDNAs corresponding to the L (6,423 nucleotides [nt]) (9), M (3,229 nt) (38), and S (1,720 nt) (42) segments have been constructed, and cDNAs encoding the open reading frames (ORFs) for the L, G1, G2, N, and NSs proteins have been derived (9, 26, 37, 44). As the first step toward the generation of infectious virus from cloned cDNAs, we show here that the pol I system can be used to synthesize chimeric RNA templates, which, despite lacking a cap structure and poly(A) tail, are transported to the cytoplasm, where they are amplified and transcribed by the UUK virus replicase components supplied either by superinfection with UUK virus or by expression of viral proteins from separate plasmids. The L and N proteins were found to be necessary and sufficient for transcription and replication, while NSs was completely dispensable. We also show that CAT activity could be transferred serially from culture to culture by passaging supernatants from transfected and superinfected cells. This indicates that the chimeric reporter RNA could be packaged into virus particles. Thus, the pol I system holds great potential as an effective alternative approach for a versatile reverse genetics system for members of the Bunyaviridae family.

Michele Bouloy - One of the best experts on this subject based on the ideXlab platform.

  • Rift Valley fever virus.
    Current Molecular Medicine, 2005
    Co-Authors: Ramon Flick, Michele Bouloy
    Abstract:

    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.

Summerpal Kahlon - One of the best experts on this subject based on the ideXlab platform.

  • Viral Hemorrhagic Fever: Bunyaviridae
    Current Treatment Options in Infectious Diseases, 2015
    Co-Authors: Summerpal Kahlon
    Abstract:

    Viruses of the family Bunyaviridae cause a variety of human diseases. Some members of this family are known to cause hemorrhagic fever syndrome in humans. Included in this group are Crimean-Congo hemorrhagic fever and Hantaan virus-induced hemorrhagic fever with renal syndrome. Rift Valley fever (RVF), a viral hemorrhagic fever in this family, merits greater attention in awareness of diagnosis and treatment options. Once thought to be an unusual source of sporadic disease outbreaks in rural east Africa, RVF continues to emerge as a viral hemorrhagic fever of note. With greater health care access, improved awareness, and newer diagnostic techniques, cases increasingly continue to be identified primarily across Sub-Saharan Africa and the Arabian Peninsula. Early clinical suspicion and identification of disease are important to implementation of appropriate, effective therapy. Early-stage RVF mimics other common febrile illnesses, such as malaria. With increasing global travel, clinicians may encounter RVF both in its local endemic geography as well as in travelers from the region. Supportive care is the traditional primary therapy, though increasing knowledge of the disease suggests additional options for consideration of prevention and treatment. This review will focus on RVF with relevant reference to other viral hemorrhagic fevers in the family.

Shchelkanov Miu - One of the best experts on this subject based on the ideXlab platform.

Francisco Gonzalezscarano - One of the best experts on this subject based on the ideXlab platform.

  • chapter 21 the Bunyaviridae
    Handbook of Clinical Neurology, 2014
    Co-Authors: Samantha S. Soldan, Francisco Gonzalezscarano
    Abstract:

    The Bunyaviridae is a large and diverse family of viruses whose members infect a wide range of arthropod vectors and animal or plant hosts. Bunyaviruses are distributed worldwide and their promiscuous use of an impressive variety of arthropod vectors amplifies the potential for bunyaviruses to increase their prevalence and geographic range given the right environmental or man-made conditions. Most bunyavirus infections are asymptomatic or present with a mild influenza-like illness. However, some members of the family are important human and veterinary pathogens that are the causative agents of devastating illnesses, including hemorrhagic fever, pulmonary disease, congenital abnormalities, and fatal encephalitis. In this chapter, we discuss the epidemiology, lifecycle, molecular biology, neuropathogenesis, and prevention and treatment strategies for emerging bunyaviruses that are predominantly associated with central nervous disease; these include members of the genera Phlebovirus (Rift Valley fever virus and Toscana virus) and Orthobunyavirus (La Crosse virus and Cache Valley virus).

  • short communicationcompletion of the la crosse virus genome sequence and geneticcomparisons of the l proteins of the Bunyaviridae
    Virology, 1995
    Co-Authors: Anjeanette Roberts, Colette Rossier, Neal Nathanson, Dan Kolakofsky, Francisco Gonzalezscarano
    Abstract:

    La Crosse virus is a member of the Bunyavirus genus in the family Bunyaviridae, viruses with trisegmented RNA genomes of mostly negative polarity composed of large (L), medium (M), and small (S) segments. The sequences of the La Crosse/ original M and S RNA segments have been previously characterized. Using reverse transcriptase in conjunction with PCR amplification, we have obtained the nucleotide sequence of the L RNA segment, which encodes the viral polymerase in a single large open reading frame. Comparison of the amino acid sequence of the LAC L protein with the sequence of other polymerases from members of the Bunyaviridae, demonstrated the presence of several conserved motifs, some of which are characteristic of many polymerase proteins. A genetic tree comparing the available polymerase proteins of the Bunyaviridae provides insights into the phylogenetic relationships within this large family. Members of the genus Bunyavirus, which are mosquito-borne and infect mammals, have a closer relationship to the plant viruses represented by tomato spotted wilt virus (Tospovirus genus) than to viruses of other genera in the family Bunyaviridae.