Poxviruses of Rabbits

McFadden, Grant

doi:10.1007/978-1-4613-2091-3_3

Cited by 16 publications

(15 citation statements)

References 104 publications

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“…Given the importance of how lymphotropism is regulated by viruses in general and the observation that the M-T5 protein appears highly specific for lymphocytes, further biochemical analysis of this protein is warranted. Since the natural history of myxoma virus and its host has been well established (11,28,29), the myxomatosis model should prove useful to further our understanding of virus-host interactions, particularly in terms of how immune system cells themselves respond to virus infection.…”

Section: Discussionmentioning

confidence: 99%

“…Myxoma virus, a member of the genus Leporipoxvirus, is one of the few poxviruses whose natural history has been well established; therefore, it provides an excellent model system in which to study virus-host interactions. Myxoma virus evolved within the South American rabbit (Sylvilagus brasiliensis), and infection of this natural host results in benign lesions which may persist for many months (11,28,29). However, infection of European rabbits (Oryctolagus cuniculus) induces a rapidly lethal infection known as myxomatosis, which is characterized by extensive fulminating internal and external lesions, severe immunodysfunction, and supervening gram-negative bacterial infection.…”

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confidence: 99%

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Disruption of M-T5, a novel myxoma virus gene member of poxvirus host range superfamily, results in dramatic attenuation of myxomatosis in infected European rabbits

Mossman

Lee

Barry

et al. 1996

J Virol

101

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Myxoma virus is a pathogenic poxvirus that induces a lethal myxomatosis disease profile in European rabbits, which is characterized by fulminating lesions at the primary site of inoculation, rapid dissemination to secondary internal organs and peripheral external sites, and supervening gram-negative bacterial infection. Here we describe the role of a novel myxoma virus protein encoded by the M-T5 open reading frame during pathogenesis. The myxoma virus M-T5 protein possesses no significant sequence homology to nonviral proteins but is a member of a larger poxviral superfamily designated host range proteins. An M-T5 ؊ mutant virus was constructed by disruption of both copies of the M-T5 gene followed by insertion of the selectable marker p7.5Ecogpt. Although the M-T5 ؊ deletion mutant replicated with wild-type kinetics in rabbit fibroblasts, infection of a rabbit CD4 ؉ T-cell line (RL5) with the myxoma virus M-T5 ؊ mutant virus resulted in the rapid and complete cessation of both host and viral protein synthesis, accompanied by the manifestation of all the classical features of programmed cell death. Infection of primary rabbit peripheral mononuclear cells with the myxoma virus M-T5 ؊ mutant virus resulted in the apoptotic death of nonadherent lymphocytes but not adherent monocytes. Within the European rabbit, disruption of the M-T5 open reading frame caused a dramatic attenuation of the rapidly lethal myxomatosis infection, and none of the infected rabbits displayed any of the characteristic features of myxomatosis. The two most significant histological observations in rabbits infected with the M-T5 ؊ mutant virus were (i) the lack of progression of the infection past the primary site of inoculation, coupled with the establishment of a rapid and effective inflammatory reaction, and (ii) the inability of the virus to initiate a cellular reaction within secondary immune organs. We conclude that M-T5 functions as a critical virulence factor by allowing productive infection of immune cells such as peripheral lymphocytes, thus facilitating virus dissemination to secondary tissue sites via the lymphatic channels.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Disruption of M-T5, a novel myxoma virus gene member of poxvirus host range superfamily, results in dramatic attenuation of myxomatosis in infected European rabbits

Mossman

Lee

Barry

et al. 1996

J Virol

101

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“…Poxvirus topoisomerases are suspected to be essential for transcription, replication, recombination and the resolution of viral telomeres (McFadden, 1988).…”

Section: Discussionmentioning

confidence: 99%

Partial transcriptional mapping of the fowlpox virus genome and analysis of the EcoRI L fragment

Jl¹,

Jb³

et al. 1996

Journal of General Virology

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Several fowlpox virus (FPV) DNA fragments were selected by differential hybridization using cDNA of transcripts that were strongly transcribed early and/or late after infection of QT-35 cells. The EcoRI L fragment contained three strongly transcribed FPV genes: L1L, a late 1452 bp partial (amino end) ORF; L2R, an early/late 522 bp ORF; and L3R, a late 948 bp ORF. The protein products of L1L, L2R and L3R shared homology with the products ofvaccinia virus ( W ) genes H4L (RAP94), H5R (Ag35) and H6R (topoisomerase), respectively, suggesting a conservation of gene structure and order between VV and FPV. The 5' upstream non-coding sequences of L1L and L3R were A + T rich and the sequence 5' TAAATG 3' overlapped the predicted translation start codon. Primer extension analysis of the L2R transcript mapped the transcriptional start sites of early and late mRNAs 14 nt downstream of a VV early promoter-like critical region sequence, AAAATTGAA-AAAAAAA. A VV-like TAAAT late transcriptional element was present 20 nt upstream of the L2R ATG translational start codon. A plasmid with the putative early L2R promoter cloned upstream of the Newcastle disease virus haemagglutinin-neuraminidase (HN) cDNA as a reporter gene was at least 6-fold more effective in generating HN mRNA than plasmids containing the P7.5 or P11 VV promoters in transient expression assays in FPV-infected CEF cells treated with cytosine arabinoside. The L2R promoter was also able to express an amount of HN mRNA equal to that expressed by the W promoters late in infection.

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“…Myxoma virus, the causative agent of myxomatosis, induces disseminated highly myxoid tumours, immunological compromise of the host and often death as a result of secondary bacterial infections (Fenner & Woodroofe, 1953). Malignant rabbit fibroma virus (reviewed by McFadden, 1987), a virus derived from recombination between SFV and myxoma virus (Block et al, 1985; & , induces malignant metastatic tumours .…”

Section: Introductionmentioning

confidence: 99%

Nucleotide sequence analysis of a unique near-terminal region of the tumorigenic poxvirus, Shope fibroma virus

Massung

McFadden

Moyer

1992

Journal of General Virology

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Shope fibroma virus (SFV), a tumorigenic poxvirus, has a DNA genome of approximately 160 kb. Previous DNA sequence analysis of SFV has been mainly limited to the terminal inverted repetitions (about 12 kb at each end of the genome) and immediately adjacent regions. We have sequenced a 4 kb fragment located approximately 20 kb from the right-terminal hairpin. Within this region three complete and two partial open reading frames (ORFs) have been identified. Each of the putative polypeptides has sequence similarity to one or more previously identified poxvirus or cellular proteins, with homology to protein kinases, erythrocyte ankyrin and a vaccinia virus virulencerelated protein (ORF NIL). The potential significance of these gene products with regard to the phenotype of SFV is discussed.

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Poxviruses of Rabbits

Cited by 16 publications

References 104 publications

Disruption of M-T5, a novel myxoma virus gene member of poxvirus host range superfamily, results in dramatic attenuation of myxomatosis in infected European rabbits

Disruption of M-T5, a novel myxoma virus gene member of poxvirus host range superfamily, results in dramatic attenuation of myxomatosis in infected European rabbits

Partial transcriptional mapping of the fowlpox virus genome and analysis of the EcoRI L fragment

Nucleotide sequence analysis of a unique near-terminal region of the tumorigenic poxvirus, Shope fibroma virus

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