Poxvirus tropism

McFadden, Grant

doi:10.1038/nrmicro1099

Cited by 474 publications

(504 citation statements)

References 189 publications

(221 reference statements)

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“…8 Within this virus family, especially vaccinia virus, the closely related cowpox virus and the rabbit pathogen myxoma virus have been studied and found to possess genes that can interfere with cellular activation pathways, such as interferon-and TNF signalling. It is noteworthy that important host regulatory genes are even conserved in the genomes of highly attenuated vaccinia virus strains, such as modified vaccinia virus Ankara (MVA) or NYVAC, candidate strains for future vaccination protocols.…”

Section: Introductionmentioning

confidence: 99%

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Fischer¹,

Ludwig

Holzapfel³

et al. 2005

Cell Death Differ

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Infection with viruses often protects the infected cell against external stimuli to apoptosis. Here we explore the balance of apoptosis induction and inhibition for infection with the modified vaccinia virus Ankara (MVA), using two MVA mutants with experimentally introduced deletions. Deletion of the E3L-gene from MVA transformed the virus from an inhibitor to an inducer of apoptosis. Noxa-deficient mouse embryonic fibroblasts (MEF) were resistant to MVA-DE3L-induced apoptosis. When the gene encoding F1L was deleted from MVA, apoptosis resulted that required Bak or Bax. MVA-DF1L-induced apoptosis was blocked by Bcl-2. When expressed in HeLa cells, F1L blocked apoptosis induced by forced expression of the BH3-only proteins, Bim, Puma and Noxa. Finally, biosensor analysis confirmed direct binding of F1L to BH3 domains. These data describe a molecular framework of how a cell responds to MVA infection by undergoing apoptosis, and how the virus blocks apoptosis by interfering with critical steps of its signal transduction.

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Section: Introductionmentioning

confidence: 99%

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Fischer¹,

Ludwig

Holzapfel³

et al. 2005

Cell Death Differ

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“…In addition to these strains, deletions of host range genes that have been identified to date from MV [66] would make excellent candidates for vaccines. Studies that have selectively deleted such genes have found no reduction in their in vitro replication levels, yet a severe defect in their ability to cause disease in rabbits (Tab.…”

Section: Prevention Control and Vaccinationmentioning

confidence: 99%

“…Studies in a mouse model of glioma has shown that this virus is quite effective in infecting tumor tissue in vivo and effectively 'cured' mice from these brain tumors [56]. These studies have fostered enthusiasm in the prospect of using this virus clinically to treat human cancers [66]. In this case, special considerations will have to be met to ensure the safety of both wild and cultivated rabbit populations.…”

Section: Prevention Control and Vaccinationmentioning

confidence: 99%

Myxoma virus in the European rabbit: interactions between the virus and its susceptible host

2007

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-Myxoma virus (MV) is a poxvirus that evolved inSylvilagus lagomorphs, and is the causative agent of myxomatosis in European rabbits (Oryctolagus cuniculus). This virus is not a natural pathogen of O. cuniculus, yet is able to subvert the host rabbit immune system defenses and cause a highly lethal systemic infection. The interaction of MV proteins and the rabbit immune system has been an ideal model to help elucidate host/poxvirus interactions, and has led to a greater understanding of how other poxvirus pathogens are able to cause disease in their respective hosts. This review will examine how MV causes myxomatosis, by examining a selection of the identified immunomodulatory proteins that this virus expresses to subvert the immune and inflammatory pathways of infected rabbit hosts. myxoma virus / immunomodulation / poxvirus / Oryctolagus cuniculus

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“…93,94 Yet, even with the newfound ability to engineer viral genomes to produce a new generation of safer, specific oncolytics, a true therapeutic frontrunner has yet to emerge. This is likely due not to inherent problems with the viruses now in circulation, but rather to their rapid clearance by the host immune system.…”

Section: Adaptation Attenuation and Engineering: Building A Bettermentioning

confidence: 99%

History of Oncolytic Viruses: Genesis to Genetic Engineering

2007

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Since the turn of the nineteenth century, when their existence was first recognized, viruses have attracted considerable interest as possible agents of tumor destruction. Early case reports emphasized regression of cancers during naturally acquired virus infections, providing the basis for clinical trials where body fluids containing human or animal viruses were used to transmit infections to cancer patients. Most often the viruses were arrested by the host immune system and failed to impact tumor growth, but sometimes, in immunosuppressed patients, infection persisted and tumors regressed, although morbidity as a result of the infection of normal tissues was unacceptable. With the advent of rodent models and new methods for virus propagation, there were numerous attempts through the 1950s and 1960s to force the evolution of viruses with greater tumor specificity, but success was limited and many researchers abandoned the field. Technology employing reverse genetics later brought about a renewal of interest in virotherapy that allowed the generation of more potent, tumor-specific oncolytics. Here, examination of early oncolytic virotherapy before genetic engineering serves to highlight tremendous advances, yet also hints at ways to penetrate host immune defenses, a significant remaining challenge in modern virotherapy research.

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Poxvirus tropism

Cited by 474 publications

References 189 publications

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Modified vaccinia virus Ankara protein F1L is a novel BH3-domain-binding protein and acts together with the early viral protein E3L to block virus-associated apoptosis

Myxoma virus in the European rabbit: interactions between the virus and its susceptible host

History of Oncolytic Viruses: Genesis to Genetic Engineering

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