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  • 1
    Language: English
    In: PLoS Pathogens, 2010, Vol.6(1), p.e1000727
    Description: [...]the history of the many consequences of smallpox on humankind reads like a long litany of human misery and calamitous events, but is juxtaposed with the more noble accomplishments that began with the discovery of vaccination by Jenner in 1798 and culminated with the World Health Organization (WHO) certifying the world free of smallpox in 1980 [2]. [...]we find ourselves still wrestling with an issue that intermingles public health policy, philosophy, national security, and bioterrorism, and affects our perceptions of research ethics with extreme pathogens in general.
    Keywords: Opinion ; Infectious Diseases ; Infectious Diseases -- Viral Infections ; Microbiology ; Microbiology -- Medical Microbiology ; Science Policy ; Virology
    ISSN: 1553-7366
    E-ISSN: 1553-7374
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  • 2
    Language: English
    In: Science, 02 January 1998, Vol.279(5347), pp.40-41
    Description: More than 5 years ago, a commentary in Science announced that viruses engage in "Star Wars" strategies against the immune system. Some of the viral invaders make receptors (viroceptors) that imitate normal cellular receptors and so can sequester and inactivate molecules that the immune system tries to use to fight the virus. Since that time, numerous other viral subterfuges for evading or subverting host defense mechanisms have been exposed, and viruses now are known to use an extraordinary spectrum of proteins to target immune molecules of the host cells. One particularly effective host defense is for the infected cell to self-destruct by programmed cell death, and in fact, cell death is triggered by infection with a wide variety of viruses. In response some viruses use specific proteins to suppress the cell suicide that would normally curtail the infection. Other classes of intracellular responses have elicited their own array of viral countermeasures as well. To this growing list, we can now add reactive oxidative species (oxidative stress) as a worthy target for viral inhibition. On page 102 of this issue, Shisler et al. report that molluscum contagiosum virus (MCV) encodes a novel anti-oxidant protein (MC066L) that functions as a scavenger of reactive oxygen metabolites and protect cells from ultraviolet- or peroxide-induced damage. Equally intriguing, MC066L is also the first bona fide selenoprotein expressed by a virus.
    Keywords: Biological sciences -- Biology -- Microbiology ; Physical sciences -- Chemistry -- Chemical compounds ; Biological sciences -- Biology -- Physiology ; Biological sciences -- Biology -- Cytology ; Biological sciences -- Biology -- Physiology ; Physical sciences -- Chemistry -- Chemical elements ; Physical sciences -- Chemistry -- Chemical compounds ; Biological sciences -- Biology -- Microbiology ; Biological sciences -- Biology -- Genetics
    ISSN: 00368075
    E-ISSN: 10959203
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  • 3
    Language: English
    In: 2015, Vol.11(6), p.e1004997
    Description: [...]when my longtime collaborator Peter Forsyth injected it into human gliomas transplanted into the brains of test immunodeficient mice, the virus grew selectively within the transplanted human brain tumors just like it does in the internal tissues of myxoma-infected rabbits! Since it is totally nonpathogenic...
    Keywords: Research Matters
    ISSN: 1553-7366
    E-ISSN: 1553-7374
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 05 April 2016, Vol.113(14), pp.3855-60
    Description: Myxoma virus (MYXV) is a rabbit-specific poxvirus, which is highly virulent in European rabbits. The attenuation of MYXV and the increased resistance of rabbits following the release of MYXV in Australia is one of the best-documented examples of host-pathogen coevolution. To elucidate the molecular mechanisms that contribute to the restriction of MYXV infection to rabbits and MYXV attenuation in the field, we have studied the interaction of the MYXV protein M156 with the host antiviral protein kinase R (PKR). In yeast and cell-culture transfection assays, M156 only inhibited rabbit PKR but not PKR from other tested mammalian species. Infection assays with human HeLa PKR knock-down cells, which were stably transfected with human or rabbit PKR, revealed that only human but not rabbit PKR was able to restrict MYXV infection, whereas both PKRs were able to restrict replication of a vaccinia virus (VACV) strain that lacks the PKR inhibitors E3 and K3. Inactivation of M156R led to MYXV virus attenuation in rabbit cells, which was rescued by the ectopic expression of VACV E3 and K3. We further show that a mutation in the M156 encoding gene that was identified in more than 50% of MYXV field isolates from Australia resulted in an M156 variant that lost its ability to inhibit rabbit PKR and led to virus attenuation. The species-specific inhibition of rabbit PKR by M156 and the M156 loss-of-function in Australian MYXV field isolates might thus contribute to the species specificity of MYXV and to the attenuation in the field, respectively.
    Keywords: Pkr ; Host–Pathogen Interaction ; Myxoma Virus ; Poxvirus ; Translational Regulation ; Myxoma Virus -- Genetics ; Viral Proteins -- Genetics ; Eif-2 Kinase -- Antagonists & Inhibitors
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    Language: English
    In: Vaccine, 06 September 2013, Vol.31(39), pp.4252-4258
    Description: Many common neoplasms are still noncurative with current standards of cancer therapy. More therapeutic modalities need to be developed to significantly prolong the lives of patients and eventually cure a wider spectrum of cancers. Oncolytic virotherapy is one of the promising new additions to clinical cancer therapeutics. Successful oncolytic virotherapy in the clinic will be those strategies that best combine tumor cell oncolysis with enhanced immune responses against tumor antigens. The current candidate oncolytic viruses all share the common property that they are relatively nonpathogenic to humans, yet they have the ability to replicate selectively in human cancer cells and induce cancer regression by direct oncolysis and/or induction of improved anti-tumor immune responses. Many candidate oncolytic viruses are in various stages of clinical and preclinical development. One such preclinical candidate is myxoma virus (MYXV), a member of the family that, in its natural setting, exhibits a very restricted host range and is only pathogenic to European rabbits. Despite its narrow host range in nature, MYXV has been shown to productively infect various classes of human cancer cells. Several preclinical modeling studies have demonstrated that MYXV is an attractive and safe candidate oncolytic virus, and hence, MYXV is currently being developed as a potential therapeutic for several cancers, such as pancreatic cancer, glioblastoma, ovarian cancer, melanoma, and hematologic malignancies. This review highlights the preclinical cancer models that have shown the most promise for translation of MYXV into human clinical trials.
    Keywords: Myxoma Virus ; Oncolytic Virotherapy ; Hematological Malignancies ; Pancreatic Cancer ; Medicine ; Biology ; Veterinary Medicine ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0264-410X
    E-ISSN: 1873-2518
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  • 6
    Language: English
    In: The Journal of Virology, 2011, Vol. 85(7), p.3270
    Description: Myxoma virus (MYXV) M062R is a functional homolog of the C7L family of host range genes from orthopoxviruses. We constructed a targeted M062R-knockout-MYXV (vMyxM062-KO) and characterized its properties in vitro and in vivo. In European rabbits, infection by vMyxM062-KO was completely asymptomatic. The surviving rabbits did not gain full protection against the subsequent lethal-dose challenge with wild-type MYXV. We also looked for cellular tropism defects in a variety of cultured cells. In all of the rabbit cells tested, vMyxM062-KO conducts an abortive infection, although it initiates viral DNA replication. In many, but not all, human cancer cells that are permissive for wild-type MYXV, vMyxM062-KO exhibited a profound replication defect. We categorized human cells tested into two groups: (i) type A, which support productive replication for wild-type MYXV but are unable to produce significant levels of progeny virus by vMyxM062-KO, and (ii) type B, which are permissive to infections by both wild-type MYXV and vMyxM062-KO. Furthermore, using proteomic strategies, we identified sterile α motif domain containing 9 (SAMD9), an interferon-regulated cellular protein implicated in human inflammatory disorders, as a unique host binding partner of M062 in human cells. Significantly, knocking down SAMD9 in type A human cancer cells led to a substantial rescue of vMyxM062-KO infection. In summary, M062 is a novel host range factor that controls productive MYXV replication in rabbit cells and in a wide variety of human cells. M062 also binds and antagonizes cellular SAMD9 in human cells, suggesting that SAMD9 is a novel innate antiviral factor against poxviruses.
    Keywords: Host Specificity ; Myxoma Virus -- Pathogenicity ; Proteins -- Antagonists & Inhibitors ; Viral Proteins -- Metabolism ; Virulence Factors -- Metabolism;
    ISSN: 0022-538X
    ISSN: 0022538X
    E-ISSN: 10985514
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  • 7
    Article
    Article
    In: Nature Medicine, 2005, Vol.11(7), p.711
    Keywords: Piperazines -- Pharmacology ; Poxviridae -- Drug Effects ; Protein Kinase Inhibitors -- Pharmacology ; Pyrimidines -- Pharmacology;
    ISSN: 1078-8956
    E-ISSN: 1546-170X
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  • 8
    Language: English
    In: PLoS ONE, 01 January 2014, Vol.9(10), p.e109801
    Description: Myxoma virus, a rabbit poxvirus, can efficiently infect various types of mouse and human cancer cells. It is a strict rabbit-specific pathogen, and is thought to be safe as a therapeutic agent in all non-rabbit hosts tested including mice and humans. Interleukin-15 (IL15) is an immuno-modulatory...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 9
    Language: English
    In: 2015, Vol.11(6), p.e1005014
    Description: In this issue of PLOS Pathogens, we are introducing a new front matter series to allow individual scientists from the many fields that encompass our community of editors, authors, and readers to comment on why the fundamental research in their labs, and...
    Keywords: Editorial
    ISSN: 1553-7366
    E-ISSN: 1553-7374
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  • 10
    Language: English
    In: 2012, Vol.7(8), p.e43298
    Description: Graft-versus-host disease (GVHD) is a potentially lethal clinical complication arising from the transfer of alloreactive T lymphocytes into immunocompromised recipients. Despite conventional methods of T cell depletion, GVHD remains a major challenge in allogeneic hematopoietic cell transplant. Here, we demonstrate a novel method of preventing GVHD by ex vivo treatment of primary human hematopoietic cell sources with myxoma virus, a rabbit specific poxvirus currently under development for oncolytic virotherapy. This pretreatment dramatically increases post-transplant survival of immunocompromised mice injected with primary human bone marrow or peripheral blood cells and prevents the expansion of human CD3 + lymphocytes in major recipient organs. Similar viral treatment also prevents human-human mixed alloreactive T lymphocyte reactions in vitro . Our data suggest that ex vivo virotherapy with myxoma virus can be a simple and effective method for preventing GVHD following infusion of hematopoietic products containing alloreactive T lymphocytes such as: allogeneic hematopoietic stem and progenitor cells, donor leukocyte infusions and blood transfusions.
    Keywords: Research Article ; Biology ; Medicine ; Immunology ; Virology ; Microbiology ; Hematology
    E-ISSN: 1932-6203
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