Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases

Bastian, Frank O.; Fermin, César D.

doi:10.1002/jemt.20223

Cited by 8 publications

(2 citation statements)

References 63 publications

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“…The role of TLR in TSE pathogenesis has been previously questioned [59] yet its up-regulation in the present model could be related to PrPres deposition. On the contrary, researchers questioning the "protein only" hypothesis suggest that classical infectious agents such as viruses [51,60-63] or bacteria [64,65] could be involved in TSE pathogenesis, in which case an innate response, such as the one suggested by the present results would also certainly fit.…”

Section: Discussioncontrasting

confidence: 50%

Central nervous system gene expression changes in a transgenic mouse model for bovine spongiform encephalopathy

Tortosa

Castells

Vidal

et al. 2011

Vet Res

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Gene expression analysis has proven to be a very useful tool to gain knowledge of the factors involved in the pathogenesis of diseases, particularly in the initial or preclinical stages. With the aim of finding new data on the events occurring in the Central Nervous System in animals affected with Bovine Spongiform Encephalopathy, a comprehensive genome wide gene expression study was conducted at different time points of the disease on mice genetically modified to model the bovine species brain in terms of cellular prion protein. An accurate analysis of the information generated by microarray technique was the key point to assess the biological relevance of the data obtained in terms of Transmissible Spongiform Encephalopathy pathogenesis. Validation of the microarray technique was achieved by RT-PCR confirming the RNA change and immunohistochemistry techniques that verified that expression changes were translated into variable levels of protein for selected genes. Our study reveals changes in the expression of genes, some of them not previously associated with prion diseases, at early stages of the disease previous to the detection of the pathological prion protein, that might have a role in neuronal degeneration and several transcriptional changes showing an important imbalance in the Central Nervous System homeostasis in advanced stages of the disease. Genes whose expression is altered at early stages of the disease should be considered as possible therapeutic targets and potential disease markers in preclinical diagnostic tool development. Genes non-previously related to prion diseases should be taken into consideration for further investigations.

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Section: Discussioncontrasting

confidence: 50%

Central nervous system gene expression changes in a transgenic mouse model for bovine spongiform encephalopathy

Tortosa

Castells

Vidal

et al. 2011

Vet Res

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“…5 Although less accepted in the scientific community, other factors (including viral and bacterial pathogens) have been suggested to play a role in the genesis and propagation of the pathogenic protein. [6][7][8][9][10] The clinical features of prion disease in humans and other animals are characterized by long incubation periods (generally intervals of years) and progressive neurologic dysfunction that invariably results in death (generally within a year after onset). Among the various human prion diseases, sporadic CJD is by far the most common.…”

Section: General Characteristics Of Tsesmentioning

confidence: 99%

Transmissible spongiform encephalopathies

Sejvar

Schonberger²,

Belay

2008

javma

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Spiroplasma

Williamson¹,

Gasparich²,

Regassa³

et al. 2015

Bergey's Manual of Systematics of Archaea and Bacteria

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Spi.ro.plas'ma. Gr. n. speira (L. transliteration spira ) a coil, spiral; Gr. neut. n. plasma something formed or molded, a form; N.L. neut. n. Spiroplasma spiral form. Tenericutes / Mollicutes / Entomoplasmatales / Spiroplasmataceae / Spiroplasma Cells are pleomorphic, varying in size and shape from helical and branched nonhelical filaments to spherical or ovoid. The helical forms, usually 100–200 nm in diameter and 3–5 µm in length, generally occur during the exponential phase of growth and in some species persist during stationary phase. The cells of some species are short (1–2 µm). In certain cases, helical cells may be very tightly coiled, or the coils may show continuous variation in amplitude. Spherical cells ~300 nm in diameter and nonhelical filaments are frequently seen in the stationary phase, where they may not be viable, and in all growth phases in suboptimal growth media, where they may or may not be viable. In some species during certain phases, spherical forms may be the replicating form. Helical filaments are motile, with flexional and twitching movements, and often show an apparent rotatory motility. Fibrils are associated with the membrane, but flagellae, periplasmic fibrils, or other organelles of locomotion are absent . Fimbriae and pili observed on the cell surface of insect‐ and plant‐pathogenic spiroplasmas are believed to be involved in host‐cell attachment and conjugation (Ammar et al., 2004; Özbek et al., 2003), but not in locomotion. Cells divide by binary fission, with doubling times of 0.7–37 h. Facultatively anaerobic. The temperature growth range varies among species, from 5 to 41°C. Colonies on solid media are frequently diffuse , with irregular shapes and borders, a condition that reflects the motility of the cells during active growth (Figure 111). Colony type is strongly dependent on the agar concentration. Colony sizes vary from 0.1 to 4.0 mm in diameter. Colonies formed by nonmotile variants or mutants, or by cultures growing on inadequate media are typically umbonate with diameters of 200 µm or less. Some species, such as Spiroplasma platyhelix , have barely visible helicity along most of their length and display little rotatory or flexing motility. Colonies of motile, fast‐growing spiroplasmas are diffuse, often with satellite colonies developing from foci adjacent to the initial site of colony development. Light turbidity may be produced in liquid cultures. Chemo‐organotrophic. Acid is produced from glucose. Hydrolysis of arginine is variable. Urea, arbutin, and esculin are not hydrolyzed. Sterol requirements are variable. An optimum osmolality, usually in the range of 300–800 mOsm, has been demonstrated for some spiroplasmas. Media containing mycoplasma broth base, serum, and other supplements are required for primary growth, but after adaptation, growth often occurs in less complex media. Defined or semi‐defined media are available for some species. Resistant to 10,000 U/ml penicillin. Insensitive to rifampicin, sensitive to erythromycin and tetracycline. Isolated from the surfaces of flowers and other plant parts, from the guts and hemolymph of various insects and crustaceans, and from tick triturates. Also isolated from vascular plant fluids ( phloem sap ) and insects that feed on the fluids . Specific host associations are common. The type species, Spiroplasma citri , is pathogenic for citrus (e.g., orange and grapefruit), producing “stubborn” disease. Experimental or natural infections also occur in horseradish, periwinkle, radish, broad bean, carrot, and other plant species. Spiroplasma kunkelii is a maize pathogen. Some species are pathogenic for insects. Certain species are pathogenic, under experimental conditions, for a variety of suckling rodents (rats, mice, hamsters and rabbits) and/or chicken embryos. Genome sizes vary from 780 to 2220 kbp (PFGE). DNA G + C content ( mol %): 24–31 ( T m , Bd). Type species : Spiroplasma citri Saglio, L'Hospital, Laflèche, Dupont, Bové, Tully and Freundt 1973, 202 AL .

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Slow virus disease: Deciphering conflicting data on the transmissible spongiform encephalopathies (TSE) also called prion diseases

Cited by 8 publications

References 63 publications

Central nervous system gene expression changes in a transgenic mouse model for bovine spongiform encephalopathy

Central nervous system gene expression changes in a transgenic mouse model for bovine spongiform encephalopathy

Transmissible spongiform encephalopathies

Spiroplasma

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