Infectious protein expression

Kastenbauer S, Angele B, Sporer B, Pfister HW, Koedel U (2005) Patterns of protein expression in infectious meningitis A cerebrospinal fluid protein ai ray analysis. J Neuroimmunol 164(1-2) 134-139. 

Hong, J.R., Y.L. Hsu and J.L. Wu. Infectious pancreatic necrosis induces apoptosis due to down-regulation of survival factor MCL-1 protein expression in a fish cell line. Virus Res. 63 75-83, 1999. 

Which mechanism could induce such a dramatic change of the 3D structure of a protein How could the a —> p conversion of PrP into PrP " account for the pathogenic properties of this protein In 1967 (25 years before Prusiner invented the term prion), a remarkably inspired mathematician, J. S. Griffith, proposed a simple but prophetic model of a disease caused by the replication of an infectious protein. One of his hypothesis was that the brain expressed a "normal" form of the protein, whereas the infectious particle contained an "abnormal" form of the same protein. The abnormal form of the protein was then supposed to bind to the normal brain protein and to convert it into a disease-causing protein. This simple mechanism... 

This long quest was marked by milestones. As already discussed, the obtention of highly purified preparations of infectious scrapie particles was necessary to identify the PrP protein. Circular dichroism studies of PrP and PrP demonstrated the existence of two totally distinct conformations of PrP, one corresponding to the physiologically expressed brain protein and the other to the infectious protein. However, the masterly demonstration of the mechanism of prion replication is that PRNP° mice, which do not express the PrP protein, failed to propagate prion infectivity. Hence, without the brain reservoir of normal PrP proteins, infectious PrP proteins are harmless and unable to cause any disease. If we link this information with the respective structures of PrP and PrP , then we have a molecular mechanism accounting for the replication, by force, of prions invaders in the brain of healthy animals (Fig. 9.5). 

The temperate virus does not exist in its mature, infectious state inside the cell, but rather in a latent form, called the provirus or prophage state. In considering virulent viruses we learned that the DNA of the virulent virus contains information for the synthesis of a number of enzymes and other proteins essential to virus reproduction. The prophage of the temperate virus carries similar information, but in the lysogenic cell this information remains dormant because the expression of the virus genes is blocked through the action of a specific repressor coded for by the virus. As a result of a genetic switch, the repressor is inactivated, virus reproduction occurs, the cell lyses, and virus particles are released. 

The majority of viruses that infect plants have single-stranded, positive-sense RNA genomes. It has therefore been necessary to use infectious cDNA clones for the in vitro manipulation of RNA viruses, allowing them to be developed as effective tools for the commercial production of target proteins in plants. This approach has also been used to study the genetic and metabolic profiles of both viruses and their host plants. Siegel [14] conceptualized the potential use of RNA viruses as expression vectors. Brome mosaic virus (BMV) and Tobacco mosaic vims (TMV) were the first two RNA viruses to be converted into expression vectors. These vectors have since been pro-... 

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