Wednesday, July 2, 2014

GMO Antibiotic Resistance Elephant in the Room

GMOs are made using antibiotic resistant bacteria... At about 8 minutes he explains how Horizontal DNA manipulation of bacteria is done to create new types that spread the anti-biotic resistance to other bacteria in the body.This is what is used to make GMOs an anti-biotic resistant mutation is added to the corn, soy or whatever to create the capacity for growth and mark the gene to be patentable.

Turns out that the process; which is always doubtful, because bacteria can make their own changes Vertically in their own DNA...has now a viral DNA not intended. And has changed their patent to an other type of product totally beyond their control.
It has been found in our bodies...floating around looking for a place to take hold... Somewhere comfortable to replicate...

This article is 2 years old...Where are all those "scientists"? To explain themselves...
...Pretending this is not happening will not work.

"How should a regulatory agency announce they have discovered something potentially very important about the safety of products they have been approving for over twenty years?

In the course of analysis to identify potential allergens in GMO crops, the European Food Safety Authority (EFSA) has belatedly discovered that the most common genetic regulatory sequence in commercial GMOs also encodes a significant fragment of a viral gene (Podevin and du Jardin 2012). This finding has serious ramifications for crop biotechnology and its regulation, but possibly even greater ones for consumers and farmers. This is because there are clear indications that this viral gene (called Gene VI) might not be safe for human consumption. It also may disturb the normal functioning of crops, including their natural pest resistance."

The researchers themselves concluded that the presence of segments of Gene VI “might result in unintended phenotypic changes”. They reached this conclusion because similar fragments of Gene VI have already been shown to be active on their own (e.g. De Tapia et al. 1993). In other words, the EFSA researchers were unable to rule out a hazard to public health or the environment.

In general, viral genes expressed in plants raise both agronomic and human health concerns (reviewed in Latham and Wilson 2008). This is because many viral genes function to disable their host in order to facilitate pathogen invasion. Often, this is achieved by incapacitating specific anti-pathogen defenses. Incorporating such genes could clearly lead to undesirable and unexpected outcomes in agriculture. Furthermore, viruses that infect plants are often not that different from viruses that infect humans. For example, sometimes
the genes of human and plant viruses are interchangeable, while on other occasions inserting plant viral fragments as transgenes has caused the genetically altered plant to become susceptible to an animal virus (Dasgupta et al. 2001). Thus, in various ways, inserting viral genes accidentally into crop plants and the food supply confers a significant potential for harm.

The Many Functions of Gene VI
Gene VI, like most plant viral genes, produces a protein that is multifunctional. It has four (so far) known roles in the viral infection cycle.
The first is to participate in the assembly of virus particles. There is no current data to suggest this function has any implications for biosafety. The second known function is to suppress anti-pathogen defenses by inhibiting a general cellular system called RNA silencing (Haas et al. 2008). Thirdly, Gene VI has the highly unusual function of transactivating (described below) the long RNA (the 35S RNA) produced by CaMV (Park et al. 2001). Fourthly, unconnected to these other mechanisms, Gene VI has very recently been shown to make plants highly susceptible to a bacterial pathogen (Love et al. 2012). Gene VI does this by interfering with a common anti-pathogen defense mechanism possessed by plants. These latter three functions of Gene VI (and their risk implications) are explained further below:

This sense of a generic failure is reinforced by the fact that this is not an isolated event. There exist other examples of commercially approved viral sequences having overlapping genes that were never subjected to risk assessment. These include numerous commercial GMOs containing promoter regions of the closely related virus figwort mosaic virus (FMV) which were not considered by Podevin and du Jardin. Inspection of commercial sequence data shows that the commonly used FMV promoter overlaps its own Gene VI (Richins et al 1987). A third example is the virus-resistant potato NewLeaf Plus (RBMT-22-82). This transgene contains approximately 90% of the P0 gene of potato leaf roll virus. The known function of this gene, whose existence was discovered only after US approval, is to inhibit the anti-pathogen defenses of its host (Pfeffer et al 2002). Fortunately, this potato variety was never actively marketed.

There are two aspects to this question. One is the length of Gene VI accidentally introduced by developers. This appears to vary but most of the 54 approved transgenes contain the same 528 base pairs of the CaMV 35S promoter sequence. This corresponds to approximately the final third of Gene VI. Deleted fragments of Gene VI are active when expressed in plant cells and functions of Gene VI are believed to reside in this final third. Therefore, there is clear potential for unintended effects if this fragment is expressed (e.g. De Tapia et al. 1993; Ryabova et al. 2002; Kobayashi and Hohn 2003).

The second aspect of this question is what quantity of Gene VI could be produced in GMO crops? Once again, this can ultimately only be resolved by direct quantitative experiments. Nevertheless, we can theorize that the amount of Gene VI produced will be specific to each independent insertion event. This is because significant Gene VI expression probably would require specific sequences (such as the presence of a gene promoter and an ATG [a protein start codon]) to precede it and so is likely to be heavily dependent on variables such as the details of the inserted transgenic DNA and where in the plant genome the transgene inserted.

Commercial transgenic crop varieties can also contain superfluous copies of the transgene, including those that are incomplete or rearranged (Wilson et al 2006). These could be important additional sources of Gene VI protein. The decision of regulators to allow such multiple and complex insertion events was always highly questionable, but the realization that the CaMV 35S promoter contains Gene VI sequences provides yet another reason to believe that complex insertion events increase the likelihood of a biosafety problem.

Even direct quantitative measurements of Gene VI protein in individual crop authorizations would not fully resolve the scientific questions, however. No-one knows, for example, what quantity, location or timing of protein production would be of significance for risk assessment, and so answers necessary to perform science-based risk assessment are unlikely to emerge soon.

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