New Israeli vaccine could save bees from colony collapse disorder

[Erna]

New Israeli vaccine could save bees from colony collapse disorder

An Israeli company has developed a revolutionary new drug that could solve the problem of Colony Collapse Disorder, the disturbing syndrome that has been wiping out bee communities and threatening agricultural production all over the world.

The drug, Remembee, which was developed by Beeologics, has completed successful clinical trials on millions of bees in North America. Not
only has it proved effective in maintaining bee health, but it also improved the longevity of bees and increased the honey in the hives.

Based on Nobel prize-winning RNAI technology, Remembee helps the bees overcome IAVP virus, also discovered in Israel, which has been associated with colony collapse in scientific literature.

"It's really a tug of war between the virus and the host. We are helping the bee tug the rope more strongly and beat the virus. We take
advantage of an immune system that the bees elicit for viral disease. But we are really using naturally occurring phenomenon. It's not a
pesticide and it's not toxic," says Nitzan Paldi, CTO of Beeologics.

The US Department of Agriculture has been accompanying Beeologics with its FDA certification process due to the urgency of the need for the drug.

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[RedFox]

RNAI technology??

_http://en.wikipedia.org/wiki/RNA_interference

RNA interference (RNAi) is a system within living cells that helps to control which genes are active and how active they are. Two types of small RNA molecules – microRNA (miRNA) and small interfering RNA (siRNA) – are central to RNA interference. RNAs are the direct products of genes, and these small RNAs can bind to specific other RNAs and either increase or decrease their activity, for example by preventing a messenger RNA from producing a protein. RNA interference has an important role in defending cells against parasitic genes – viruses and transposons – but also in directing development as well as gene expression in general.

The RNAi pathway is found in many eukaryotes including animals and is initiated by the enzyme Dicer, which cleaves long double-stranded RNA (dsRNA) molecules into short fragments of ~20 nucleotides. One of the two strands of each fragment, known as the guide strand, is then incorporated into the RNA-induced silencing complex (RISC). The most well-studied outcome is post-transcriptional gene silencing, which occurs when the guide strand base pairs with a complementary sequence of a messenger RNA molecule and induces cleavage by Argonaute, the catalytic component of the RISC complex. This process is known to spread systemically throughout the organism despite initially limited molar concentrations of siRNA.

The selective and robust effect of RNAi on gene expression makes it a valuable research tool, both in cell culture and in living organisms because synthetic dsRNA introduced into cells can induce suppression of specific genes of interest. RNAi may also be used for large-scale screens that systematically shut down each gene in the cell, which can help identify the components necessary for a particular cellular process or an event such as cell division. Exploitation of the pathway is also a promising tool in biotechnology and medicine.

Historically, RNA interference was known by other names, including post transcriptional gene silencing, and quelling. Only after these apparently unrelated processes were fully understood did it become clear that they all described the RNAi phenomenon. In 2006, Andrew Fire and Craig C. Mello shared the Nobel Prize in Physiology or Medicine for their work on RNA interference in the nematode worm C. elegans,[2] which they published in 1998.[3]

RNA interference is a vital part of the immune response to viruses and other foreign genetic material, especially in plants where it may also prevent self-propagation by transposons.[61] Plants such as Arabidopsis thaliana express multiple dicer homologs that are specialized to react differently when the plant is exposed to different types of viruses.[62] Even before the RNAi pathway was fully understood, it was known that induced gene silencing in plants could spread throughout the plant in a systemic effect, and could be transferred from stock to scion plants via grafting.[63] This phenomenon has since been recognized as a feature of the plant adaptive immune system, and allows the entire plant to respond to a virus after an initial localized encounter.[64] In response, many plant viruses have evolved elaborate mechanisms that suppress the RNAi response in plant cells.[65] These include viral proteins that bind short double-stranded RNA fragments with single-stranded overhang ends, such as those produced by the action of dicer.[66] Some plant genomes also express endogenous siRNAs in response to infection by specific types of bacteria.[67] These effects may be part of a generalized response to pathogens that downregulates any metabolic processes in the host that aid the infection process.[68]

Although animals generally express fewer variants of the dicer enzyme than plants, RNAi in some animals has also been shown to produce an antiviral response. In both juvenile and adult Drosophila, RNA interference is important in antiviral innate immunity and is active against pathogens such as Drosophila X virus.[69][70] A similar role in immunity may operate in C. elegans, as argonaute proteins are upregulated in response to viruses and worms that overexpress components of the RNAi pathway are resistant to viral infection.[71][72]

The role of RNA interference in mammalian innate immunity is poorly understood, and relatively little data is available. However, the existence of viruses that encode genes able to suppress the RNAi response in mammalian cells may be evidence in favour of an RNAi-dependent mammalian immune response.[73][74] However, this hypothesis of RNAi-mediated immunity in mammals has been challenged as poorly substantiated.[75] Alternative functions for RNAi in mammalian viruses also exist, such as miRNAs expressed by the herpes virus that may act as heterochromatin organization triggers to mediate viral latency.[42]

GM Bees?! Good greif......it does make me wonder about the whole swine flu thing too....