rense.com feb 23 2016 Dr Bill Deagle Zike Virus Fears Grow

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The Gene Plague - Zika Virus Weaponized by OX513A Jumping Gene Complex in GMO Mosquitoes and Hosts under Oxidative Stress
March 10, 2016    
http://www.nutrimedical.com/news.jhtml?method=view&news.id=4458

  "The Gene Plague
   Oxitec Transposon Jumping genes in Fraken-mosquitoes
   from the Gates Foundation
   
   2012 OXITECH RELEASE OF MALE GMO MOSQUITOES
   
   
   Oxitech was aware that the terminator jumping genes inserted in
   Brazilian mosquitoes, may allow up to 15 % first generation survivors,
   due to ambient Tetracycline in the environment.  One in 200 hand sorted
   mosquitoes were female, and add another variable.  Because selection
   bread out lethal genetic traits, the piggyBAC gene transposon moves to
   a different place in the 10 thousand codon sequence to make the changes
   less lethal, but maintaining high oxidative stree.  This will speed
   viral mutagenic pathogenic evolution, due to peroxynitrate and
   hydroperoxy radicals in gene imbalanced host vector organisms. Thus we
   now have a platform to weaponized any pathogenic bacteria or virus via
   known mechanisms, causing expected future pandemics.   Other unexpected
   genetic and epigenetic changes may occur that cannot be anticipated. 
   Oxitech is therefore resulted in creating a weapon arising platform to
   speed the a pathogenic evolution of RNA and DNA viruses as well as
   bacterial and other parasitic pathogens. Unexpected gene changes would
   also possibly occur during insertion of the piggyBAC gene insertion to
   one or multiple points in the animal or human or plant genome.  Changes
   in structure and function, fertility and organ and tissue development
   may occur that are very unexpected.
   
   
   
   There are two problems that have been potentially identified. The first
   is an increased oxidative stress host caused by an unstable genetics
   with the insertion of the transposon gene. This will result in
   increased level of pathogen evolution to cause more lethal effects. The
   second problem is the presence of normal gene control mechanism
   disruption by this jumping gene. Unexpected effects may felt affect
   organ development, fertility, disease states such as autoimmune
   diseases and cancer. Because the virus is neurotrophic it may result in
   other neurological syndromes such as cortical atrophy damage to a
   nuclei of the brain that regulate hormones and the autonomic nervous
   system, and end organ failure.
   Intrexon, which has acquired Oxitech has developed other technological
   platforms for grading genetically engineered ActoBiotics , fuel
   conversion genetic technology, and other pathogen control technologies
   such as the monster affects cotton. ActoBiotics, result from the
   insertion in lactobacillus that are designed to have terminator gene so
   they will not persist in the bowel. This may be wishful thinking and
   the gene complex maybe unstable address or other bacteria within the
   got or other tissues. You continue to generate multiple peptides that
   have any pathogenic effects on body pathogens and unexpected epigenetic
   effects.
   The virus should be protected at for transfer at points of entry at
   ports and airlines. PCR testing for the virus and buccal smears for
   fluorescent markers of the presence of one or more copies of the
   piggyBAC gene in human genome.   Capture of mosquitoes and wild animals
   and pets for the presence of the virus or genetic pollution from the
   piggyBAC transposon should be undertaken with geographic mapping and
   cataloging epigenetic changes caused by specific gene insertion.
   Unexpected effects may result in changes it and food vegetables in
   terms of taste, vitamin content, mineral content and appearance. Animal
   epigenetic may be affected that may change behavior, organ development,
   and fertility. Ecological effects may disrupt the ecosystem web of
   life. The unexpected changes may result in loss of species and
   imbalance of the ecosystem causing loss of crops and predators or food
   and the spread of super pathogens animals in the wild or to humans as
   pandemics. eBook on The Gene Plaque will be available soon at
   NutriMedical.com or phone 888-212-8871.  Updates are given daily at 12
   Noon to 3 PM PST, Mondays to Fridays on The NutriMedical Report Show on
   Genesis Network with free mp3 access.
   
   PROOF PUBLISHED OF NO LINK BETWEEN LARVICIDE AND MICROCEPHALY
   Published proof that Pyriproxyfen is not linked with microcephaly.
   February 2016 rumors that microcephaly was the caused by the larvicide
   Pyriproxyfen have now been refuted by scientists. The Brazilian
   government statement is also identified some local authorities do not
   use Pyriproxyfen and have reported cases of microcephaly. The following
   four references clearly dismiss the theory that the pesticide was
   directly linked to the Zika microcephaly and other birth defects.
   Reference number one scientist of debunk. Pesticides related to the
   zinc at the birth defects but not to seek a virus. Reference number
   two, reports his month sent a link pesticide is to blame for
   microcephaly outbreakv
   . There a review of the report showed no scientific evidence forming a
   link. Reference number three, dismiss the a linkage previously placed
   between the microcephaly and Guillaine Barre paralysis and the
   pesticide. finally, the Brazilian government has dismissed the link
   proposed between the pesticide and larvicide and the presence of birth
   defects of microcephaly optic atrophy and Guillaine barre paralysis
   
   1/ Szabo, Liz (16 February 2016). "Scientists debunk theory linking
   pesticide, not Zika, to birth defects". USA Today.
   2/  "Report says Monsanto-linked pesticide is to blame for microcephaly
   outbreak – not Zika". Science Alert (Australia). 16 February 2016. But
   let's be clear – there is no scientific evidence to support that link.
   3/ a b Jacobs, Andrew (February 16, 2016). "Conspiracy Theories About
   Zika Spread Along With the Virus". The New York Times. Retrieved
   February 16, 2016.
   4/ Bowater, Donna (February 15, 2016). "Zika virus: Brazil dismisses
   link between larvicide and microcephaly". Daily Telegraph. Retrieved
   February 16, 2016.
   
   
   
   ZIKA VIRUS PROTECTION PROTOCOL
   AllicinMed 1 to 2 capsules three times a day
   Nutriodine 10 to 20 drops three times a day diror three drops per 10
   pounds body weight scrrs fon water
   Silver 101 spray or three drops per 10 pounds body weight three times a
   day orally
   NutriDefense one to two capsules three times a day
   Power C PLUS three capsules three times a day
   MyCell D3 5,000 IU three to five softgels twice per day
   STD protection with condoms, NIOSH N95 if proof of droplet spray,
   Defense Wipes on all contact surfaces
   Ports of Entry PCR Saliva, Urine of Zika and Buccal Scaping for
   Fluorecent piggyBAC gene with microscopy > Quarantine until PCR
   negative 72 hours, on repeated testing
   Ozonated Water Cleansing surfaces, Seal Aircraft Ozonated Air with
   Silver 100 aerosols for kill period 10 to 20 minutes, UV Light Curtains
   and Reverse Protection in Clinics and Hospitals with Carrier Zika Cases.
   Prevention of pregnancy with positive Zika PCR test or gene on buccal
   fluorescent smear microsocopy
   
   Dr Bill Deagle MD  A4M AAEM ACAM
   NutriMedical.com
   888-212-8871
   The NutriMedical Report Show on Genesis Network 12 Noon to 3 PM M-F
   Worldwide "

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Aedes Aegypti mosquito feeding on human blood. This is the species that transmits Zika, and that was genetically engineered by Oxitec using the piggyBac transposon. Photo: James Gathany via jentavery on Flickr (CC BY).
Pandora's box: how GM mosquitos could have caused Brazil's microcephaly disaster
Oliver Tickell
1st February 2016
http://www.theecologist.org/News/news_analysis/2987024/pandoras_box_how_gm_mosquitos_could_have_caused_brazils_microcephaly_disaster.html

  "In Brazil's microcephaly epidemic, one vital question remains
   unanswered: how did the Zika virus suddenly learn how to disrupt the
   development of human embryos? The answer may lie in a sequence of
   'jumping DNA' used to engineer the virus's mosquito vector - and
   released into the wild four years ago in the precise area of Brazil
   where the microcephaly crisis is most acute.
   
   ` ` These 'promiscuous' transposons have found special favour with
   genetic engineers, whose goal is to create 'universal' systems for
   transferring genes into any and every species on earth. Almost none of
   the geneticists has considered the hazards involved ' '
   
   Since August 2015, a large number of babies in Northeast Brazil have
   been born with very small heads, a condition known as microcephaly, and
   with other serious malformations. 4,180 suspected cases have been
   reported.
   
   Epidemiologists have found a convincing correlation between the
   incidence of the natal deformities and maternal infections with the
   Zika virus, first discovered in Uganda's Zika Valley in 1947, which
   normally produces non-serious illness.
   
   The correlation has been evidenced through the geographical
   distrubution of Zika infections and the wave of deformities. Zika virus
   has also been detected in the amniotic fluids and other tissues of the
   affected babies and their mothers.


Map showing the concentration of suspected Zika-related cases of microcephaly in Brazil. Image: Claire Bernish / AntiMedia.


Map showing the location of Juazeiro, Bahia, Brazil. Image: thanks to John Fedor-Cunningham.
   
   

Important update: Since this article was written, two things have
   become apparent that cast doubt on the hypothesis advanced in this
   article as regards the Zika virus.
   
   First the connection between the Zika virus and Brazil's outbreak of
   microcephaly as set out in this article appears increasingly tenuous
   with the announcement on 6th February of the Colombian President, Juan
   Manuel Santos (reported by the Washington Post), that there is no
   evidence that Zika has caused any cases of microcephaly in his country.
   Health officials have diagnosed 3,177 pregnant women with the virus,
   but in no case has microcephaly been observed in foetal scans. We also
   note that the Melo Oliveira paper referred to below is based on an
   examination of just two women.
   
   This among the topics covered in a newly published article on The
   Ecologist: 'Argentine and Brazilian doctors suspect mosquito
   insecticide as cause of microcephaly' by Claire Robinson of GMWatch.
   
   Second, bioinformatician David Murphy has examined recent genomes of
   the Zika virus and found no trace of the piggyBac transposon in its
   genetic material. This is set out in detail in Notes 1 & 2 at the foot
   of this article. This effectively rules out the possibility of the
   mutation of the virus by the proposed mechanism.
   
   However important questions raised in this article remain unanswered.
   In particular, it would be precautionary to know if any of the genetic
   material inserted into the Aedes aegypti mosquitos using the piggyBac
   transposon survives in wild populations in and around the area in which
   the Oxitec mosquitos were released in 2011 and 2012. This is something
   that would be relatively easy to test for using PCR techniques however
   I am not aware that this has been done. If indeed such genetic material
   does persist in the wild this fact would need to be taken into account
   by regulators as a significant risk factor in their consideration of
   any future releases.
   
   Please also see Notes 1, 2 and 3 at the foot of this article.

   This latter finding was recently reported by A S Oliveira Melo et al in
   a scientific paper published in the journal Ultrasound in Obstetrics &
   Gynecology, which noted evidence of intra-uterine infection. They also
   warn:
   
   "As with other intrauterine infections, it is possible that the
   reported cases of microcephaly represent only the more severely
   affected children and that newborns with less severe disease, affecting
   not only the brain but also other organs, have not yet been diagnosed."
   
   The Brazilian Health Minister, Marcelo Castro, says he has "100%
   certainty" that there is a link between Zika and microcephaly. His view
   is supported by the medical community worldwide, including by the US
   Center for Disease Control.
   
   Oliveira Melo et al draw attention to a mystery that lies at the heart
   of the affair: "It is difficult to explain why there have been no fetal
   cases of Zika virus infection reported until now but this may be due to
   the underreporting of cases, possible early acquisition of immunity in
   endemic areas or due to the rarity of the disease until now.
   
   "As genomic changes in the virus have been reported, the possibility of
   a new, more virulent, strain needs to be considered. Until more cases
   are diagnosed and histopathological proof is obtained, the possibility
   of other etiologies cannot be ruled out."
   
   And this is the key question: how - if indeed Zika really is the
   problem, as appears likely - did this relatively innocuous virus
   acquire the ability to produce these terrible malformations in unborn
   human babies?
   
   Oxitec's GM mosquitoes
   
   An excellent article by Claire Bernish published last week on AntiMedia
   draws attention to an interesting aspect of the matter which has
   escaped mainstream media attention: the correlation between the
   incidence of Zika and the area of release of genetically modified Aedes
   aegypti mosquitos engineered for male insterility (see maps, above
   right).
   
   The purpose of the release was to see if it controlled population of
   the mosquitos, which are the vector of Dengue fever, a potentially
   lethal disease. The same species also transmits the Zika virus.
   
   The releases took in 2011 and 2012 in the Itaberaba suburb of the city
   of Juazeiro, Bahia, Northeast Brazil, about 500 km west of the coastal
   city of Recife. The experiment was written up in July 2015 in the
   journal PLOS Neglected Tropical Diseases in a paper titled 'Suppression
   of a Field Population of Aedes aegypti in Brazil by Sustained Release
   of Transgenic Male Mosquitoes' by Danilo O. Carvalho et al.
   
   An initial 'rangefinder of 30,000 GM mosquitos per week took place
   between 19th May and 29th June 2011, followed by a much larger release
   of 540,000 per week in early 2012, ending on 11th February.
   
   At the end of it the scientists claimed "effective control of a wild
   population of Ae. aegypti by sustained releases of OX513A male Ae.
   aegypti. We diminished Ae. aegypti population by 95% (95% CI:
   92.2%-97.5%) based on adult trap data and 78% (95% CI: 70.5%-84.8%)
   based on ovitrap indices compared to the adjacent no-release control
   area."
   
   So what's to worry about?
   
   The idea of the Oxitec mosquitoes is simple enough: the males produce
   non-viable offspring which all die. So the GM mosqitoes are
   'self-extinguishing' and the altered genes cannot survive in the wild
   population. All very clever, and nothing to worry about!
   
   But in fact, it's not so simple. In 2010 geneticist Ricarda
   Steinbrecher wrote to the biosafety regulator in Malaysia - also
   considering a release of the Oxitec mosquitoes - with a number of
   safety concerns, pointing out the 2007 finding by Phuc et al that 3-4%
   of the first generation mosquitos actually survive.
   
   The genetic engineering method employed by Oxitec allows the popular
   antibiotic tetracycline to be used to repress the lethality during
   breeding. But as a side-effect, the lethality is also reduced by the
   presence of tetracycline in the environment; and as Bernish points out,
   Brazil is among the world's biggest users of anti-microbials including
   tetracycline in its commercial farming sector:
   
   "As a study by the American Society of Agronomy, et. al., explained,
   'It is estimated that approximately 75% of antibiotics are not absorbed
   by animals and are excreted in waste.' One of the antibiotics (or
   antimicrobials) specifically named in that report for its environmental
   persistence is tetracycline.
   
   In fact, as a confidential internal Oxitec document divulged in 2012,
   that survival rate could be as high as 15% - even with low levels of
   tetracycline present. 'Even small amounts of tetracycline can repress'
   the engineered lethality. Indeed, that 15% survival rate was described
   by Oxitec."
   
   She then quotes the leaked Oxitec paper: "After a lot of testing and
   comparing experimental design, it was found that [researchers] had used
   a cat food to feed the [OX513A] larvae and this cat food contained
   chicken. It is known that tetracycline is routinely used to prevent
   infections in chickens, especially in the cheap, mass produced, chicken
   used for animal food. The chicken is heat-treated before being used,
   but this does not remove all the tetracycline. This meant that a small
   amount of tetracycline was being added from the food to the larvae and
   repressing the [designed] lethal system."
   
   So in other words, there is every possibility for Oxitec's modified
   genes to persist in wild populations of Aedes aegypti mosquitos,
   especially in the environmental presence of tetracycline which is
   widely present in sewage, septic tanks, contaminated water sources and
   farm runoff.
   
  'Promiscuous' jumping genes
   
   On the face of it, there is no obvious way in which the spread of
   Oxitec's GM mosquitos into the wild could have anything to do with
   Brazil's wave of microcephaly. Is there?
   
   Actually, yes. The problem may arise from the use of the 'transposon'
   ('jumping' sequence of DNA used in the genetic engineering process to
   introduce the new genes into the target organism). There are several
   such DNA sequences in use, and one of the most popular is known as
   known as piggyBac.
   
   As a 2001 review article by Dr Mae Wan Ho shows, piggyBac is
   notoriously active, inserting itself into genes way beyond its intended
   target: "These 'promiscuous' transposons have found special favour with
   genetic engineers, whose goal is to create 'universal' systems for
   transferring genes into any and every species on earth. Almost none of
   the geneticists has considered the hazards involved ...
   
   "It would seem obvious that integrated transposon vectors may easily
   jump out again, to another site in the same genome, or to the genome of
   unrelated species. There are already signs of that in the transposon,
   piggyBac, used in the GM bollworms to be released by the USDA this
   summer.
   
   The piggyBac transposon was discovered in cell cultures of the moth
   Trichopulsia, the cabbage looper, where it caused high rates of
   mutations in the baculovirus infecting the cells by jumping into its
   genes ... This transposon was later found to be active in a wide range
   of species, including the fruitfly Drosophila, the mosquito
   transmitting yellow fever, Aedes aegypti, the medfly, Ceratitis
   capitata, and the original host, the cabbage looper.
   
   "The piggyBac vector gave high frequencies of transpositions, 37 times
   higher than mariner and nearly four times higher than Hirmar."
   
   In a later 2014 report Dr Mae Wan Ho returned to the theme with
   additional detail and fresh scientific evidence (please refer to her
   original article for references): "The piggyBac transposon was
   discovered in cell cultures of the moth Trichopulsia, the cabbage
   looper, where it caused high rates of mutations in the baculovirus
   infecting the cells by jumping into its genes ...
   
   "There is also evidence that the disabled piggyBac vector carrying the
   transgene, even when stripped down to the bare minimum of the border
   repeats, was nevertheless able to replicate and spread, because the
   transposase enzyme enabling the piggyBac inserts to move can be
   provided by transposons present in all genomes.
   
   "The main reason initially for using transposons as vectors in insect
   control was precisely because they can spread the transgenes rapidly by
   'non-Mendelian' means within a population, i.e., by replicating copies
   and jumping into genomes, thereby 'driving' the trait through the
   insect population. However, the scientists involved neglected the fact
   that the transposons could also jump into the genomes of the mammalian
   hosts including human beings ...
   
   "In spite of instability and resulting genotoxicity, the piggyBac
   transposon has been used extensively also in human gene therapy.
   Several human cell lines have been transformed, even primary human T
   cells using piggyBac. These findings leave us little doubt that the
   transposon-borne transgenes in the transgenic mosquito can transfer
   horizontally to human cells. The piggyBac transposon was found to
   induce genome wide insertion mutations disrupting many gene functions."
   
   Has the GM nightmare finally come true?
   
   So down to the key question: was the Oxitec's GM Aedes aegypti
   male-sterile mosquito released in Juazeiro engineered with the piggyBac
   transposon? Yes, it was. And that creates a highly significant
   possibility: that Oxitec's release of its GM mosquitos led directly to
   the development of Brazil's microcephaly epidemic through the following
   mechanism:
   
   1. Many of the millions of Oxitec GM mosquitos released in Juazeiro in
   2011/2012 survive, assisted, but not dependent on, the presence of
   tetracycline in the environment.
   
   2. These mosquitos interbreed with with the wild population and their
   novel genes become widespread.
   
   3. The promiscuous piggyBac transposon now present in the local Aedes
   aegypti population takes the opportunity to jump into the Zika virus,
   probably on numerous occasions.
   
   4. In the process certain mutated strains of Zika acquire a selective
   advantage, making them more virulent and giving them an enhanced
   ability to enter and disrupt human DNA.
   
   5. One way in which this manifests is by disrupting a key stage in the
   development of human embryos in the womb, causing microcephaly and the
   other reported deformations. Note that as Melo Oliveira et al warn,
   there are almost certainly other manifestations that have not yet been
   detected.
   
   6. It may be that the piggyBac transposon has itself entered the DNA of
   babies exposed in utero to the modified Zika virus. Indeed, this may
   form part of the mechanism by which embryonic development is disrupted.
   
   In the latter case, one implication is that the action of the gene
   could be blocked by giving pregnant women tetracycline in order to
   block its activity. The chances of success are probably low, but it has
   to be worth trying.
   
   No further releases of GM insects!
   
   While I am certainly not claiming that this is what actually took
   place, it is at least a credible hypothesis, and moreover a highly
   testable one. Nothing would be easier for genetic engineers than to
   test amniotic fluids, babies' blood, wild Aedes mosquitos and the Zika
   virus itself for the presence of the piggyBac transposon, using well
   established and highly sensitive PCR (polymerase chain reaction)
   techniques.
   
   [See Notes 1 & 2, below. Recent Zika genome snapshots examined as a
   result of this article are, in fact, free of the piggyBac transposon.]
   
   If this proves to be the case, those urging caution on the release of
   GMOs generally, and transgenic insects bearing promiscuous transposons
   in particular, will have been proved right on all counts.
   
   But most important, such experiments, and any deployment of similar GM
   insects, must be immediately halted until the possibilities outlined
   above can be safely ruled out. There are plans, for example, to release
   similarly modified Anopheles mosquitos as an anti-malarial measure.
   
   There are also calls for even more of the Oxitec Aedes aegypti
   mosquitos to be released in order to halt the transmission of the Zika
   virus. If that were to take place, it could give rise to numerous new
   mutations of the virus with the potential to cause even more damage to
   the human genome, that we can, at this stage, only guess at.
   
   
   Note 1: A reader of this article, David Murphy, reports on Facebook
   (see thread here) as follows:
   
   Zika, 4 strains, 2016 from the Center for Technological Innovation,
   Brazil
   
   http://www.ncbi.nlm.nih.gov/nuccore/KU365777.1
   http://www.ncbi.nlm.nih.gov/nuccore/KU365778.1
   http://www.ncbi.nlm.nih.gov/nuccore/KU365779.1
   http://www.ncbi.nlm.nih.gov/nuccore/KU365780.1
   
   The releases of GM mosquitos took place in 2011 and 2012. Fortunately
   people sequenced zika before that.
   
   Zika 01-AUG-2006
   
   http://www.ncbi.nlm.nih.gov/nuccore/GU937109.1
   id:AY632535.2
   
   So lets compare. This isn't anything amazing, the viruses are tiny,
   this is rare in biology but we can actually eyeball the data since you
   could fit a whole viral genome on a single A4 sheet of paper.
   
   View the alignment online:
   http://web.archive.org/web/20160204113740/http://www.ebi.ac.uk/Tools/ser
   vices/web/toolresult.ebi?jobId=mview-I20160203-123326-0036-25505577-pg
   
   http://toolkit.tuebingen.mpg.de/alnviz/results/8144137
   
   If you take a peek at the last 2 links you can see that while they're
   not identical the differences are almost all small changes with no big
   new chunks of code added.
   
   From a quick scan through eyeballing it, the only chunk of new bases
   was a 15 base sequence that doesn't show up in any piggyBac.
   
   Zika is small, only 10000 bases long and it's hard to hide anything big
   in it.
   
   piggyBac is not tiny, (
   http://www.ncbi.nlm.nih.gov/nuccore/?term=piggybac ), you wouldn't have
   to do any amazing analysis to see that it's not been added in there.
   Zika virus strain BeH818995 polyprotein gene, complete cds - Nucleotide
   - NCBI National Center for Biotechnology Information, U.S. National
   Library of Medicine 8600 Rockville Pike, Bethesda MD, 20894
   USANCBI.NLM.NIH.GOV
   
   Note 2: I'm grateful to David Murphy for carrying out this work, and to
   James Babcock for drawing it to my attention. It appears that the
   hypothesis set out above is probably incorrect, and this must be a
   matter of considerable relief to all concerned. However it remains my
   opinion that considerable caution should be exercised with releases of
   GE insects containing 'promiscuous' DNA sequences such as piggyBac.
   
   The Zika virus, as a pure RNA virus, is resistant to the uptake of DNA
   of any kind (more on this in Note 3), and being very small, any such
   uptake would be rapidly detectable. However there are many other
   viruses, bacteria, disease vectors, etc, for which this remains a
   possiblity.
   
   Another check that should also be made is to test for the presence of
   piggyBac in wild Aedes mosquitos around the release sites to see if, in
   fact, these 'programmed to die out' sequences are indeed as evanescent
   as claimed.
   
   Note 3: I have received this comment by Dr Michael Antoniou, respected
   researcher in this field, originally posted on a GM news list, and
   reproduce it here in full.
   
   "I urge great caution in viewing and using the message of this article
   in the Ecologist as it contains a number of technical errors with what
   it says especially about the piggyBac transposon system used to
   generate the GM mosquitos.
   
   "Native transposons by their very nature do move around the genome of
   the host into which they have inserted and do so by the action of an
   enzyme called a 'transposase' for which they carry the gene.
   
   "However, when adapted for use as a gene transfer vehicle ('vector') as
   was used to generate the GM mosquitos they have been stripped of their
   own genes including the one encoding the transposase, which as I
   mentioned is responsible for the insertion and mobility of the DNA
   transposon element. Thus following insertion of the GM transposon
   vector into the target cell genome by the transient provision (over a
   small time scale) of the transposase via a separate gene construct, the
   inserted GM transposon has no mechanism for subsequent mobilisation
   from its initial site of genome integration. Also, please note that
   transposases are specific for a given transposon. I worked with a
   transposon vector called Sleeping Beauty; the Sleeping Beauty
   transposase can only interact and move around its cognate transposon
   and not that of another type such as piggyBack, which has its own
   specific transposase.
   
   "Furthermore, the suggestion that the transposon vector inserted into
   the GM mosquitos can be mobilised and insert itself into the Zika virus
   genome that may be carried by these GM mosquitos is even more
   farfetched. The Zika virus genome is made of RNA and resides/replicates
   after infection completely in the part of the cell known as the
   cytoplasm, which surrounds the cell nucleus, which is where the cell
   DNA with its inserted transposon are located. Not only are the Zika
   virus RNA in the cell cytoplasm and transposon DNA in the cell nucleus
   separated spatially and thus incapable of physically interacting but
   the piggyBack transposase enzyme even if somehow present is totally
   incapable of inserted mobilised transposon DNA into the Zika virus RNA
   genome.
   
   "Overall, I believe the link between the release the GM mosquitos and
   increased incidence of microcephaly is at best highly tenuous. I draw
   your attention to what some other individuals have highlighted as a far
   more likely cause of the increase in microcephaly; that is, escalation
   and spread in the use of toxic larvicides used to combat mosquito
   reproduction."
   
   Dr Mae Wan Ho responds:
   
   "Michael Antoniou claimed and argued with me for a long time that it
   was impossible for the CaMV 35S promoter to move into genomes. This has
   been proven to happen.
   
   "I think the whole issue of horizontal gene transfer, not just of
   piggyBac, but the other bits of the construct cannot be ignored.
   
   "Also, interaction between construct and virus could simply be
   mutagenic, as you suggested originally. And of course, there is now a
   suggestion that the 'killing gene product' from the transgenic mosquito
   may have been transferred into pregnant women, thereby causing
   microcephaly.
   
   "If the female mosquito can transfer protein and viruses, why not
   nucleic acids? Both RNA (transcripts) and DNA can undergo horizontal
   gene transfer and recombination, and are hence also mutagenic."
   
   I also add a highly relevant comment received in an earlier email from
   Dr Mae Wan Ho which addresses the same points as those raised by Dr
   Antoniou, though in another context:
   
   "The point in the follow-up email is the most serious objection.
   piggbac is a DNA transposon that has no RNA intermediate, and zika
   virus is a flavivirus that has no DNA intermediate, therefore on the
   face of it, recombination between them is impossible.
   
   "However, this has recently been proven wrong. See Stedman KM. Deep
   Recombination: RNA and ssDNA Virus Genes in DNA Virus and Host Genomes.
   Annual Review of Virology Vol. 2: 203-217 (Volume publication date
   November 2015).
   
   "It states: 'genetic exchange across viral kingdoms, for instance
   between nonretroviral RNA viruses or ssDNA viruses and host genomes or
   between RNA and DNA viruses, was previously thought to be practically
   nonexistent. However, there is now growing evidence for both RNA and
   ssDNA viruses recombining with host dsDNA genomes and, more
   surprisingly, RNA virus genes recombining with ssDNA virus genomes.
   Mechanisms are still unclear, but this deep recombination greatly
   expands the breadth of virus evolution and confounds virus taxonomy.'
   
   "The contention that disabled piggyBac cannot transpose is known to be
   false from studies cited in articles submitted by Cummins & Ho to the
   USDA in 2001, see here, for example:
   http://www.i-sis.org.uk/terminsects-pr.php. That is because
   transposases are abundant in genomes.
   
   "A more recent article confirming this is Aziz RK, Breitbart M and
   Edwards RA. Transposases are the most abundant, most ubiquitous genes
   in nature. Nucleic Acid Res 2010,
   http://nar.oxfordjournals.org/content/early/2010/03/09/nar.gkq140.full "
   
   My conclusion: there are obstructions to the onward transfer of genetic
   material from the transposon into the Zika virus, as suggested in my
   article. But it would be wrong to declare it impossible, as a number of
   critics have done in firm and absolute terms. These are obstructions,
   not hard barriers, and similar obstructions are proven to have been
   breached. It appears (from examination of the Zika genome) not to have
   taken place in the manner proposed on this occasion, however there is
   no guarantee that something similar may not happen in the future.
   
   Dr Mae Wan Ho also refers to two additional possibilities as deserving
   of consideration, first, that "interaction between construct and virus
   could simply be mutagenic", and second, "that the 'killing gene
   product' from the transgenic mosquito may have been transferred into
   pregnant women, thereby causing microcephaly".
   
   There remains every reason to take a highly precautionary approach to
   the release of genetically modified organisms and especially those that
   contain promiscuous transposons whose DNA may, as in the case of
   mosquitos, enter into people with potentially dangerous impacts.
   
   Oliver Tickell edits The Ecologist."

[rmstock]

Deep Pockets Recombination

01-20FEB2007-Genetic-Mosquito-Control-BMC-Biology-20MAR2007.pdf
01a-09JUN2010-Aedes-AEgypti-Strains-History-J.Med.Entomol.Aug27.2010.pdf
02-14MAR2008-Antibiotic-Resistance-Genes-J.Environ.Qual.May-June2009.pdf
03-21DEC2009-Transposases-Nucleic-Acids-Research-Mar9.2010.pdf             
04-04FEB2009-OX513A-MosquitoDocOriginal.pdf                               
05-06AUG2010-OX513A-announcement.pdf                                       
06-11AUG2010-OX513A-factsheet.pdf                                         
07-03SEP2010-OX513A-Submission-Application-for-Approval.pdf               
08-04MAR2013-Evolution-of-Zika-Virus-PLOS.Neglec.Trop.Dis-Jan9.2014.pdf   
09-09MAY2014-Mosquito-Control-in-Brazil-PLOS.Neglec.Trop.Dis-Jul2.2015.pdf
10-17DEC2015-Zika-Virus-Microcephaly-Ultrasound.Obstet.Gynecol.2016.pdf

[rmstock]

So what is the difference between a Yellow fever virus and the Zika virus ?
Not much, the two could be brothers in disease :

Yellow fever virus (YFV)
Virus classification
Group:    Group IV ((+)ssRNA)
Order:    Unassigned
Family:    Flaviviridae
Genus:    Flavivirus
Species:    Yellow fever virus

dengue virus (DENV)
Virus classification
Group:    Group IV ((+)ssRNA)
Order:    Unassigned
Family:    Flaviviridae
Genus:    Flavivirus
Species:    Dengue virus

Zika virus (ZIKV)
Virus classification
Group:    Group IV ((+)ssRNA)
Family:    Flaviviridae
Genus:    Flavivirus
Species:    Zika virus

According the Institut Pasteur de Dakar, Dakar, Senegal and Biomedical Sciences Institute,
University of Sao Paulo, Sao Paulo, Brazil :
08-04MAR2013-Evolution-of-Zika-Virus-PLOS.Neglec.Trop.Dis-Jan9.2014.pdf


  "[ ... ]
   Introduction
      Zika virus (ZIKV) is a mosquito-borne flavivirus, a member of
   the Spondweni serocomplex, whose natural transmission cycle
   involves mainly vectors from the Aedes genus (A. furcifer, A. taylori, A.
   luteocephalus and A. africanus) and monkeys [1], while humans are
   occasional hosts. Clinical pictures range from asymptomatic cases
   to an influenza-like syndrome associated to fever, headache,
   malaise and cutaneous rash [2,3]. Likewise, direct contact is also
   considered a potential route of transmission among humans,
   probably during sexual intercourse [4]. The first isolation of ZIKV
   was in 1947 from the blood of a sentinel Rhesus monkey No. 766,
   stationed in the Zika forest, near the Lake Victoria in Uganda, and
   in 1948 ZIKV was also isolated in the same forest from a pool of A.
   africanus mosquitoes [5]. Thereafter, serological and entomological
   data indicated ZIKV infections in the African continent in Nigeria
   in 1971 and 1975 [6], Sierra Leone in 1972 [7], Gabon in 1975
   [8], Uganda in 1969 and 1970 [9], Central African Republic in
   1979 [10], Senegal from 1988 to 1991 [11] and Coˆ te d'Ivoire in
   1999 [12]. Recently, ZIKV was detected in Senegal in 2011 and
   2012 (unpublished data). In addition, ZIKV infections in Asia
   were reported in Pakistan [13], Malaysia [14], Indonesia in 1977
   and 1978 [15], Micronesia in 2007 [16,17] and Cambodia in 2010
   [18]. Although ZIKV was repeatedly isolated, only 14 human
   cases were reported before April 2007, when a Zika fever (ZF)
   epidemic occurred in Yap island in Micronesia, where 49
   confirmed cases and 73% of the residents older than 3 years
   provided serologic evidence for recent ZIKV infection [16]. This
   outbreak showcased the potential of ZF as an emerging disease,
   which could be misdiagnosed as dengue fever, as happened during
   the beginning of the Micronesian outbreak [16,17].
      The ZIKV genome consists of a single-stranded positive sense
   RNA molecule with 10794 kb of length with 2 flanking noncoding
   regions (59 and 39 NCR) and a single long open reading
   frame encoding a polyprotein: 59-C-prM-E-NS1-NS2A-NS2BNS3-
   NS4A-NS4B-NS5-39, that is cleaved into capsid (C), precursor
   of membrane (prM), envelope (E) and seven non-structural
   proteins (NS) [19,20].

   1. Hayes EB (2009) Zika virus outside Africa.
      Emerg Infect Dis 15: 1347–1350.  doi:10.3201/eid1509.090442.
   2. Simpson DI (1964) Zika virus infection in man.
      Trans R Soc Trop Med Hyg 58: 335–338.
   3. Bearcroft WG (1956) Zika virus infection experimentally induced in
      a human volunteer. Trans R Soc Trop Med Hyg 50: 442–448.
   4. Foy BD, Kobylinski KC, Chilson Foy JL, Blitvich BJ, Travassos da Rosa A,
      et al. (2011) Probable non-vector-borne transmission of Zika virus,
      Colorado, USA. Emerg Infect Dis 17: 880–882. doi:10.3201/eid1705.101939.
   5. Dick GWA, Kitchen SF, Haddow AJ (1952) Zika virus. I. Isolations and
      serological specificity. Trans R Soc Trop Med Hyg 46: 509–520.
   6. Fagbami AH (1979) Zika virus infections in Nigeria: virological and
      seroepidemiological investigations in Oyo State. J Hyg (Lond) 83: 213–219.
   7. Robin Y, Mouchet J (1978) Serological and entomological study on yellow
      fever in Sierra Leone. Bull Soc Pathol Exot Filiales 68: 249–258.
   8. Jan C, Languillat G, Renaudet J, Robin Y (1978) A serological survey of
      arboviruses in Gabon. Bull Soc Pathol Exot Filiales 71: 140–146.
   9. McCrae AW, Kirya BG (1982) Yellow fever and Zika virus epizootics and
      enzootics in Uganda. Trans R Soc Trop Med Hyg 76: 552–562.
   10. Saluzzo JF, Gonzalez JP, Herve´ JP, Georges AJ (1981) Serological survey
       for the prevalence of certain arboviruses in the human population of the
       south-east area of Central African Republic. Bull Soc Pathol Exot
       Filiales 74: 490–499.
   11. Monlun E, Zeller H, Le Guenno B, Traore´-Lamizana M, Hervy JP,et al.(1993)
       Surveillance of the circulation of arbovirus of medical interest in the
       region of eastern Senegal. Bull Soc Pathol Exot 86: 21–28.
   12. Akoua-Koffi C, Diarrassouba S, Be´nie´ VB, Ngbichi JM, Bozoua T,
       et al. (2001) Investigation surrounding a fatal case of yellow fever
       in Coˆte d'Ivoire in 1999.  Bull Soc Pathol Exot 94: 227–230.
   13. Darwish MA, Hoogstraal H, Roberts TJ, Ahmed IP, Omar F (1983) A
       seroepidemiological survey for certain arboviruses (Togaviridae) in
       Pakistan. Trans R Soc Trop Med Hyg 77: 442–445.
   14. Marchette NJ, Garcia R, Rudnick A (1969) Isolation of Zika virus from
       Aedes aegypti mosquitoes in Malaysia. Am J Trop Med Hyg 18: 411–415.
   15. Olson JG, Ksiazek TG, Suhandiman, Triwibowo (1981) Zika virus, a
       cause of fever in Central Java, Indonesia.
       Trans R Soc Trop Med Hyg 75: 389–393.
   16. Duffy MR, Chen T-H, Hancock WT, Powers AM, Kool JL, et al. (2009)
       Zika virus outbreak on Yap Island, Federated States of Micronesia.
       N Engl J Med 360: 2536–2543. doi:10.1056/NEJMoa0805715.
   17. Lanciotti RS, Kosoy OL, Laven JJ, Velez JO, Lambert AJ, et al. (2008)
       Genetic and serologic properties of Zika virus associated with an
       epidemic, Yap State, Micronesia, 2007. Emerg Infect Dis 14: 1232–1239.
   18. Heang V, Yasuda CY, Sovann L, Haddow AD, Travassos da Rosa AP, et al.
       (2012) Zika virus infection, cambodia, 2010.
       Emerg Infect Dis 18: 349–351. doi:10.3201/eid1802.111224.
   19. Chambers TJ, Hahn CS, Galler R, Rice CM (1990) Flavivirus genome
       organization, expression, and replication.
       Annu Rev Microbiol 44: 649–688. doi:10.1146/annurev.mi.44.100190.003245.
   20. Kuno G, Chang G-JJ (2007) Full-length sequencing and genomic
       characterization of Bagaza, Kedougou, and Zika viruses.
       Arch Virol 152: 687–696.  doi:10.1007/s00705-006-0903-z.
   [ ... ]"

According the  Oxitech OX513A Mosquito manufacturing team :
01-20FEB2007-Genetic-Mosquito-Control-BMC-Biology-20MAR2007.pdf :
  "[ ... ]
   Results: We investigated by mathematical modeling the effect of
   manipulating the stage of development at which death occurs (lethal
   phase) in an SIT program against a density-dependence-limited insect
   population. We found late-acting lethality to be considerably more
   effective than early acting lethality. No such strains of a vector
   insect have been described, so as a proof-of-principle we constructed a
   strain of the principal vector of the dengue and yellow fever viruses,
   Aedes ( Stegomyia) aegypti, with the necessary properties of dominant,
   repressible, highly penetrant, late-acting lethality.
   [ ... ]
   Mosquito transformation and rearing
   Aedes aegypti of the Rockefeller strain (obtained from Roger Wood,
   University of Manchester), were reared in an insectary maintained at
   28°C and 75–80% relative humidity with 12-hour light/dark cycle.
   Mosquitoes were transformed by standard micro-injection methods [44],
   using a vector plasmid (e.g. pLA513) concentration of 500 ng/l
   coinjected with a 400 ng/l concentration of piggy-Bac 'helper plasmid'
   phsp-pBac [45] as the source of piggy-Bac transposase.
   
   [44] Jasinskiene N, Coates C, Benedict M, Cornel A, Rafferty C,
     James A, Collins F: Stable transformation of the yellow fever mosquito,
      Aedes aegypti, with the Hermes element from the housefly.
      Proc Natl Acad Sci USA 1998, 95(7): 3743-3747.
   [45] Handler AM, McCombs SD, Fraser MJ, Saul SH: The lepidopteran
      transposon vector, piggyBac, mediates germ-line transformation in the
      Mediterranean fruit fly. Proc Natl Acad Sci USA 1998, 95(13): 7520-7525.
   [ ... ]"

While Zika or Yellow fever virus from the Rockefeller strain are considered relatively
harmless, as they have been around since the 1930s 1940s, the piggy-Bac transposase
variant used to control Mosquito populations has relatively new and yet not fully
known side effects ...