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Now tracking the new emerging South Africa Omicron Variant

Genetics & Microcephaly

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    Posted: February 11 2016 at 9:01am
Brazil's mysteroius microcephaly disaster.

Zika appears to be linked to a rise in microcephaly wherever it appears be it French Polynesia or Brazil, exactly how this occurs is still a mystery, the prevalent theory for the moment is OAS or Original Antigenic Sin (as discussed below).

Background to the French Polynesia Outbreak
Since the beginning of this epidemic, and as up to 8,200 cases of ZIKA infection have already been reported of a 268,000 total population, the incidence of GBS has been multiplied by 20 in French Polynesia (data not shown), raising the assumption of a potential implication of ZIKA.

Pacific Island of Yap Zika Outbreak (2007)
Zika was identified as having acquired a glycoprotein very similar to the Dengue virus so similar in fact the Zika can show a false positive for Dengue infection during testing, It is also the reason why Zika finds it easier to infect humans.

Since these islands were seeing a concurrent Dengue outbreak there was speculation that co-infection by Dengue and Zika  - or sequential arboviral immune stimulation - might predispose one to more severe illness.  Adding some credence to this notion, with dengue, it is usually a person's second infection that causes severe illness, while the first infection is usually mild.

The prevailing theory is that the host’s immune system - which already has neutralizing antibodies to the first DENV infection - mistakenly identifies the second DENV infection as being the same strain. Rather than creating new neutralizing antibodies to fight the infection, it deploys its existing cross reactive, but non-neutralizing (read: ineffective) antibodies to the field of battle.

Sometimes called OAS or Original Antigenic Sin, this is the immunological equivalent of taking a knife to a gun fight.

This could a plausible reason why Zika is able to breach the immune system to invade the Central Nervous System (CNS) and testes triggering cases of microcephaly, It would also seem reasonable that pregnant females would be predominantly hit the hardest as pregnancy is immune-depressive by natural design to avoid fetal rejection.

In Brazil the Microcephaly Mystery Deepens

Here we have the introduction of Oxitec GM Mosquito's that appears to be directly linked to a explosion of microcephaly cases and attention is drawn to an interesting aspect of the matter of correlation between the incidence of Zika and the area of release of genetically modified Aedes aegypti mosquitos engineered for male insterility.

More recently their are new concerns that Mosquito Insecticide may be also be a contributing factor to Microcephaly cases, I refer you to Medclinician's thread on this new development >> http://www.avianflutalk.com/insecticide-suspected-cause-of-microcephaly_topic35391.html


More background on Oxitec GM Mosquitos project in Brazil

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.

I wrote about the Oxitec Mosquito & Tetracycline problem in the thread THE BIOWARS for those unfarmilar with the topic >> http://www.avianflutalk.com/the-biowars_topic35201.html

Also see http://theantimedia.org/zika-outbreak-epicenter-in-same-area-where-gm-mosquitoes-were-released-in-2015/

Genetics of Microcephaly

Aurthor Dr MaeWan Ho (a scientist involved in the early negotiations on the Catagena Protocol on Biosafety, as well as a member of their roster of experts.)

The '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.

piggyBac is notoriously active, inserting itself into genes way beyond its intended target: "These 'promiscuous' transposons have found special favour with genetic engineers

"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."

More on Genetics & Microcephaly at jacksdads thread http://www.avianflutalk.com/zika-epicenter-connected-to-gm-mosquitoes_topic35252_page2.html which includes a basic breakdown of the very lengthy scientific findings of Dr MaeWan Ho,  however links to her full scientific findings are included for the more adventurous.

DISCLAIMER
I would like to emphasis that while it has been demonstrated that Horizontal Gene Transfer (HGT) can and does take place it has not been demonstrated the (HGT) occurs between Oxitecs GM Mosquito's and Humans only that it is a technical possibility at this stage of the investigation.

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First documented case of mother-to-fetus Zika transmission, moving one step closer to pinpointing the link between serious birth defects and the virus sweeping across the Americas.

The study published in the New England Journal of Medicine by scientists from the University of Ljubljana http://www.nejm.org/doi/pdf/10.1056/NEJMoa1600651

An autopsy performed after the surgery showed that the fetus had no other anomalies, while the detailed medical background of the woman revealed no sign of genetic disorders.

The study explicitly indicates the connection between the virus and abnormalities found in newborns.



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Genetics of Microcephaly
Microcephaly can be complex with many with different sources, types and causes, furthermore some forms of microcephaly are caused by a change in someone’s DNA I am going to look at SLC25A19 gene as a possible candidate for the cause of ZIKA related microcephaly.

Previous autopsy
An autopsy revealed that particles of the Zika virus and a significant amount of viral genomic RNA were present in the brain, but not other organs.

“The findings of this case report do not provide absolute proof that Zika virus causes microcephaly,” Eric J. Rubin, associate editor of the New England Journal of Medicine said, but added that it “makes the link stronger.”


Mutations in the SLC25A19 gene cause lethal microcephaly.

The SLC25A19 gene provides instructions for producing a protein that is a member of the solute carrier (SLC) family of proteins. Proteins in the SLC family transport various compounds across the membranes surrounding the cell and its component parts. The protein produced from the SLC25A19 gene transports a molecule called thiamine pyrophosphate into the mitochondria, the energy-producing centers of cells. Thiamine pyrophosphate is involved in the functioning of a group of mitochondrial enzymes called the alpha-ketoglutarate dehydrogenase complex. This complex acts on a compound called alpha-ketoglutaric acid as part of an important series of reactions known as the citric acid cycle or Krebs cycle. The transport of thiamine pyrophosphate into the mitochondria is believed to be important in brain development.

The SLC25A19 gene is located at Cytogenetic Location: 17q25.3
Molecular Location on chromosome 17: base pairs 75,272,980 to 75,289,957
(Homo sapiens Annotation Release 107, GRCh38.p2)


The protein produced from the SLC25A19 gene, transports a molecule called thiamine pyrophosphate into the mitochondria, the energy-producing centers of cells. This compound is involved in the activity of a group of mitochondrial enzymes called the dehydrogenase complexes, one of which is the alpha-ketoglutarate dehydrogenase complex. The transport of thiamine pyrophosphate into the mitochondria is believed to be important in brain development.

All known individuals with this lethal microcephaly have a mutation in which the protein building block (amino acid) alanine is substituted for the amino acid glycine at position 177 of the SLC25A19 protein, written as Gly177Ala or G177A. Researchers believe that this mutation interferes with the transport of thiamine pyrophosphate into the mitochondria and the activity of the alpha-ketoglutarate dehydrogenase complex, resulting in the abnormal brain development and alpha-ketoglutaric aciduria seen in lethal microcephaly.

In addition to brain and skull abnormalities, babies with this type of microcephaly have elevated levels of the biochemical alpha-ketoglutarate in their urine, a finding that is directly related to this microcephaly but still not clearly understood. Scientists also are investigating the mystery of why the children's other organs, such as the heart and liver, seemingly are not affected, even though they rely on energy production from mitochondria at a metabolic rate similar to the brain during development.

This type of microcephaly is inherited in an autosomal recessive pattern, which means that it is necessary for a baby to inherit two copies of the mutated gene to have the disorder. In affected families, each parent contributes one changed copy of the gene to the child who has the disorder. The parents are called microcephaly carriers because they have one normal copy of the gene and one changed copy of the gene, but do not show symptoms of the disorder. When both parents are carriers of the changed gene, each of their children has a 25 percent chance of having the disorder, a 50 percent chance of being a carrier of the disorder (like their parents) and a 25 percent chance of neither being a carrier nor having the disorder. These risks are the same for each pregnancy.

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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 12 2016 at 6:39am
That is terrifying, Guest!  

Taratogenesis is bad enough, genetic change is so much worse.  That was not what I wanted to hear.  

Additionally, recessive genetic changes, though apparently less terrible first time round, are fantastically difficult to weed out.  That just goes one step further to concealing the nasties.  This rollercoaster is not just bumpy - it is a very long ride.

This is a VERY big threat our species is facing.  Short of genetically engineering ourselves, I can see no end to it.
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Detection of Zika Virus in Semen UPDATE !!!


In 2014, a 68-year-old man had onset of fever, marked lethargy, and an erythematous rash 1 week after returning from the Cook Islands. Serum samples taken 3 days into the febrile illness tested negative for dengue and chikungunya viruses by real-time reverse transcription PCR (rRT-PCR). Test results for dengue virus IgM and chikungunya virus IgM also were negative; a test result for dengue virus IgG was indeterminate.

Convalescent-phase serum, urine, and semen samples were requested; only semen was positive for ZIKV by rRT-PCR, , at 27 and 62 days after onset of febrile illness.

Although we did not culture infectious virus from semen, our data may indicate prolonged presence of virus in semen, which in turn could indicate a prolonged potential for sexual transmission of this flavivirus.

http://wwwnc.cdc.gov/eid/article/22/5/16-0107_article

Centre of Disease Creation (CDC)Wink

As I stated many times in the past,

Similarities between Ebola and Zika are striking

The similarities between Ebola and Zika are striking, Ebola essentially sets up the immune system to self destruct it's called a cytokine storm, the reason for the explosive bleed out in ebola victims is that blood vessels are particularity susceptible to the antigen antibody complex.

With the Zika virus it breaches the immune system in a similar fashion to Ebola then hides in the CNS and testes as does ebola,  when the immune system eventually produces antibodies they attack the CNS and testes but the CNS and Testes are privileged areas that the immune system is not supposed to attack by default.

Two reasons why Zika does not appear as deadly as EBOLA,

1) The antibody antigen complex is not attacking the endothelium.

2) the CNS and Testes are Immuno depressive by natural design.

Zika does not appear to posses the contagiousness of ebola as it's not got ebolas main glycoprotein spike but the mere fact that Zika has been identified as a bioweapon I would treat the Zika virus as a BIO-HAZARD same as Ebola, 3ft-6ft aerosol infectivity as per close contact would be a sensible precaution until we learn more)

How long does Zika remain in the seminal fluid of it's male victims, I would guess 9 months as per Ebola.

Females previously infected with the Zika Virus
NEED URGENT GENETIC PROFILING to determine if they are genetically predisposed to having future children with
Microcephaly as this is also linked to genetic markers.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote CRS, DrPH Quote  Post ReplyReply Direct Link To This Post Posted: February 12 2016 at 1:08pm
Thanks, Guest, this is good information! 

I should point out that, as a professional epidemiologist, we need to really dig into this and determine if Zika causes microcephaly vs. is simply associated with the condition. 

This article suggests association, not causation:


Large numbers of babies with borderline normal head sizes were born in Brazil as far back as 2012, two years before the Zika virus is thought to have entered the country, say researchers searching for answers to urgent questions.

Pediatric cardiologist Dr. Sandra Mattos had been collecting data on 100,000 newborns in the Brazilian state of Paraiba as part of her work studying and treating congenital heart disease.

The microcephaly fears linked to the Zika virus drove her team to check back into hospital records for head circumferences of more than 1,600 babies born in the state in the last four years.

"We were very, very surprised," Mattos said. Babies with mild microcephaly were present in the population dating back to at least 2012.

Having a head slightly smaller than the limit doesn't mean there's neurological disease. "Borderline cases seem to be present all along," she said.

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The Rise of Mild Microcepaly in Brazil 2012.

Oxitec's GM Aedes aegypti male-sterile mosquito released in Juazeiro was engineered with the piggyBac transposon which is "Genetically Promiscuous"

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.[1]

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.

The problem with the use of the 'transposon' ('jumping' sequence of DNA used in the genetic engineering process to introduce the new genes into the target organism), and there are several such DNA sequences in use, one of the most popular is known as piggyBac which is notoriously active, inserting itself into genes way beyond its intended target .

The facts as I currently understand them,

It has been demonstrated that Horizontal Gene Transfer (HGT) can and does take place, it has not been demonstrated the (HGT) occurs between Oxitecs GM Mosquito's and Humans only that it is a technical possibility not fully appreciated by the Brazilian risk assessment team for the Oxitec GM Mosquito project .

Starting from 19th of May 2011 the Introduction of Oxitec GM Mosquito's appears to coincide with the 2012 appearance of a large number of apparently mild cases of Microcepaly and attention is drawn to an interesting aspect of the matter of correlation between the recent incidence of Zika and the previous Oxitec release site.

I suspect that the mild cases of Microcephaly from 2012 could well be related to HGT from the Mosquito to humans currently their is no evidence, we need a urgent investigation to estabilish if there is a possibility for Oxitec's modified genes persist in wild populations of Aedes aegypti mosquitoes especially in the presence of enviromental tetracyclines.

The genetic material inserted into the Aedes aegypti mosquitos using the piggyBac transposon could be detected via PCR Techniques.


[1] http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0003864  

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Zika Virus Associated with Microcephaly
Jernej Mlakar, M.D., Misa Korva, Ph.D., Nataša Tul, M.D., Ph.D.,
Mara Popović, M.D., Ph.D., Mateja Poljšak‑Prijatelj, Ph.D., Jerica Mraz, M.Sc.,
Marko Kolenc, M.Sc., Katarina Resman Rus, M.Sc., Tina Vesnaver Vipotnik, M.D.,
Vesna Fabjan Vodušek, M.D., Alenka Vizjak, Ph.D., Jože Pižem, M.D., Ph.D.,
Miroslav Petrovec, M.D., Ph.D., and Tatjana Avšič Županc, Ph.D.


Summary

A widespread epidemic of Zika virus (ZIKV) infection was reported in 2015 in
South and Central America and the Caribbean. A major concern associated with
this infection is the apparent increased incidence of microcephaly in fetuses born
to mothers infected with ZIKV. In this report, we describe the case of an expectant
mother who had a febrile illness with rash at the end of the first trimester of
pregnancy while she was living in Brazil. Ultrasonography performed at 29 weeks
of gestation revealed microcephaly with calcifications in the fetal brain and placenta.
After the mother requested termination of the pregnancy, a fetal autopsy
was performed. Micrencephaly (an abnormally small brain) was observed, with
almost complete agyria, hydrocephalus, and multifocal dystrophic calcifications in
the cortex and subcortical white matter, with associated cortical displacement and
mild focal inflammation. ZIKV was found in the fetal brain tissue on reversetranscriptase–
polymerase-chain-reaction (RT-PCR) assay, with consistent findings
on electron microscopy. The complete genome of ZIKV was recovered from the
fetal brain.




Download full report here
http://www.nejm.org/doi/pdf/10.1056/NEJMoa1600651
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 13 2016 at 2:45pm
Thank you, Guest!  I do love proper peer reviewed scientific journals and that one you just posted is a cracker!

This confirms what I suspected:  page 5 notes normal karyotyping of the damaged fetus and pages 6 and 7 note the teratogenic affects of zika as being consistent with Zika's cousins the other flaviviurses.

To say this is a relief is something of an understatement.  Thank God (who apparently does listen to our prayers) this is a taratogenic not a genetic effect.  Whereas, this does not mean that Zika cannot harm our societies by interfering with our breeding, it does suggest that the alteration to fetuses is for one generation only and those microcephalics who do manage to breed will not necessarily pass the damage on.

The analysis of the genome of the Zika virus present contained a whole new set of worries:  the apparent suitability of neural tissue to the growth of Zika and the only partial answers regarding its route to present-day Brazil.  But I am just happy that it turns out to be teratogenic after all.  PHEW!
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Zika Virus Associated with Microcephaly
Jernej Mlakar, M.D., Misa Korva, Ph.D., Nataša Tul, M.D., Ph.D., Mara Popović, M.D., Ph.D., Mateja Poljšak-Prijatelj, Ph.D., Jerica Mraz, M.Sc., Marko Kolenc, M.Sc., Katarina Resman Rus, M.Sc., Tina Vesnaver Vipotnik, M.D., Vesna Fabjan Vodušek, M.D., Alenka Vizjak, Ph.D., Jože Pižem, M.D., Ph.D., Miroslav Petrovec, M.D., Ph.D., and Tatjana Avšič Županc, Ph.D.

Download Report excluding Supplementary Appendix
http://www.nejm.org/doi/pdf/10.1056/NEJMoa1600651


Detailed description of molecular methods is provided in the Supplementary Appendix

Download Supplementary Appendix
http://www.nejm.org/doi/suppl/10.1056/NEJMoa1600651/suppl_file/nejmoa1600651_appendix.pdf



Zika Virus and Microcephaly
Eric J. Rubin, M.D., Ph.D., Michael F. Greene, M.D., and Lindsey R. Baden, M.D.

Download full report here
http://www.nejm.org/doi/pdf/10.1056/NEJMe1601862
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 14 2016 at 3:53am
Thanks again.  'Got the full data now.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Guests Quote  Post ReplyReply Direct Link To This Post Posted: March 04 2016 at 4:57pm
Recently Brazilian researches infected Culex Mosquitoes in the lab but powers at be stopped the publication.

Now we have new reports of the Zika Virus Experimentally Introduced Into Culex Mosquitoes, Ebola too is very good at crossing the species barrier expect more species to become competent Zika vectors.


02/03/2016 17h36 - Updated 03/02/2016 17h36  Fiocruz research shows virus zika in salivary gland stilt


Still can not confirm that the common mosquito transmits the disease. The end result of the research will be known within eight months.

The ease of spread of zika virus in Culex mosquitoes infected in the laboratory was confirmed on Wednesday (2) by the researcher Constance Ayres, of vector design of the Oswaldo Cruz Foundation institution ( Fiocruz ) in Pernambuco . "This means that, in the laboratory, the virus managed to escape some barriers in the mosquito and reached the salivary gland," the researcher explained. The Culex is the common mosquito, popularly known as muriçoca or stilt.

During the second day of the workshop A, B, C, D, E Zika virus, held in Recife , the biologist presented the preliminary results of research showing the spread of the virus to the mosquito 's salivary gland, where happen to transmission disease to humans. After performing three infections in 200 Culex mosquitoes (the first two in December last year and the third in February), research shows the vector competence of mosquito in the laboratory.

The survey results are still partial, it is still not possible to say whether the mosquito is capable of transmitting the virus to zika people. "To complete this, lack identify in the field the species of mosquito infected with the virus zika," says the biologist.


Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth


Highlights

    •Zika virus (ZIKV) infects human embryonic cortical neural progenitor cells (hNPCs)
    •ZIKV-infected hNPCs produce infectious ZIKV particles
    •ZIKV infection leads to increased cell death of hNPCs
    •ZIKV infection dysregulates cell cycle and transcription in hNPCs


Summary

The suspected link between infection by Zika virus (ZIKV), a re-emerging flavivirus, and microcephaly is an urgent global health concern. The direct target cells of ZIKV in the developing human fetus are not clear. Here we show that a strain of the ZIKV, MR766, serially passaged in monkey and mosquito cells efficiently infects human neural progenitor cells (hNPCs) derived from induced pluripotent stem cells. Infected hNPCs further release infectious ZIKV particles. Importantly, ZIKV infection increases cell death and dysregulates cell-cycle progression, resulting in attenuated hNPC growth. Global gene expression analysis of infected hNPCs reveals transcriptional dysregulation, notably of cell-cycle-related pathways. Our results identify hNPCs as a direct ZIKV target. In addition, we establish a tractable experimental model system to investigate the impact and mechanism of ZIKV on human brain development and provide a platform to screen therapeutic compounds.

Received: February 24, 2016; Received in revised form: February 28, 2016; Accepted: February 29, 2016; Published: March 4, 2016
© 2016 Elsevier Inc. Published by Elsevier Inc. All rights reserved.

http://www.cell.com/cell-stem-cell/abstract/S1934-5909%2816%2900106-5

Download Report Here
http://www.cell.com/cell-stem-cell/pdfExtended/S1934-5909(16)00106-5

The Presentation Slides
http://www.cell.com/cell-stem-cell/ppt/S1934-5909(16)00106-5.ppt


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