Role of viruses in human evolution

Altair

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Recently I finished Diseases From Space: Astrobiology, Viruses, Microbiology, Meteors, Comets, Evolution written by several authors including Chandra Wickramasinghe. The book consists of 8 chapters each written by a particular author. Basically, they provide evidence to support panspermia but the last chapter (Viruses, Genetic Libraries, Evolution, Interplanetary Horizontal Gene Transfer) written by R. Gabriel Joseph stood out with some very interesting conclusions. So here are some notes (the chapter is available online.)

Viral genes can insert themselves into a variety of locations within the host genome where they may promote gene expression or duplication; and this has been shown to be true even in the human genome. Endogenous retroviral (ERV) sequences, such as promoters, enhancers, and silencers determine when and which genes should be turned on or off and play important roles in the evolution of new species. Once inserted into a host, these viral genes can also rapidly replicate and increase in number (Doolittle & Sapienza 1980; Tsitrone et al., 1999) enabling them to grain greater control over the expanding Eukaryotic genome.

Further, just as Prokaryotes have supplied Eukaryotes with “silent genes” viruses have done likewise. Retroviruses, for example, intwine their genes with the host genome and manufacture enzymes (reverse transcriptase) to reverse transcribe the host’s RNA to create a complementary viral DNA which then becomes an integral part of the host genome. Numerous copies of this viral DNA and RNA are then replicated and then transmitted via the Eukaryotic germline through daughter cells, to subsequent generations and species.

Eight percent of the human genome consists of around 200,000 endogenous retroviruses (IHGSC 2001; Medstrand et al., 2002), and 3 million retro elements (Medstrand et al., 2002). Some of these retroviruses are still active whereas others are silent or have been deactivated (Conley et al. 1998; Medstrand & Mager, 1998).

These, “silent” viral genes, such as those promoting the duplication of genes and whole genomes, have shown sudden bursts of activity which has corresponded with the evolution and divergence of species. Further, once a new species has been genetically manufactured, many of these viral elements become inactive or they are deleted from the genome of subsequent species. Having acted out their role in the metamorphosis of specific species, they are deleted.

Several endogenous retroviruses (ERV) families are still active in present-day humans (Belshaw et al., 2005; Löwer et al., 1993; Medstrand & Mager 1998) which suggests that evolutionary activity will not stop with modern humans. Retroviral sequences encode tens-of-thousands of active promoters and thus regulate human transcription on a massive scale (Conley et al., 2008). In fact, about one quarter of all analyzed human promoter regions harbor sequences derived from viral elements (Jordan et al. 2003). Coupled with the 158,000 mammalian retrotransposons inherited from common ancestors, genome sequencing reveals that 8% of the “modern” human genome consists of human endogenous retroviruses (HERVs); and, if we extend this to HERV fragments and derivatives, the retroviral legacy amounts to roughly half of Homo sapien DNA (Bannert & Kurth 2005; Medstrand et al., 2002). Thus, viral genes have accumulated in those genomes leading to humans and have increased after the metamorphosis of humans; which again suggests that evolution of the human lineage may continue well in the future.

Viruses can also make copies of genes and then exit the host, only to insert them into the genomes of other species, including other viruses. Therefore, each time a virus is jettisoned into space, it would carry copies of these genes which would then be inserted into the genomes of new hosts when that virus falls upon the surface of another planet. Likewise, these viruses would obtain genes from the denizens of the planets upon which they fell; genes which would be added to the growing viral genetic library. As the number of viruses is innumerable, then so too would be the number of genes and multiple genomes stored collectively within these viral libraries (Joseph 2009b,c,d).

Viruses maintain a large reservoir of excess genes. Up to 25% of viruses studied in fact contain up to 3 complete genomes (Goff et al., 2012).

Considerable evidence has been marshaled which demonstrates that viruses are utilized by bacteria as vast storehouses of genes and DNA, which may be transferred from viruses to bacteria, and then back again, depending on environmental and other conditions which impact bacterial needs and requirements. Moreover, viruses, as well as bacteria and archae, can store their genes within the Eukaryotic genome (Conley et al., 1998; López-Sánchez et al., 2005; Romano et al., 2007).

For example, viruses maintain a store-house of genes which code for photosynthesis (Lindell et al., 2004; Sullivan et al., 2005, 2006; Williams et al., 2008). These genes, including those coding for photoadaptation and the conversion of light to energy remain in viral-storage and are only transferred to bacteria under conditions of reduced sunlight and increased environmental stress resulting in nutrient depletion. When these conditions threaten the bacteria with starvation, viruses will transfer the necessary genes to the genome of these starving bacteria.

Once incorporated into the bacterial genome, these genes enhance the cell’s photosynthetic machinery so as to obtain the necessary energy and nutrients by capturing additional sunlight (Sullivan et al., 2006). When sufficient sunlight and nutrients become available, these genes are transferred from the bacteria genome back to the virus genome for storage (Lindell et al., 2004; Sullivan et al., 2005, 2006). Viruses and prokaryotes maintain a genetic co-dependency such that genes are commonly transferred back and forth between them on an “as needed basis.”

Viruses, or viral-like plasmids, may also be periodically ejected from the archae and bacteria genome as packets of DNA. When these genes are needed, these packets are opened and the necessary genes extracted and inserted into prokaryotic and eukaryotic genomes (Sullivan et al., 2006; Williamson et al., 2008).

Viruses are so numerous and come in so many varieties their numbers and genetic storage capacity are essentially infinite. This also means that in total, these viral libraries may contain an infinite number of genes which code for innumerable functions that are held in reserve unless required by the host.

By acting as a genetic storehouse, with the capacity to maintain up to three separate genomes, viruses free up genetic space in the host’s genetic machinery which need only maintain those genes necessary for its survival and functional integrity, or the next step in evolutionary change or speciation. Thus, viruses act as gene and genomic conservatories and can increase the gene pool within the genome of a host when necessitated by environmental or other conditions (Sullivan et al., 2006; Zeidner et al., 2005) including those impacting evolution (Joseph 2009b,c,d,e). And they can insert the necessary genes which can produce products which change the environment (which acts on gene selection), and the later retrieve these genes and store them in the viral genetic library.


Viruses Serve the Host: Diseases Are Rare


The defining feature of viruses including retroviruses, is they precisely target specific species and host cells. Further, the viral RNA genome is actually a template for DNA which must have been copied from another source of DNA. However, if that perfect host has not yet evolved, on Earth, then the virus remains dormant. Thus the dormant virus must have obtained its template from a specific extraterrestrial host. This explains why the virus acts purposefully, targeting and inserting its RNA or DNA into specific species after they evolve. By contrast, if there is not a 100% perfect genetic match, errors are introduced thereby harming the host.

Therefore, in some instances, when viruses invade Eukaryotes, they may sicken or even kill the host. However, that is not advantageous to the virus which may also die. Given that viruses exist in vast numbers, and considering that so many viral genes have benefited the host, it appears that it is only relatively rarely that a virus may sicken or kill those they infect. Rather, it could be said that when sickness results, its because these viruses introduced genetic errors into the genetic hardware of the host--perhaps due to a slight mismatch between the inserted gene or viral element, and the genome of the targeted species (Joseph 2009b,c,d).

Viruses store multiple genomes and vast amounts of genetic information which provide no direct benefit to the virus. Viruses instead, serve potential hosts by storing genes which can be selectively transferred to the host depending on need and which provide substantial benefits to the recipient (Lorenc & Makalowski. 2003; Miller et al., 1999; Parseval & Heidmann 2005). For example, some viral genes enhance host cell carbon metabolism, nitrogen fixation, antibiotic resistance, the biosynthesis of vitamin B12, and the creation of heat shock proteins during times of stress (Evans et al., 2009; Sherman & Pauw, 1976; Sullivan et al., 2005; Williams et al., 2008).

Endogenous retro-viruses (ERVs) are responsible for the generation of proteins involved in the formation of mammalian placenta (Mi et al., 2000; Blond et al., 2000) and provide a protective function allowing for nutrients to pass from mother to fetus while simultaneously protecting the fetus against infection or rejection by the mother’s immune system (Ponferrada et al., 2003; Prudhomme et al., 2005). ERVs are also highly expressed in many human fetal tissues including heart, liver, adrenal cortex, kidney, the central nervous system, and human brain (Anderson et al., 2002; Conley et al., 2008; Patzke et al., 2002; Seifarth et al., 2005; Wang-Johanning et al., 2001, 2003).

In fact, one of the purposes of viral gene storage is to enable the transfer of specific genes into specific species, just before or after these hosts evolve. The evolution of numerous species including humans, has been shaped by successive waves of viral invasions.

Viruses Target Specific Hosts Before And After They “Evolve”

Viruses and retroviruses are host specific and precisely target specific species and cells. In order to invade, or for viral genes to become activated, requires the existence of specific species or the evolution of a new host. In other words, each viral key had to await the evolution of a specific genetic lock. Once that lock evolved, the key was inserted opening the door to the next stage in evolutionary metamorphosis.

For example, ERV sequences encompass 42.2% of the human genome and almost half of the mammalian genome (Deininger & Batzer 2002; van de Lagemaat et al. 2003); many of which were inserted during key points of evolutionary divergence and speciation. Retroviral sequences encode tens-of-thousands of active promoters and regulate human transcription on a massive scale (Conley et al., 2008).

Each stage of evolution and each viral infection event preceded or required that the host first evolve
; at which point viruses invaded and inserted genes which interacted with ancient genes which had been donated by Prokaryotes hundreds of millions if not billions of years before. That is, it is only when specific hosts evolve that viral genes or regulatory elements which have been held in abeyance within these viral genetic storehouses, are retrieved, inserted and activated or silenced; all of which is associated with evolutionary divergence and speciation, such as the split between new world and old world monkeys, and the split between hominids and chimpanzees (López-Sánchez et al., 2005; Romano et al., 2007).

The human genome contains 200,000 copies of endogenous retroviruses grouped in three classes (Lander et al. 2001), which have been introduced through at least 31 separate infection events (Belshaw et al. 2005). And yet, there is virtually little or no trace of ERV activity in prosimians--the ancestors of monkeys, apes and humans. Thus, humans, apes, and monkeys have been repeatedly and selectively targeted by viruses which can only infect humans or apes or monkeys. However, numerous viral genes and retro-elements inserted into monkeys did not become active until just before or after the evolution of apes, whereas many of those viral genes inserted into the ape genome did not become active until hominids and then humans had evolved.

There is a precise key lock relationship between a virus and host. The viral RNA or viral DNA genome must perfectly match the DNA genome of the host or there can be no infection. If the match is not completely perfect, then errors are produced which result in disease (Joseph & Wickramasinghe 2010). If the viral-key cannot fit into the genetic-lock, there is no infection and the virus remains dormant and inactive until a host evolves and becomes available.


The fact that the viral genetic key must wait for the evolution of a specific genomic lock, indicates that these genetic keys and locks had evolved long before suitable hosts became available on this planet. That is, since the viral RNA or viral DNA is actually a template for species-specific DNA, and since these viruses exist before these species evolve, then then these viral templates must have been copied from an identical source of host-specific DNA which must have long evolved evolved on another planet. The ease at viral insertion and integration, the fact that the viral gene-host genome are a perfect fit, indicates that the original viral source for this RNA/DNA template of DNA was the DNA of an identical species who long ago lived on other worlds. This explains why host specific viruses exist before the species evolves, why the virus acts purposefully, targeting and inserting its RNA or DNA into specific species or cells, and why errors are introduced if the match is not perfect.


After reading this the following C's remarks appear in a different light:

Session 23 August 2014
(Odyssey) If different people catch the same virus, does that virus have the possibility of being beneficial or detrimental depending on the person's FRV?

A: Yes.

Session 16 August 2014
(Puck) On the topic of Ebola, what's causing the rapid transmission of the virus?

A: Mutating and becoming more virulent.

Q: (L) So, it's becoming stronger?

A: Yes.

Q: (Perceval) Is it a contender for wiping out millions of people?

A: A lot, of course. Isn't it interesting the similarity between psychopaths as virii of the human kind, and the activation and spread of the infectious kind?

Q: (L) So, are you suggesting that this is one of those, "As above, so below" interactive things? That as psychopaths become more virulent and present in human society, so will Ebola become more virulent in the physiological realm? Is that what we're getting at here?

A: Yes close enough.

Q: (L) So in order to stop the progress of Ebola and any other following pathogens, human society would have to take care of the psychopathy problem? The mind virus, the Wetiko virus...

A: Yes

Session 6 February 2016
(L) Yeah, we've got this thing called the Zika virus. They're saying it's responsible for causing these cranial and brain malformations in babies. I'm not too sure that the Zika virus is always correlated. I haven't read any serious studies on it. It just seems to me that there are a lot of assumptions being made. Is it the Zika virus causing it? Is the Zika virus caused because of genetically modified mosquitoes, or are birth defects being caused by vaccinations?

(Galatea) What's the cause?

[Noko gets up and moves to the floor, goes back to sleep]

A: Mutations began in humans due to vaccine and then collected by mosquitoes, undergoing further mutations by combining with modifications of the insects.

Q: (L) In other words, the mutation began in the human beings. Then the mosquitoes bit them and sucked up their blood. The blood mixed with the genetic modifications in the mosquitoes, and then the mosquitoes went and bit somebody else which injected it into them? So it was a combination of the genetic modifications of the mosquitoes and the mutation of the vaccinated human? Is that what we're getting at there?

A: Yes


Session 18 July 2015
(Pierre) There seems to be something else. The way they refer to parasites is that they are preventing not only the gaining of knowledge and growth of awareness, but also this quantum leap. Maybe if you have parasites, you can still increase your knowledge and awareness, but you'll reach a sort of glass ceiling that prevents you from graduating.

A: Yes

Q: (L) What's the tinkering there?

A: The parasites act as receivers.

Q: (Pierre) Yeah. The parasites act as receivers. So when you are full of parasites, you are more under the influence of bad waves, or waves sent by bad entities. You're more susceptible to those messages. There's a bad influence on you beyond the parasites.

A: Getting free of parasitic microorganisms is one of the first orders of business for transformation.

Q: (Galatea) Would you say that the closer somebody gets to graduating, the worse things get? Like they start to feel worse?

A: In many cases, yes.

Q: (L) If you get too smart, then something happens. I wonder if they even have something designed into the system that makes that happen?

A: Yes

Q: (Pierre) They have a back door.

(Perceval) When they said that the parasites act as receivers, receivers of what?

A: Waves of information.


Q: (Perceval) The reference to bloodlines becoming parasitically infected, does that refer to certain bloodlines that were particularly targeted for infestation?

A: Yes


Q: (Perceval) As in bloodlines or genetic profiles that were more likely to have an increase in awareness or to be more of a threat to the system?

A: Yes

Q: (L) That's pretty freaking depressing.

(Pierre) That's cunning.

(Perceval) What did they say about the tinkering?

(L) Okay, how is the tinkering done?

A: Most often via viruses.

Q: (L) Is the campaign to vaccinate everyone part of this project to make sure that everybody gets the viruses that are needed to stop them from progressing?

A: Yes

Q: (L) I know you said that the mark of the beast is something that relates to anybody who accepts torture and that sort of thing, but some of those old ideas about the mark of the beast, it's like DNA is code... So, maybe have these virally implanted genetic instructions could be considered as the mark of the beast.

A: It goes together!

Q: (L) So if they get these virally implanted DNA codons or something, that then makes them of the type of person who is accepting of the bad waves and the torture and so forth...

A: Yes


Q: (Perceval) Can we assume that most of the population of the planet is infected with these kinds of parasites?

A: Many, not most. Some have strong resistance. And also, some have compensatory counteractive codons.
 

Laura

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The whole topic of panspermia is fascinating. Of course, it does not deal with the question of evolution, as such. Because if you displace evolution onto panspermia, you still haven't explained the evolution of the virii in their natural habitat.
 

Eboard10

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This is topic is indeed fascinating. I always revert back to Shiller's "The Origin of Life: The 5th Option", where he makes a compelling case using a systems approach that life on Earth was the result of rational design rather than panspermia. But it's clear that viruses are being continually brought to this planet through meteors and that they influence our genetic makeup primarily through epigenetic changes.

Thanks for sharing Altair - will add this to my reading list.
 

Cosmos

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I can't remember where I heard or read the following, but it came to my mind again after reading the above. I've tried to find a source for that idea, without much success so far.

Basically I recently heard somewhere that the actual underlying reason for racism, or more generally speaking, of being afraid of other foreign tribes or people, might actually be a deep seated fear, about those others not being clean in the sense of possibly carry deadly or harmful viruses, that could endanger oneself and/or the own tribe. Apparently, this has to do with the deep seated fear that was instilled in human beings through deadly pandemics in the past.

As an example Hitler was brought up (among other famous racist) and his obsession with cleanness and orderliness. Then the actual content of his and other racist spoken and written words was analyzed, basically concluding that the words he and other use to express their racism suggested that they are actually afraid to get dirty and the other being dirty.
 

Laura

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Pashalis said:
I can't remember where I heard or read the following, but it came to my mind again after reading the above. I've tried to find a source for that idea, without much success so far.

Basically I recently heard somewhere that the actual underlying reason for racism, or more generally speaking, of being afraid of other foreign tribes or people, might actually be a deep seated fear, about those others not being clean in the sense of possibly carry deadly or harmful viruses, that could endanger oneself and/or the own tribe. Apparently, this has to do with the deep seated fear that was instilled in human beings through deadly pandemics in the past.

As an example Hitler was brought up (among other famous racist) and his obsession with cleanness and orderliness. Then the actual content of his and other racist spoken and written words was analyzed, basically concluding that the words he and other use to express their racism suggested that they are actually afraid to get dirty and the other being dirty.

Along that line, "Cognitive Science and the New Testament" is an interesting read.

https://www.amazon.fr/Cognitive-Science-New-Testament-Christian/dp/0198779860/ref=sr_1_1

It gives a much better explanation for the "cleanliness" fetish and fear of "the other" based on science.
 

Altair

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Laura said:
The whole topic of panspermia is fascinating. Of course, it does not deal with the question of evolution, as such. Because if you displace evolution onto panspermia, you still haven't explained the evolution of the virii in their natural habitat.

Indeed. The most fascinating is the idea that virii function as a low-level genetic library borrowing their genes to other species and then taking back their updated/improved versions to their library. I would rather say that they are just tools of evolution. Especially interesting is the connection between FRV and how hosts may even benefit from virii:

Viruses and retroviruses are host specific and precisely target specific species and cells. In order to invade, or for viral genes to become activated, requires the existence of specific species or the evolution of a new host. In other words, each viral key had to await the evolution of a specific genetic lock. Once that lock evolved, the key was inserted opening the door to the next stage in evolutionary metamorphosis.

(Odyssey) If different people catch the same virus, does that virus have the possibility of being beneficial or detrimental depending on the person's FRV?

A: Yes.

And that virii only then pathogenic when there is a mismatch in "key lock relationship" between them and the hosts:

There is a precise key lock relationship between a virus and host. The viral RNA or viral DNA genome must perfectly match the DNA genome of the host or there can be no infection. If the match is not completely perfect, then errors are produced which result in disease (Joseph & Wickramasinghe 2010). If the viral-key cannot fit into the genetic-lock, there is no infection and the virus remains dormant and inactive until a host evolves and becomes available.
 

Eboard10

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Viruses and retroviruses are host specific and precisely target specific species and cells. In order to invade, or for viral genes to become activated, requires the existence of specific species or the evolution of a new host. In other words, each viral key had to await the evolution of a specific genetic lock. Once that lock evolved, the key was inserted opening the door to the next stage in evolutionary metamorphosis.

Does this mean that the virus in some way already knows the most likely path that the host's "genetic lock" is going to take? It's hard to imagine that a virus would have much chance of activating itself if it had to wait for the hosts DNA to evolve in a specific manner out of a myriad of possible combinations. This would suggest some form of intelligence either inherent to the virus or acting behind it.

There is a precise key lock relationship between a virus and host. The viral RNA or viral DNA genome must perfectly match the DNA genome of the host or there can be no infection. If the match is not completely perfect, then errors are produced which result in disease (Joseph & Wickramasinghe 2010). If the viral-key cannot fit into the genetic-lock, there is no infection and the virus remains dormant and inactive until a host evolves and becomes available.

I'm a bit confused by this paragraph, maybe I'm just not reading it correctly. It starts by saying that there must be a match between the virus and the hosts genome in order for the former to infect the latter, which I guess can eventually lead to a disease to manifest in the host. It then says that if there is no match between the two, this produces a disease in the host.
 

Keit

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Eboard10 said:
I'm a bit confused by this paragraph, maybe I'm just not reading it correctly. It starts by saying that there must be a match between the virus and the hosts genome in order for the former to infect the latter, which I guess can eventually lead to a disease to manifest in the host. It then says that if there is no match between the two, this produces a disease in the host.

It does appears to be a bit confusing. The text appears to be saying:

- If there is a match - it leads to infection;
- If there is an incomplete match and errors are produced - it leads to a disease;
- If there is no match - the virus is dormant

Maybe I misunderstood the text, but according to the text there appear to be differences between infection and the disease? Something else? It isn't clear.

In añy case, this topic is really fascinating! Lots to think about.
 

Siberia

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Thank you for sharing, Altair. This topic is very interesting in so many ways. For example, this passage from your post caught my attention:

For example, viruses maintain a store-house of genes which code for photosynthesis (Lindell et al., 2004; Sullivan et al., 2005, 2006; Williams et al., 2008). These genes, including those coding for photoadaptation and the conversion of light to energy remain in viral-storage and are only transferred to bacteria under conditions of reduced sunlight and increased environmental stress resulting in nutrient depletion. When these conditions threaten the bacteria with starvation, viruses will transfer the necessary genes to the genome of these starving bacteria.

Once incorporated into the bacterial genome, these genes enhance the cell’s photosynthetic machinery so as to obtain the necessary energy and nutrients by capturing additional sunlight (Sullivan et al., 2006). When sufficient sunlight and nutrients become available, these genes are transferred from the bacteria genome back to the virus genome for storage (Lindell et al., 2004; Sullivan et al., 2005, 2006).

I read this Sott article about Ebola the other day:

Ebola virus leaves unique scar inside survivor's eyes

which says:

When asked to read letters on an eye chart, the Ebola survivors tended to perform just as well as those who'd never had the disease, meaning their infection didn't seem affect their vision.

But about 15 percent of Ebola survivors had a unique scar on their retina — the light-sensitive tissue at the back of the eye. The people who had never contracted Ebola did not have this particular type of scar, the study found.

This scar, "often resembling a diamond or wedge shape, appears unique," the researchers said. The scar was next to the eye's optic disc, the spot where nerve fibers exit the eye to connect to the brain. This suggests that the Ebola virus enters the eye by traveling along the optic nerve, the researchers said.

Previous studies have found that up to 60 percent of Ebola survivors experience eye symptoms, including eye inflammation and temporary vision loss, but little is known about the patients' long-term vision outcomes, the researchers said.

About 7 percent of the Ebola survivors in the new study had white cataracts, or cloudy areas in the lens of the eye that can affect vision. In contrast, no white cataracts were found in the participants who'd never had Ebola, the researchers said.

I wonder if Ebola could be a way of possible adaptation of people to our stressful environmental conditions - a way for humans to better absorb light via our retina and thus obtain more energy? And in some cases it may also cause damage to the retina. FWIW

Also, this session comes to mind:

(L) Well, I think that obviously "tribal" means physiological spiritual union profile, and that that may have something to do with what we were talking about at a previous session when we asked about Caesar's soul group. Physiological spiritual union profile would be what defines what tribe you belong to, but it's a spiritual tribe and not necessarily specifically physical. You can grow into it according to some criteria... “graduate” was the term used. Am I correct here about a tribal group being like a soul group? Is that an accurate way of putting it?

A: Very close.

Q: (L) Is there anything that can get me closer?

A: In some cases there is also a supersensory component.

Q: (L) What is a supersensory component?

A: Externally driven mutation.

Q: (L) Externally driven by what?

A: Most often by the occupying soul itself.

Q: (L) So are you saying that if a soul selects a body or gets a close frequency match to a body that it wants to use, that it can also modify that body for its own purposes if it needs to and if the DNA match isn't quite to its taste or purposes?

A: Yes.

Q: (Andromeda) So our souls can cause mutations?

A: Yes.

Q: (Perceval) Does that happen pre-birth?

A: No, it can happen once the soul is seated and as needed.

Q: (L) So, what are some of the processes that can effect this in a physical way?

A: Diet is one. Also "arrangement" to contract the needed sickness.

Q: (Pierre) So you contract a sickness because the soul wants to learn something and experience something, and it's through this sickness that this learning will occur?

A: No. The soul and its helpers wants to trigger DNA modification!

Q: (L) They're saying no, that it's far more pragmatic. Okay, next question... I'm never going to get to my questions that I have! [laughter] Okay, when you say, "the soul and its helpers", what the heck are the soul's helpers?

A: Tribal unit members both in the body and out.

Q: (L) So if you're a member of a tribal unit, you are in a way connected via DNA connections or signals or frequencies with your other tribal members, whether they are incarnated or not? Is that what we're saying here?

A: Pretty much; no man is an island!
 

Altair

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Keit said:
Eboard10 said:
I'm a bit confused by this paragraph, maybe I'm just not reading it correctly. It starts by saying that there must be a match between the virus and the hosts genome in order for the former to infect the latter, which I guess can eventually lead to a disease to manifest in the host. It then says that if there is no match between the two, this produces a disease in the host.

It does appears to be a bit confusing. The text appears to be saying:

- If there is a match - it leads to infection;
- If there is an incomplete match and errors are produced - it leads to a disease;
- If there is no match - the virus is dormant

Maybe I misunderstood the text, but according to the text there appear to be differences between infection and the disease? Something else? It isn't clear.

In añy case, this topic is really fascinating! Lots to think about.

Yes, as far as I understood, infection doesn't mean disease in this context but rather docking of the virus to your cells (key lock relationship)
 

Keit

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Altair said:
Yes, as far as I understood, infection doesn't mean disease in this context but rather docking of the virus to your cells (key lock relationship)

Hmm...does it mean that only when this key lock relationship happens, only then the virus releases its "programming", i.e infection? If so, it is a completely different way of looking at infection. At the moment we believe that infection leads to a disease, but here it does...what exactly? Rearranges DNA? Well, if so, it is no less than a revolutionary idea, because it means that viruses are not to blame for the disease per se, but the disease is a consequence of a mismatch, or the host not being "ready" enough. Fascinating.

As for the disease being the result of "errors" made me think about the mismatch of FRVs between different people, and how it can lead to a variety of symptoms, including catching a cold, etc.
 

Altair

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Keit said:
Altair said:
Yes, as far as I understood, infection doesn't mean disease in this context but rather docking of the virus to your cells (key lock relationship)

Hmm...does it mean that only when this key lock relationship happens, only then the virus releases its "programming", i.e infection? If so, it is a completely different way of looking at infection. At the moment we believe that infection leads to a disease, but here it does...what exactly? Rearranges DNA? Well, if so, it is no less than a revolutionary idea, because it means that viruses are not to blame for the disease per se, but the disease is a consequence of a mismatch, or the host not being "ready" enough. Fascinating.

As for the disease being the result of "errors" made me think about the mismatch of FRVs between different people, and how it can lead to a variety of symptoms, including catching a cold, etc.

The following excerpt from the same article explains it to some extent:

The fact that the viral genetic key must wait for the evolution of a specific genomic lock, indicates that these genetic keys and locks had evolved long before suitable hosts became available on this planet. That is, since the viral RNA or viral DNA is actually a template for species-specific DNA, and since these viruses exist before these species evolve, then then these viral templates must have been copied from an identical source of host-specific DNA which must have long evolved evolved on another planet. The ease at viral insertion and integration, the fact that the viral gene-host genome are a perfect fit, indicates that the original viral source for this RNA/DNA template of DNA was the DNA of an identical species who long ago lived on other worlds. This explains why host specific viruses exist before the species evolves, why the virus acts purposefully, targeting and inserting its RNA or DNA into specific species or cells, and why errors are introduced if the match is not perfect.

And since there are planets which are not just habitable but billions of years older than this planet and upon which intelligent life may have evolved long before Earth became Earth, this also explains why evolution on this planet will continue into the future.

On the other hand, given the infinite variety of viruses in existence, it may be that most viruses, at least on Earth, never become active, and that the lock-key genetic relationship between host and virus is due to chance. By happenstance the viral key fits the genomic lock of specific cells and species because there are so many viruses.

But then, where did this infinite variety of viruses obtain their genetic libraries and their specific RNA and DNA templates? Why are viral genes beneficial to the host and promote speciation?

Then there is the step wide progression of increasingly intelligent species, and then evolutionary quantum leaps without intermediate forms; all of which are linked to changes in the environment acting on genes inserted into the Eukaryotic genome by Prokaryotes and the activity of viruses on gene duplication and expression.

Rather than random chance secondary to an infinite variety of viruses which lay in wait, it may be that life on Earth is merely a sample of life’s evolutionary possibilities some of which are expressed on planets with their own varied environments. And this genetic potentiality is represented in the genomes of viruses and Prokaryotes, these genetic seeds of life which germinated upon falling to Earth.

What is called “evolution” is like metamorphosis and embryogenesis, all of which are under precise genetic regulatory control.

Thus, the data on evolution and metamorphosis presented here, can be interpreted in two ways: 1) archae, bacteria, and viruses from this world or other planets, have repeatedly inserted genes into the Eukaryotic genome thereby influencing the direction and trajectory of life’s evolution on this planet. Or 2) Extraterrestrial viruses and microbes have repeatedly inserted genes into the Eukaryotic genome, and contain all the genes, genetic elements, and genetic instructions for altering the environment which acts on those genes donated by viruses and Prokaryotes, and that evolution is a form of embryogenesis and metamorphosis: the recreation of creatures who long ago evolved on other worlds.
 

Chu

Administrator
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FOTCM Member
Super interesting!

Reading the thread and this in particular:

Altair said:
Viral genes can insert themselves into a variety of locations within the host genome where they may promote gene expression or duplication; and this has been shown to be true even in the human genome. Endogenous retroviral (ERV) sequences, such as promoters, enhancers, and silencers determine when and which genes should be turned on or off and play important roles in the evolution of new species. Once inserted into a host, these viral genes can also rapidly replicate and increase in number (Doolittle & Sapienza 1980; Tsitrone et al., 1999) enabling them to grain greater control over the expanding Eukaryotic genome.

Further, just as Prokaryotes have supplied Eukaryotes with “silent genes” viruses have done likewise. Retroviruses, for example, intwine their genes with the host genome and manufacture enzymes (reverse transcriptase) to reverse transcribe the host’s RNA to create a complementary viral DNA which then becomes an integral part of the host genome. Numerous copies of this viral DNA and RNA are then replicated and then transmitted via the Eukaryotic germline through daughter cells, to subsequent generations and species.

reminded me of a video I'd like to recommend.


https://youtu.be/3wy6EmhhR7I

Particularly starting from minute 20 or so, if you can't watch the whole thing. It talks about viruses not being the "bad guys" all the time, and about the huge role they may have played in evolution. For example, a study made with sheep showed that, without a specific retrovirus in the placenta, a baby sheep could not develop. Another study was made on bonding after the injection of a virus in prairie voles, and I found the results pretty amazing, FWIW.


These viruses are often found in "junk DNA", which makes one question the importance of that "junk".
 

Gaby

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Fascinating topic, quotes and food for thought. Downloaded the documentary into an mp3 so I can listen to it later.

I remember reviewing a couple of articles that seem to support the information quoted in this thread:

https://www.sott.net/article/257631-On-viral-junk-DNA-a-DNA-enhancing-Ketogenic-diet-and-cometary-kicks

I think it is very relevant in the sense that the fragments of hemorrhagic viruses that were speculated to be the cause of the Black Death (for more information see New Light on the Black Death: The Viral and Cosmic Connection), are listed as part of our genome, indicating that life on Earth has been exposed to rather dangerous viruses through our evolutionary history which then effected changes in our DNA:

Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes

Vladimir A. Belyi, Arnold J. Levine, and Anna Marie Skalka. PLoS Pathog. 2010 July; 6(7): e1001030.

[...]

This second paper was linked in the first one and is even more interesting. It expands and backs up Bryant M. Shiller's explanations on Origin of Life: The 5th Option. Keeping in mind that "transposable elements" (TE) - which were once considered "junk" DNA - are viral in their origin, it would explain why humanity benefits from periodic plague diseases to give a kick-start or "reformation" to our genetic makeup and accelerate evolution or change through cometary impacts:

Transposable elements and viruses as factors in adaptation and evolution: an expansion and strengthening of the TE-Thrust hypothesis

Keith R Oliver and Wayne K Greene. Ecol Evol. 2012 November; 2(11): 2912 - 2933.

[...]

The frustrating thing is that it just transfers all the evolution theory into another planet so to speak, which then comes to this reality via a comet. But how did it originate in the "other planet"? The Cs had some very interesting things to say:

https://cassiopaea.org/forum/index.php/topic,27027.0.html

After reading this book about viruses, we have the idea that viruses may be the means by which genetic manipulation {as in intentional coming from other densities} has taken place on this planet for millions, if not billions, of years.

A: Yes

Q: (L) Does that mean that a virus is a transdimensional manifestation?

A: Yes. Thoughts made manifest! Compare to some crop circles!

Q: (Psyche) Some viruses in the atlas DO look like crop circles. [wind noise muffles Ark's question] (Ark)...of course virus is just pure DNA, or what? (Psyche) It can be both DNA or RNA depending on the type of virus, and usually coated to protect itself. There are so many types of viruses; it can be just a piece of genetic code. (Ark) Okay, so my question is whether there is a particular part of the virus that has the property that is not just described by normal quantum physics or quantum chemistry and so on, or its the whole organization of virus that has this property?

A: Yes. Information field aggregates matter.


Q: (talk of thought vs. information) (Belibaste) Does information command or direct the aggregation of different proteins or amino acids to form a virus? Materialization?

A: Yes.

Q: (Psyche) It's very interesting because they have found in our "junk" DNA, properties of viruses that are close in location to those of stem cells, and also cells that end up producing cancer. It is quite interesting. (Perceval) That means our DNA is thought made manifest?

A: More or less!

Q: (Perceval) Except when we do the thinking, we mess it up. So we should stop thinking and interfering with the manifestation of our DNA! (laughter)

(Ark) My question is that I moved from my shape of the universe with time being like a loop to another shape of the universe in which time is infinite but can wind an absolute infinite number of times. (L) Why? (Ark) Why? Yes... I liked before my time as a loop, but now I'm a little bit hesitant… but something tells me to follow the way with infinite time. Am I doing it right?

A: Yes. And you may find a bigger loop!

Q: (Ark) A bigger loop. Alright. Next question is now I came back to my old paper about the shape of photons which contains errors, and I thought I will fix these errors, but at the same time I thought, "Well, let me add what I learned during these thirty years, and also this new idea of time and space." But I am not really sure if I should go back to this old idea because who cares about the shape of the photon?

A: It may reveal something important.

Q: (Ark) It may be... but is it?

A: You like it!

Q: (Ark) Alright. I am done. (L) anybody else got anything? (Bubbles) Why have I for the past year or two felt so weak and pathetic lately? Where did my energy go?

A: Onset of autoimmune reactions. It should get better with your current regime. Be patient!

Q: (Bubbles) Why did these autoimmune reactions suddenly happen?

A: Reacting to virus.

Q: (L) Probably chicken pox. (Ark) It takes awhile.

And then, "junk" AKA "non-coding" DNA is related to stem cells:

UCLA Scientists Find 3000 New Genes in “Junk DNA” of Immune Stem Cells

https://blog.cirm.ca.gov/2015/10/28/ucla-scientists-find-3000-new-genes-in-junk-dna-of-immune-stem-cells/

Another important function that non-coding RNAs control is cell differentiation, or the maturation of immature cells into adult cells. Differentiation is a complicated process, and because non-coding RNAs are relatively new to the scientific world, we haven’t figured out their exact roles in the differentiation of stem cells into adult cells.

Understanding Immune Cell Development

In a study published this week in Nature Immunology, UCLA scientists reported the discovery of 3000 new genes that make a type of non-coding RNA called a long non-coding RNA (lncRNA) that regulates the differentiation of stem cells into mature immune cells like B and T cells, which play a key role in fighting infection. This important study was funded in part by CIRM....

‘Junk DNA’ tells mice—and snakes—how to grow a backbone
http://www.sciencemag.org/news/2016/08/junk-dna-tells-mice-and-snakes-how-grow-backbone

Most mice have 13 pairs of ribs, but a few strains of mutant mice bred by Mallo and colleagues have 24 pairs. Their rib cages extend all the way along their backbone, down to the hind legs, similar to those of snakes.

The research team traced the extra ribs to a mutation deactivating a gene called GDF11, which puts the brakes on another gene that helps stem cells retain their ability to morph into many cell types. Without GDF11 to slow down that second gene—OCT4—the mice grew extra vertebrae and ribs. But GDF11 seemed just fine in snakes. So what was regulating vertebrate growth in snakes? The researchers decided to look at the DNA surrounding OCT4 to see whether something else was going on.

The OCT4 gene itself is similar in snakes, mice, and humans, but the surrounding noncoding DNA—which also plays a role in slowing down OCT4—looks different in snakes. To see whether this junk DNA gives snakes a longer-lasting growth spurt, Mallo and his colleagues spliced noncoding snake DNA into normal mouse embryos near OCT4. The embryos grew large amounts of additional spinal cord, suggesting that this junk DNA does indeed play a role in body shape regulation, the team reports this month in Developmental Cell.

Ancient Virus DNA Gives Stem Cells the Power to Transform
http://news.nationalgeographic.com/news/2014/03/140330-embryonic-stem-cell-virus-science/

A virus that invaded the genomes of humanity's ancestors millions of years ago now plays a critical role in the embryonic stem cells from which all cells in the human body derive, new research shows.

The discovery sheds light on the role viruses play in human evolution and could help scientists better understand how to use stem cells in advanced therapies or even how to convert normal cells into stem cells.

Embryonic stem cells are pluripotent, meaning they are capable of becoming any other kind of cell in the body. Scientists around the world hope to use this capability to help patients recover from injury and disease.

Researchers have struggled for decades to figure out how pluripotency works. These new findings reveal that "material from viruses is vital in making human embryonic stem cells what they are," said computational biologist Guillaume Bourque at McGill University in Montreal, a co-author of the study published online March 30 in Nature Structural & Molecular Biology.

Viral Invasion

To make copies of itself, a virus has to get inside a cell and co-opt its machinery. When one type of virus called a retrovirus does this, it slips its own genes into the DNA of its host cell. The cell is then tricked into assembling new copies of the retrovirus. The most infamous retrovirus is HIV, the virus behind AIDS.

In rare cases, retroviruses infect sperm or egg cells. If that sperm or egg becomes part of a person, their cells will contain retrovirus DNA, and they can pass that DNA on to their descendants. Past research suggests that at least 8 percent of the human genome is composed of these so-called endogenous retroviruses-leftovers from retroviral infections our ancestors had millions of years ago.

Scientists long thought that endogenous retroviruses were junk DNA that didn't do anything within the human genome, said study co-author Huck-Hui Ng, a molecular biologist at the Genome Institute of Singapore.

However, recent studies have revealed that might not be true for one class of endogenous retroviruses known as human endogenous retrovirus subfamily H. HERV-H DNA was surprisingly active in human embryonic stem cells but not in other regular types of human cells.

Now scientists have found that HERV-H is not only active in these stem cells, but also is key in keeping them pluripotent.

In the new study, the researchers treated human embryonic stem cells with tiny bits of RNA that suppressed HERV-H activity. The treated cells stopped acting like stem cells. Instead, they acted much like fibroblasts, the most common kind of cell found in animals' connective tissue.

Further analysis confirmed that curbing HERV-H quashed the production of proteins that are associated with pluripotency.

"It's pretty wild to see these elements at play in embryonic stem cells, which one intuitively might not want to fiddle around with too much," said computational biologist David Kelley of Harvard University, who did not participate in this study.

A better understanding of how HERV-H works might help researchers chemically reprogram ordinary cells into becoming pluripotent stem cells, which "could help lead to regenerative medicine therapies," Bourque said. Those therapies could treat conditions such as diabetes, stroke, multiple sclerosis, Parkinson's disease, and brain and spinal cord injury.

Converting an Enemy

More than 1,000 copies of HERV-H litter the human genome. The DNA sequences are unique to humans and great apes, apparently invading primates less than 20 million years ago, said evolutionary geneticist Cedric Feschotte of the University of Utah, who did not take part in this research.

But HERV-H isn't necessary for pluripotency in stem cells of other organisms. Non-primates have stem cells that work without this viral material.

"Whatever these elements are doing for stem cell biology, which remains unclear but the study suggests is important, it must have emerged recently and rapidly in evolution," Feschotte said.

Human embryonic stem cells are the ultimate source of the more than 200 known types of cells in the body. That such critical building blocks of human biology would depend on genetic material from an outside source—a virus, no less—runs counter to intuition.

However, eons of evolution have honed viruses' ability to manipulate the biology of a host cell. These findings suggest that once an organism absorbs a retrovirus, it can then use some of this viral material to better control its own biology. "That can be faster than just relying on random mutations to get something that might work," Bourque said.

Future work should explore other families of endogenous retroviruses "to see if they have also evolved new functional roles, like HERV-H did in stem cells," said functional genomicist John Rinn at Harvard University, who did not participate in this study. "We suspect that these genes may play important roles in other cell types as well, such as liver, kidney, and brain."

These relics from ancient infections may turn out to be more treasure than junk.
 

Phill4

The Living Force
A disease may be the result of altering the existing balance of a person, I mean the immune system will react to any agent and the effects of a viral infection will be present.

What I was thinking is that being there so many viruses and "thought forms" some that match our genome and some that do not, that those that are dissonant with our genetic code are there to inhibit certain sections of our DNA, and do nothing for the body at this point, while it may eventually lead to a mutation that helps the body.

A disease, seems like a karma, and it makes sense that the individual has to be tuned to integrate the coded information of the virus, being that we can alter our DNA via genetic changes from the environment and those that come as a result of change, I.e work. diet, etc.

I think that those parasitic agents, affect the DNA all the way down to perception.

I don't have this information, and actually I heard it , but I heard that when a person gets candida, the body actually craves sugar, so my question was how does the virus or bacteria re-wires or signals the brain so that it craves exactly what the virus needs to survive? as if candida had a mind of its own, it made me think that attachments, entities, pathogens agents, bacteria, viruses affect and thrive in our emotional states providing the conditions for further growth of disease. I don't know..
My question was how does that signaling happens? because it it can alter our craving , it is not far fetched to thing that it can affect our mood and our thinking patters, hence why they act as antennas for negative waves....
 
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