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.)
After reading this the following C's remarks appear in a different light:
Session 23 August 2014
Session 16 August 2014
Session 6 February 2016
Session 18 July 2015
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?
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?
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...
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?
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.
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?
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?
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?
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?
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...
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.