Longevity and Biblical Plagues 2

Kinkajou:. Compare the situation to CoVid. With CoVid over the space of two years, there are dozens of variants and the trend is increasing. The immune system clears the infection - eventually, faster in some than others. The virus can always be isolated from the tissues of the respiratory tract.
Dr Axxxx: .  With CRRI, the disease is not present in the bloodstream once active immunity emerges after the initial infection. The virus essentially cannot be isolated. This is abetted by the difficulty of searching for tissue persistence of the bio-agent – in effect giving the “stealth” characteristics typical of a good bio-weapon. The disease is stable. variants / mutants do not function as well and do not replicate successfully.
Goo: . Disconcerting! In knowing you were at war, you can write the specifications of your perfect weapon. It emerges immediately in the light of day, not just meeting your expectations but exceeding them. Disconcerting!

Kinkajou:. But there were three steps were talking about. The last?
Erasmus: . Hang on. This I can see a few problems with the theory so far. The biggest issue I have is “granularity”. Not everyone is affected to the same extent. This means that they will be a trend for some people to show greater or lesser anti-longevity effects than others. The discrepancy is a problem in a stealthy bio-weapon because it highlights the disparity of normal versus non-normal. Why is this happening to one person and not to another?

Granularity in grains of sugar :
No two identical, all somewhat different: Asks the question Why?

Dr Xxxxx: . And that brings us to the third agent (LLIAP) responsible for the third intervention. And this one has characteristics that outshine its predecessors . I believe the third agent is a bacterium – but a complex bacterium. You would normally expect considerable evolution/devolution of such an organism over time. And it appears that there have been substantial changes in the DNA sequence but with a surprisingly small number of variants emerging over several thousand years with retention of stealthy effectiveness. And – an unusual solution to the issue of granularity.

It is a lethal disease, shortening your life essentially to- threescore and 10 years. But it is a disease which you can catch 100 to 1000 times in your lifetime, but still not die one day sooner than if you had only caught it just once.
It is a disease that you would in fact probably catch many times in your life.
Dr Axxxx: .  And its distribution agent is invisible!
Dr Xxxxx: . The best simple analogy I can give is owning a car. Most of us have probably owned many cars over our lives. The exterior look and the paintwork may change, but the basic design with the internal combustion engine has shown very little variance over decades. Same with LLIAP.

Car Evolution

This organism similarly is likely to have developed a large number of serovars (serological variants) which you can catch again and again and again, but all having the same basic internal DNA programming. In effect an infection that you can catch many times.

And because everyone is likely to have caught the infection many times in their lives, it removes the issue of granularity. There are no: “gets” and “don’t gets”. This is because everyone has experienced the infection so repetitively and so often, that it appears to have an even effect profile across the entire population – or as close to it as you could possibly expect.

Having caught the disease once, your immune system produces antibodies effectively clearing the germ from the systemic circulation. However it persists with apparently minuscule effect within the bone marrow affecting macrophage antigen presentation. This slowdown of the immune mechanism causes immune cell anergy resulting in sluggish disease immune response and in slow repair of tissue damage.
Erasmus: . You have told me personally before how the first two infections spread. Paill Spectrum enters the body through a nasal lying infection – penetrating the nerve tissue of the nasal mucosa which penetrates the Cribiform plate underlying the frontal lobes of the brain. The bacterium sets up an infection within the frontal lobes giving the characteristics symptoms of anger, irritability, poor memory and concentration.

The second agent is spread by respiratory droplets. Viral particles are in the droplets attached to lymphocytes in the sub nasal mucosa and there is persistent viral shedding to a small extent over the years. A mother just speaking or breathing over her child is likely to infect the baby. The agent lurks in lymph nodes throughout the body affecting lymphocyte selection and differentiation in immune processes.
But the third agent you tell me is spread by “invisible flying insects”.

Dr Xxxxx: . Will they are not really invisible. They are just too small to routinely see.
Erasmus: . Well since you have made me aware of these little critters, I am highly sensitive and aware of their presence. I remember once a bus stopping on the side of a hill in Italy. The insects alighted on the passengers in the bus within 15 seconds of the bus stopping. And I could see no one aware of their presence. I can remember being in a restaurant, effectively in a basement with no greenery for hundreds of metres. And yet I could see a couple of the critters buzzing around again effectively invisible to everybody, everyone in the room being unaware of their presence.

Invisible Insects

I would even accept that these little critters have an attack rate or an aggression rate far above that of the average mosquito. In fact I would even say you are 10 times more likely to be bitten by one of these things then you are by a mosquito.

Erasmus: . But the insect example gives me some concern about being a 100% solution. Malaria parasites, many arbo- viruses, and many mosquito borne viruses need to infect the mosquito first before the mosquito is able to transmit the infection. And this does not guarantee 100% infection to a target population.

No See Ums

Dr Xxxxx: . Ah! This organism has a unique solution to this problem. Absolutely unique. The organism is present within the ovaries and the salivary glands of the infected biting insects. A typical ovarian cell in such an insect contains 30 to 40 chromosomes. However, within the body of the insect, each cell will often have only about 10 chromosomes.

So here’s how I think it works.

The organism is present in every germ cell (ovaries and sperm) of every insect. As the baby insect grows within its “egg” excess chromosomes are dumped from the somatic cells of the insect, and the double double chromosomes set exists only within the salivary glands and the ovaries. It must exist within the ovaries to ensure transmission from one insect generation to another in effect guaranteeing 100% transmission. It must exist within the salivary glands to guarantee 100% transmission to human beings.

> Proboscis > Note the saw tooth edge which damages skin on obtaining a feed and maximises infection success through maximised skin damage, possibly even the secondary infection facilitating lymphocyte and macrophage attraction to the site, also maximising infection. The irritation favours scratching which increases immune cell migration to the area, facilitating the infection.

The insects have a number of modifications to maximise transmission. Mosquitoes have a pointy beak – like a little pike that they stick into humans to suck out blood. LLIAP vectors have a sawtooth proboscis which maximises superficial skin damage thereby increasing the likely exposure of the human being to the infecting agent.

The insect vectors are one of the very few species on the planet that can stop their reproductive development. In adverse circumstances, egg maturation can freeze and can stay frozen until circumstances are more favourable for egg development into the adult insect vector. There are very few organisms on the planet they can stop/start the growth cycle to adapt to external circumstances.

Goo: . What you mention is awesome biotechnology here. The ability to regulate growth cycles is not common in many animals or insects on this planet. But we find it here in association with a deadly bio-agent.

Erasmus: . Using mosquitos by comparison, mosquito larvae/pupae have a set growth cycle. If circumstances get difficult, they die. The LLIAP vector by comparison can stop and start, requires substantially less water and less consistent watery environment for the completion of its growth cycle and can breed in micro-climes. (The microclimate of a crack in a brick may be sufficient to maintain an adequate growth environment for a LLIAP vector egg).

Erasmus: . . Yes but I still see problems. How can you guarantee that every insect vector will be infected? One infected bug is easy : but to infect ALL bugs that is a challenge. To infect the entire biosphere is an incredible triumph of scientific biotechnology over nature.
Dr Xxxxx: . A very good question. I think the solution is what I call the bootstrap chromosome. When an egg or sperm is formed, it would typically have half the chromosomes of the adult. When this unites with the other half (egg or sperm), this creates a single full chromosome set typical of the organism.

I believe that the LLIAP agent has the ability to initiate an extra chromosome replication cycle. So once a fertilised embryo within an egg is formed, it will have a chromosome set from each of its parents but only a single chromosome set from the infecting organism. The solution is for the infecting organism’s DNA to initiate an extra replication cycle doubling up the chromosomes present that are sourced from the infecting agent. In short ,converting a haploid DNA sequence from the infecting organism into a diploid DNA sequence by initiating an extra replication cycle for these chromosomes. The process that I call bootstrapping.

It runs in reverse as well. Somatic cells of the insect lose the extra chromosomes. In the long run, just the ovaries and the salivary glands carry the germs.

Goo: . If an infected insect mates with a non-infected insect, you would expect a dilution affect. However, not if there is an extrachromosomal replication cycle. it becomes obvious that the chromosomes need to boost or have an extra replication cycle to ensure that every child of an infected/non-infected mating has a complete chromosome set of the infecting organism. This is an even more amazing example of biotech. So simple, so necessary, so effective, so subtle and so deadly.

Kinkajou:. The LLIAP vector must incorporate chromosome replication segments. Chromosomes can be lost from the initial “zygote” formed from the union of sperm and egg. (The mating of an infected with an uninfected vector will give a diploid chromosomal set for the carrier organism but only a haploid chromosome set for the infecting agent/ germ).

So DNA technology guarantees that chromosomes can be replicated within meiosis to guarantee that every fertilised “zygote” will have a full chromosome set from the LLIAP insect vector (diploid) and from the LLIAP organism itself (diploid).

Dr Axxxx: . A very elegant solution in effect entrenching infection within the biosphere and guaranteeing one hundred percent penetration of insect vector populations and perfect (100%) exposure of target populations to the germ with bites.

Goo: . And being invisible helps too. As I said before, you cannot hide the signs of superior technology - and especially superior bio-technology.

Kinkajou:. Well, they are not really invisible. They just too small to be easily seen. Effectively invisible. But if you really start looking for them you start seeing the little critters absolutely everywhere.

Dynamite:
the invention which created the basis of the Nobel Prizes.

Goo: . I think technology of this order deserves a Nobel Prize.
Erasmus: . Generally, we give Nobel Prizes to things that help humanity. Not to weapons developers and murderers.
Kinkajou:. Yes but the very concept of a Noble Prize is based on the earnings from the patents on the development of dynamite. In short the proceeds of the developers of weapons and of murderers are used to fund a prize for the good of mankind.

Nobel's most famous invention was dynamite, a safer and easier means of harnessing the explosive power of nitro-glycerine; it was patented in 1867 and was soon used worldwide for mining and infrastructure development.

Swedish chemist, inventor, engineer, entrepreneur and business man Alfred Nobel had acquired 355 patents worldwide when he died in 1896. He invented dynamite and experimented in making synthetic rubber, leather and artificial silk among many other things. The money for the Nobel Prizes comes from the estate of Alfred Nobel. The capital is invested in "safe securities" per his instructions, and the interest (return) is paid out as prizes.

Erasmus: . . I don’t think we also give Nobel Prizes to nonhumans. It becomes obvious that the only sapients with technology advanced enough to produce weaponised bio-agents thousands of years ago, are unlikely to have a terrestrial (Earth) origin.

Kinkajou:. There is nothing noble about this technology, but it certainly is exceptional technology. I think the ability to catch a lethal disease 100 times and not die a day sooner is remarkable. From what I can see much of the power of its effect is based on its effect on macrophages. If you have multiple infections running at the same time, there are only a limited number of macrophages to share between them. Hence the overall effect on human organism is the same.

And if the effect on macrophages is too intensive the macrophages supply dwindles in effect limiting the ability of the infecting organism to effect the human immune system. It forms a natural feedback loop limiting the extent and severity of infection – in effect making it much less obvious and detectable.

Human mutations with fewer macrophages, suffer illnesses worse and would survive no longer.

Goo: . The basic technology is stealthy – effectively invisible. An invisible agent with an invisible vector and invisible effects on the body. And some truly remarkable adaptations to make it infective and effective. And so efficient: beyond 100% and lethal.

I think the chromosomal replication control technology is also remarkable.

Dr Axxxx: .  Having an insect lose chromosomes from its originating zygote to develop into an adult reliably and effectively, would appear to be an impossible task. And if you can do something that remarkable, you should be able to guarantee that every haploid fertilised germ cell will change to generate a diploid insect vector zygote with a diploid chromosomal set of the infecting organism.

Goo: . As I said before, every serial killer gives himself (or herself) away. So what are the clues for this.
Dr Xxxxx: . I think the basic “modus operandi” of stealth and immune subversion would be a substantial clue. I suspect that CCR5 receptor technology is also a giveaway.

CCR5 receptor facilitates Cell Entry

Goo: . Strangely, studying other's weapons teaches us about defending against these weapons and is the basis of immense understanding of the immune system.

Kinkajou:. What is a CCR5 receptor?
Dr Xxxxx: . CCR5 Is short for calcium channel receptor number 5. The calcium channel receptor is essentially form a gateway from the outside of the cell to the inside of the cell. And it is a complex gateway to understand and manipulate. Once you have worked out a solution, the temptation must be to use the solution or the basic science related to the solution again and again to save you time and money in future work.

Goo: . I understand. Once you have worked out how doors work, you tend to put a door into every building you design. And once you work out a basic design for a door, there is almost no reason to change it. It takes someone approaching the problem from a different angle to realise that you have made a mistake in using doors. For example someone else may decide that it is easier to access your building through a window, a chimney or through a landing pad on the roof, rather than a door.

And hence the serial killer is revealed.

Dr Xxxxx: . Exactly!

Goo: . So you have to wonder whether any features of the above technologies would appear in our history in other interventions/events? It would be difficult to hide the hallmarks of high-technology. High-technology guarantees efficiency and effectiveness.

You are automatically looking for the meanest and ugliest and most successful in its category in terms of “intervention/agents”.

Dr Xxxxx: . And I think there is evidence in our history of exactly that. If you think of illnesses that are capable of exterminating the human race and that are adapted to our circumstances, you cannot go past the Black Death. (Yesinia pestis). This is a germ designed to be a bio- weapon. It is designed to evade and subvert the immune system. It is designed to take advantage of circumstances present in Middle Ages human civilisation. It is designed to kill.

Yersinia pestis :
the bacteria causing the Black Death.

Goo: . And kill it certainly did and certainly does.
Kinkajou:. Yersinia pestis pneumonia is capable of killing 90% of the people it infects. Even the usual typical skin infection easily causes 50% mortality in the human hosts
Dr Xxxxx: . I think it uses the CCR5 receptor to gain cellular entry. Although outbreaks have been present throughout history to small extents, there was a pervasive extensive infectious and lethal pandemic which is so efficient and effective at killing humans, that it is unique in human history. (Early 1300s).

Kinkajou:. So would you think that this organism if it were present today would be less dangerous because the human population is healthier and better nourished?
Dr Axxxx: .  No I think the weapon planners stuffed up on this one. If you are poorly nourished and have a barely adequate immune system, the disease is less likely to kill you. Fewer lymphocytes will arrive in infected areas and thus there will be less spread of infection. Lymphocyte activity will be reduced again causing less spread of infection. The only thing that would stop this infection taking a substantial foothold today is the biotechnology that the human race possesses. The ability to make antibiotics. The ability to make vaccines targeting T cells. The ability to understand disease spread and the role of vectors.

Erasmus: . I agree there is an issue in the action of the plague bacillus. It is a much more deadly agent in healthy immune competent populations. Where there are deficiencies in vitamins, minerals and proteins, the immune response is sluggish. This results in a slowed infection in an agent designed to evade immune response. And a slowed infection results in a less virulent infection process. Something like this could easily be the difference between a 60% death rate and a 90% death rate amidst infected people.

Dr Xxxxx: . The difference between effect in the laboratory and the effect in the world at large. Often science that works well laboratory needs to be adjusted and tweaked to work well in the field. And I think the plague bacillus is one of those scenarios. A slightly less aggressively virulent and slower bacteria may well have given higher death rates.

Goo: . So that’s it?
Dr Xxxxx: . No. Approximately 500 to 600 years later after this pandemic, ( a time gap we have noticed before), there appears another pandemic of another immune evasive agent, affecting lymphoid cells, working by stealth and subverting the effects of the immune system with lethal effect. Its action is adapted to human circumstances (sexuality). Onset approximately 1950s. We call this one HIV. And this germ also has some unusual DNA coding aspects which suggest high-technology and optimisation.

HIV: the new agent using CCR5 receptors
Dr Axxxx: .  In this case the tendency for mutation gives the organism the ability to resist targeted anti-viral drugs.
Goo: . A technological adaptation to a new target population. Perhaps purposeful but perhaps just accidental luck in design.

Erasmus: . RNA viruses like CoVid have a very rapid mutation rate. However HIV seems to have stabilised mutation rate minimising the tendency for devolution of the infecting virus.
Goo: . I think the serial killers have really blown it. Dirty footprints, visible for thousands of years, using the same modus operandi and crawling with the hallmarks of high-technology and optimisation for purpose. And there is evidence of familiarity with human behaviour in terms of adapting the disease agent to its target population. Disconcerting!
Erasmus: . The most obvious conclusion is that someone somewhere wants humans controlled.

The diseases are aimed at controlling human populations.
The Flood of the Bible was aimed at controlling human populations and was rapidly followed by the introduction of the first intervention agent. The question of course in terms of the Great Deluge was did we (God and the angels) do this to ourselves to hide what we had done from external scrutiny or was there and external agency (EBE) involved in initiating the catastrophic intervention – which caused the Biblical Flood.

We (humanity and God/ the angels) certainly did know that the Flood was coming. And history shows it as something which was experienced around the world. The flood occurred in many continents and was witnessed by many different people. Many different recorded histories give evidence that something did happen.

And in considering why, by looking at the pattern of behaviour and the interventions that humanity has experienced, we can begin to see the purpose inherent.

Goo: . Do you think the ET’s made a mistake in the strategy?
Kinkajou:. I think definitely. There is a sci-fi book called Enders Game written by Orson Scott Card. It quotes “The enemy is your teacher. The enemy teaches you where you are strong. The enemy teaches you where you are weak.”

I think there are definite aspects of this in the HIV scenario. Humanity’s understanding of the immune system has burgeoned significantly in its fight the HIV virus. Deploying this weapon has taught us about the use of this technology as a weapon. The Plague Bacillus is possibly a similar scenario. When you look at the structure of the bacterium, you realise is designed to evade the immune system and to kill. A school for bio warfare.101 .

Erasmus: . I think there are also elements of desperation in the deployment both of these agents. HIV deployed 600 years ago would be a devastating agent which humanity would have few defences against. HIV deployed in the 1950s is an agent which teaches us to the technology of immunity and which by 2022 is controllable with simple treatment.

And there are other factors to consider than just the killing efficiency of an agent. Deployment of the plague bacillus in the early 1300s, reduced the human population to the point where the feudal system of government was unable to function. There were too few peasants and too few low level people to allow minimal payments for labour. The individual began to be valued and paid more and to develop new rights. And the Renaissance was born.

Goo: . Technology began to blossom. The introduction of a devastating bio-agent guaranteeing innovation in the march of technology, rather than stopping it.

Black Death: Buboes on skin : an infection

Kinkajou:. Let’s talk a little bit about the Plague Bacillus before we go on and talk about the Flood . I think it’s important to try to see how unique an event the Black Death of the 1300s truly was. To see how it stood out from the background of human history.
Erasmus: . Current Human Beliefs:
There have been three great world pandemics of plague recorded, in 541, 1347, and 1894 AD, each time causing devastating mortality of people and animals across nations and continents. On more than one occasion plague irrevocably changed the social and economic fabric of society.  The plague created religious, social and economic upheavals, with profound effects on the course of European history. The three great plague pandemics had different geographic origins and paths of spread..

Goo: . Hard to say, but I have an itchy feeling about that 600 year logistics gap. Perhaps ??

Dr Axxxx: .  Logically if you are developing a bio-weapon, it is best to start with nature. Get an existing design and optimise it. So you will find that some agents may well have been around for a long time. But it is the efficient and effective redesign of a few key DNA sequences and the adjustment of immune identifiers of the agent that give an agent its impact, (its ability to kill).

Dr Xxxxx: . The plague of Justinian or Justinianic plague (541–549 AD) was the first major plague caused by the bacterium Yersinia pestis.

The Justinian Plague of 541 started in central Africa and spread to Egypt and the Mediterranean. The contagion arrived in Roman Egypt in 541, spread around the Mediterranean Sea until 544, and persisted in Northern Europe and the Arabian Peninsula, until 549.The plague is named for the Byzantine Emperor Justinian I (r. 527–565) who, according to his court historian Procopius, contracted the disease and recovered in 542, at the height of the epidemic which killed about a fifth of the population in the imperial capital.

The strain of Yersinia pestis responsible for the Black Death, the devastating pandemic of bubonic plague, does not appear to be a direct descendant of the Justinian plague strain. However the Justinian plague may have caused the evolutionary radiation that gave rise to the currently extant 0ANT.1 clade of strains.

Dr Xxxxx: . The Black Death (also known as the Pestilence, the Great Mortality or simply, the Plague or the bubonic plague was a pandemic occurring in Afro-Eurasia from 1346 to 1353. The Black Death of 1347 originated in Asia and spread to the Crimea then Europe and Russia. It is the most fatal pandemic recorded in human history, causing the death of 75–200 million people in Eurasia and North Africa, peaking in Europe from 1347 to 1351. 

Bubonic plague is caused by the bacterium Yersinia pestis spread by fleas and their bites but it can also be spread directly from person to person via aerosols, (the variant called the pneumonic plague).

The Black Death is estimated to have killed 30 percent to 60 percent of the European population, as well as about one-third of the population of the Middle East. The plague might have reduced the world population from around 475 million to 350–375 million in the 14th century, the European population did not regain its level in 1300 until 1500. 

Outbreaks of the plague recurred around the world until the early 19th century.

Dr Xxxxx: . The third pandemic, that of 1894, originated in Yunnan, China, and spread to Hong Kong and India, then to the rest of the world. The third pandemic waxed and waned throughout the world for the next five decades and did not end until 1959, in that time plague had caused over 15 million deaths, the majority of which were in India.

Currently around 2,000 cases occur annually, mostly in Africa, Asia and South America, with a global case fatality rate of 5% to 15%.

But scientists have since found DNA evidence that Yersinia pestis could have existed much further back than previously thought -- there's evidence it existed in Europe some 5,000 years ago.

Goo: . But DNA provides an indelible fingerprint and records the characteristics of the organism. It Is the ultimate technology catching out serial killers.

Dr Axxxx: .  In the recent past, our study of the bacteria is limited to what we know about its physiology (biochemistry). Traditional classification has identified biological variants (bio-vars): the inability to ferment glycerol, the inability to reduce nitrate and the ability to ferment glycerol and reduce nitrate.

There are also atypical biological variants such as pestoides, which cause disease in a variety of rodents in Central Asia and, unlike the three classical biovars, can ferment rhamnose and melibiose. Some enzootic Y. pestis isolates from a wide variety of rodents in China also do not readily fit into the classical biovars , resulting in a new biovar designation, Microtus, for Y. pestis that do not cause disease in larger mammals and cannot reduce nitrate or ferment arabinose.

Yersinia pestis evolution
Dr Xxxxx: . A better classification system for identifying the evolution of this organism should be based on molecular signatures in particular the genomic patterns of IS100 insertion elements, supernumerary DNA islands, or multilocus variable number of tandem repeat analysis (MLVA). This technology reveals that the causative organism is so unusually monomorphic.

Goo: . Just researching online : MLVA, an abbreviation for multiple locus variable number of tandem repeats analysis, is another technique used by microbiologists to generate a DNA fingerprint or a bacterial isolate. Microbiologists usually perform MLVA after they have performed Pulsed-Field Gel Electrophoresis (PFGE) so they can get more details about the type of bacteria that may be causing an outbreak.

Dr Axxxx: .  Devignat suggested on the basis of geographical sources and epidemiological observations that each of the three biovars was responsible for an independent pandemic wave. The age estimates presented here confirm that Y. pestis is old enough to have caused historical pandemics of plague.

Yersinia pestis evolution

Dr Xxxxx: . This may not be true.
However, Y. pestis, like other young pathogens ,has evolved too recently to allow the accumulation of extensive sequence diversity. Indeed, no sequence polymorphisms were detected in six gene fragments from 36 isolates from the three classical biovars, indicating that Y. pestis evolved from Yersinia pseudotuberculosis within the last 1,500-20,000 years.

Deducing the evolutionary history of a species with so little sequence diversity is difficult, especially when markers with high mutation rates are used that may yield inaccurate branch orders caused by homoplasies and irregular molecular clock rates.

Such inaccurate branch orders are method-specific and can be recognized by comparing the results from independent methods with different clock rates.

One study therefore investigated the evolutionary history of Y. pestis by three independent high-resolution methods that have been applied to monomorphic species: synonymous SNPs (sSNPs) defined by genome scanning ,MLVA, and screening for the presence of IS100 at defined locations.

These results demonstrate that Y. pestis initially evolved from Y. pseudotuberculosis along one branch, called branch 0, from which strain 91001 split off, before splitting into branch 1 (CO92) and branch 2 (KIM).

It has been previously calculated that the age of Y. pestis is the 1,500-20,000 years on the basis of a lack of sequence diversity in the six gene fragments described above.
Those age calculations were based on two estimates of mutation clock rates, a short-term rate derived from laboratory experiments with E. coli  and a long-term rate based on the divergence time between E. coli and Salmonella enterica Typhimurium.

Unfortunately, neither clock rate estimate was applicable to the genomic analyses. The short-term rate is inappropriate because it measures all mutations, most of which are rapidly lost because of drift, whereas the sSNPs described here represent fixed nucleotides that were uniform within populations (see below). The long-term rate is appropriate but incorrect, because it ignored the fact that the time since separation of two organisms is only half of the elapsed time during which mutations have accumulated.

Dr Xxxxx: . Some super complex stuff:read at your peril, included so you can see the complexity ia assessing germ evolution. The correct synonymous mutation rate between E. coli and Typhimurium is the synonymous distance between them (0.94) divided by twice the time since these organisms separated (140 million years ago), or 3.4 × 10-9 per year. The frequency of sSNPs per potential sSNP divided by that rate then yields the age estimates for Y. pestis that are shown above.

Yersinia pestis evolution

Dr Xxxxx: . So the study suggests that approximately 13,000 years of evolutionary history separate CO92 and KIM and that the time since strain 91001 separated from branch 0 is longer (10,000 years) than since CO92 or KIM diverged from their common ancestor (average of 6,500 years).

Goo: . The key issue is the optimization. The organism may well be good at what it does. But making it work better , faster and be more deadly is the work of superior biotechnology. Any changes we would just put down to chance mutation and nature.

There is one other facet of interest. There are gaps of several hundred years between flareups. Again suggestive of logistic constraints in research/ transport and implementation.

Kinkajou:. The world of the scientist can be an ugly place.

Evolutionary branch order within Y. pestis. (a-d) Simplified branch order of the major groups as indicated by sSNPs (a), MLVA (b), and IS100 insertions (c and d Fig. 3.

A neighbour-joining dendrogram was constructed from Hamming distances based on 43 variable numbers of tandem repeat loci.

Discussion
New scientific methods involving organism identification by molecular sequencing rather than by biovars (biological variants). Are likely to give us better and less ambiguous information on the evolution of organisms.

Detecting Phylogenetic Structure in a Highly Monomorphic Species. Each of the three screening methods used here has distinct advantages and disadvantages for deducing the phylogenetic structure of Y. pestis. MLVA was the most discriminatory but the boundaries of population groupings were somewhat ambiguous. Furthermore, the high mutation rate of variable number of tandem repeat loci resulted in very long branch lengths, with corresponding problems for tree reconstruction. As a result, MLVA did not correctly detect the binary split between branches 1 and 2. It was hoped that IS100 analyses would combine adequate discrimination with reliable classification.

Of the three methods, sSNP analyses are the easiest to interpret from an evolutionary viewpoint. No homoplasies were detected, and most branches were supported by multiple, independent sSNPs. However, Y. pestis is so monomorphic that three complete genome sequences of 4.5 MB differed by only 76 conservative sSNPs,
. A definitive sSNP-based classification will probably only be possible after at least one genome has been sequenced from each of the other five populations.

With time, as additional genomes are sequenced, sSNP analysis may become the method of choice for determining the evolutionary branch structure and molecular groupings within highly uniform species. Genotyping of bacteria might then be efficiently performed by a hierarchical approach in which molecular markers for the branch structure are used to group bacteria into populations before using more variable methods with higher resolution, such as high-throughput SNP typing, whole gene microarrays or MLVA, for subdivision into genotypes.

Goo: . There is a basic problem with these analyses. They assume that random evolution produced the changes observed. Intelligence can do efficiently in short time frames things that nature at random never will.

To assess for the actions of intelligence , there needs to be a much different type of analysis. Are the hallmarks of random here or are there hallmarks of purposeful action.

Dr Axxxx: . God does things purposefully.

Goo: . Yes, but last I looked around, i think he was on our side.

Dr Axxxx: . Maybe they have a god too. Evil gods for the evil ones.

Erasmus: . Leave it. Kinkajou, give us the benefit of you eyeballing of all that we've said.

Kinkajou:. The issues that I have seen which may be significant in this discussion include:
the causative organism is so unusually monomorphic
the iterations of infection spaced by approximately 500- 600 years show a suspicious similarity to other previously noticed infection patterns. The timeframe suggests logistical restraints in deployment and implementation.

Erasmus: . Perhaps. You can look at the history with interest but perhaps there may never been answer. One thing remains obvious. The germ is a weapons grade germ. It is a killing machine. If there were multiple deployments over time frames we have noticed, there does seem to be a distinct clumsiness in the process, not at all what you would expect from intelligence that would be capable of designing such an organism.

Still deployment of weapons and remote sites and without supervision is was problematical. The difference between the laboratory and the field can be very significant.

Goo: . Let’s move on. Remember our primary purpose is to look at aliens. The three great plague pandemics had different geographic origins and paths of spread.. A distinct pattern is starting to emerge and not a very pleasant one at that. I’m sure history and the Bible has more to tell us.