Genetic Virology, In Silico Genome . Manufacturing theoretical viruses and variants, Part 2


Part 2- The Variants in Virology.

In  Part 1  covered briefly  genetic virology, in silico genome and the NGS technology used to manufacture theoretical viruses.

"To this day, no virus has been seen in or isolated from humans, animals, nor plants or their fluids. It has not even been possible to isolate a nucleic acid that would correspond to the length and composition of the genetic strands of the claimed disease causing viruses, although the isolation, presentation and analysis of the composition of nucleic acids of this length has long been possible using the simplest standard techniques."
( - Dr Stefan Lanka)

Karl Popper- Theory of Falsification
According to Popper, scientific theory should make predictions which can be tested, and the theory rejected if these predictions are shown not to be correct.

Dr Stefan Lanka:
"The definition of what can be called a scientific statement and the resulting obligations are clearly defined. Summarised:

A. Every scientific statement must be verifiable, comprehensible and refutable.

B. Only if the refutation of a scientific statement by laws of thought, logic and, if applicable, by control experiments has not succeeded, a statement may be called scientific.

C. Every scientist is obliged to check and question his statements himself."

Dr Stefan Lanka has put forward 7 argument ,  each on its own is sufficient to refute the existence claims of all 'pathogenic viruses .'


1. The fact of Alignment
Virologists have never isolated a complete genetic strand of a virus and displayed it directly, in its entire length. They always use very short pieces of nucleic acids, whose sequence consists of four molecules to determine them and call them sequences. From a multitude of millions of such specific, very short sequences, virologists mentally assemble a fictitious long genome strand with the help of complex computational and statistical methods. This process is called alignment.
The result of this complex alignment, the fictitious and very long genetic strand, is presented by virologists as the core of a virus and they claim to have thus

2. The fact of the lack of control experiments for alignment
Virologists have never performed and documented an alignment using equally short nucleic acids from control experiments.

3. Alignment is only done by means of mental constructs
In order to be able to mentally/computationally assemble the very short sequences of the nucleic acids used into a long genome, the virologists need a template to align the short sequences into a very long, supposedly viral genome strand.

4. Viruses have never been seen in a human/animal/plant or in liquids thereof.
To date, however, not a single virus has been photographed in saliva, blood or other places in human/animal/plant or fluids, although electron microscopic imaging is now an easy and routine standard technique..

5.The composition of the structures that are claimed to be viruses has never been biochemically characterized

6. Electron microscopic images, which are output as viruses, are known typical artifacts or cell- specific structures
Virologists publish a large number of electron microscopic images of structures that they pass off as viruses. They do not mention the fact that ALL of these images are typical structures of dying cell cultures or are laboratory-produced protein-fat soap bubbles and have never been photographed in human/animal/plant or liquids from them.

7. the animal experiments of the virologists refute the virus- existence assertions.
It is clear from every single publication in which such animal experiments have been conducted that the way the animals are treated produces exactly the symptoms that are claimed to be caused by the virus. In each of these publications, it is clear that no control experiments have been performed where the animals would have been treated in the same way with sterilized starting material.

So how come there are variants in virology( if viruses refuted)  and  also such an increase in variants especially  in the last two decades?
Are we basing theory on theory and refining theories to fit the originally disproved theories ?   Are scientist  aware  and discussing the inconsistancies and scrutanising their work and that of their colleagues in an ethical scientific way?

The  origin of RNA viruses , the quasispecies theory  of species the new computer NGS  sequencing technology and emergence of bioinformatics seem to have  given rise to the escalation of variants in virology. 
Some background on retroviruses and quasispecies.

Retroviruses Dr Stefan Lanka

Retroviruses were postulated as being that species of micro-organism which caused reverse transcription to occur, which, as a working hypothesis at the time in the early 1970s, was entirely reasonable. The mistake was to elevate the hypothesis to a dogma. Early gene detection techniques lent some credence to the existence of an entity that could be transmitted from one cell to another, which was unfortunate, because this, too, turned out to be wrong. Errors of this kind occur whenever technology makes available for general use a new experimental procedure, which propels a whole army of researchers into mass producing experimental data, heedless of what the biological significance, if any, of their work might be. Even worse, is the habit of making countless ad hoc adjustments to the original theory, which completely distort the original hypothesis. Correct science demands that there should be a radical re-think when this happens. If there isn't, as in this case, a fundamentally flawed concept goes haywire ending in disaster.

To the astute observer, it should have been apparent as early as 1973 that the working hypothesis of ascribing the experimentally observed phenomenon of reverse transcription to retroviruses had become untenable, when it became known that reverse transcription was anything but rare; by 1980 at the latest, the hypothesis should have been abandoned by everyone. Indeed, the extraordinarily artificial and circumscribed conditions under which reverse transcription could be induced in the laboratory should have alerted everyone to the extreme improbability of such exclusively laboratory conditions having any bearing whatsoever on naturally occurring phenomena. All the more so, as no retrovirus was ever shown to exist-for example, by being able to isolate and characterise it, and to demonstrate its transmissibility. These failures (obviously not for want of trying) should have sufficed to kill off the whole concept. It may be hard to believe that all maps purporting to represent a whole retrovirus, including HIV, are always compilations, many bits and pieces cobbled together by their authors to the best of their beliefs. They are collages. No complete retrovirus nor its RNA in its entirety has ever been proved to exist either in vivo or in vitro.

A further difficulty for the hypothesis was that it had never proved possible to show that the experimental observations attributed to retroviruses were exogenous to the cells used in experiments, i.e. that they came from outside of the cell; indeed, all the evidence pointed to the opposite, i.e. that they were endogenous (inherent) to the cells themselves.

History furnishes an unhappy precedent for this form of research. At the turn of the century experiments were conducted using highly in-bred laboratory animals. Under strictly circumscribed conditions, these displayed higher disease susceptibilities than animals which were not in-bred; the phrase 'highly in-bred' was forgotten about, and generalisations about viral infectivity were made which turned out to be wrong, from which medicine has not recovered to this day. 

In like manner, experiments are nowadays performed with cell cultures instead of whole animals, for the very good reason that they greatly speed up experiments. The disadvantage is that this limits experimentation to just one of a few cell lines, which are always cancerous, because only they will grow continuously in the laboratory. History is repeating itself: generalisations are made about the behaviour of normal cells on the basis of results obtained from highly abnormal cells.

 Such cells can incorporate extraneous pieces of DNA (into their own DNA) when added to growth medium (as normal cells can, too, only more slowly). Cells, which have incorporated such DNA, will obviously manifest characteristics for which the DNA coded, making it appear that a virus had been at work, when nothing of the sort had happened. It is easy to see, therefore, how the bizarre notion of 'infectious' DNA arose, and to conclude (wrongly) that a virus, in the conventional use of the word, is involved. The whole argument collapses, however, when it can be shown that non-viral DNA can be made to do this too, both in vivo and in vitro. If that DNA happens to be DNA arbitrarily defined to be HIV DNA (or part thereof), then clearly the cell, which has incorporated the DNA, will behave as if it had been infected by HIV.

The rules demonstrating the existence of HIV (and retroviruses in general) were never adhered to by those who devised them nor were they ever validated.

They clearly had a slight worry at the back of their minds all along that the term was used in retrovirology rather as in Alice in Wonderland-"it means what I say it means."

Until AIDS was invented, retrovirologists were a minority sect who were happy to accept each others' flights of fancy without being too critical. They could fiddle around to their hearts' content, safe in the knowledge that "retroviruses were the least dangerous of all viruses." Well-meaning and credulous colleagues, as well as aspiring virologists, journalists and, through them, laymen were mesmerized by incomprehensible jargon into believing that the mass of data on HIV and retroviruses somehow meant something. Each property relating to HIV, and retroviruses generally, can be shown to pertain to the cells used in the co-cultivation experiments. At no time have there ever been any credible grounds for thinking that these properties and components had anything to do with viruses in general, nor with "HIV" in particular.


Origins of the Concept

Quasispecies describes a type of population structure in which collections of closely related genomes are subjected to a continuous process of genetic variation, competition and selection. Quasispecieshas become very important in virology because it provides an interpretation for the extensive plasticity, both genetic and phenotypic (of biological features), displayed by many viruses, in particular RNA viruses. The quasispecies concept originated in theoretical studies on early informational macromolecules by Eigen and colleagues.
(Esteban Domingo, in Encyclopedia of Virology (Second Edition), 1999)

Scientific Context

Quasispecies theory is a population genetics theory. Population genetics, which took its first steps in the beginning of the twentieth century, addresses how changes in gene frequencies depend on measurable parameters such as selection coefficients, population sizes, mutation rates, or recombination rates, and provides a well-grounded theory for the study of evolution. Nevertheless, evolution is a very complex process and its mathematical treatment requires the use of simplifying assumptions. Choosing the appropriate assumptions is critical to build accurate models of evolution
(R. Sanjuán, in Encyclopedia of Virology (Third Edition), 2008) 


Conclusions and Prospects

Quasispecies is a theory of molecular evolutionadequate to describe the behavior of replicating entities characterized by high-mutation rates. It has found its maximum interest in the interpretation of adaptability of RNA viruses, chiefly with the recognition that populations of RNA viruses consist of complex mutant spectra, as predicted by the theory. Although the term quasispecies applies mostly to RNA viruses, the concept is also valid for other biological entities. Some DNA viruses that are replicated by low-fidelity DNA polymerases display a dynamics comparable to that of RNA viruses.
( E. Domingo, C. Perales, in Encyclopedia of Evolutionary Biology, 2016)

Some Key Points on the Impact of Quasispecies in Virology

Quasispecies insights have been instrumental for the understanding of the nature of viral populations, and to interpret intrahost evolution and pathogenesis of RNA viruses for the following reasons:

Quasispecies provides a new definition of wild type

One of the most inspiring departures from classic concepts contributed by quasispecies theory is that the wild type is no longer a defined genome with a precise nucleotide sequence, but a collection of related genomes. This means that forces that promote evolution (selection acting on phenotypes and random drift acting on genotypes (Sections 3.5and 3.6)) can operate on collections of genomes
As the complexity of mutant spectra of RNA viruses is unveiled, aided by the zooming-in power of NGS, additional implications of quasispecies become apparent,
 ( Esteban Domingo, in Virus as Populations, 2016)


Quasispecies Theory and the Behavior of RNA Viruses

Adam S. Lauring1, Raul Andino2*
PLoS Pathogens |, July 2010 | Volume 6 | Issue 7 


A large number of medically important viruses, including HIV, hepatitis C virus, and influenza, have RNA genomes. These viruses replicate with extremely high mutation rates and exhibit significant genetic diversity. This diversity allows a viral population to rapidly adapt to dynamic environments and evolve resistance to vaccines and antiviral drugs. For the last 30 years, quasispecies theory has provided a population-based framework for understanding RNA viral evolution. A quasispecies is a cloud of diverse variants that are genetically linked through mutation, interact cooperatively on a functional level, and collectively contribute to the characteristics of the population. Many predictions of quasispecies theory run counter to traditional views of microbial behavior and evolution and have profound implications for our understanding of viral disease. Here, we discuss basic principles of quasispecies theory and describe its relevance for our understanding of viral fitness, virulence, and antiviral therapeutic strategy.


From the available scientific evidence, using  logic , if ‘pathogenic ‘ viruses refuted ( see 7 reasons, each one, by itself should be enough) then all the consequent deductions eg. existence of RNA viruses and variants based on theoretical model of ‘quasispecies ‘ are false . With the introduction of NGS technology   and in silico genome new viruses and variants can be constructed via computer software . 

Are variants the inability to reproduce or validate the orginal results  ? ( see attached slide , 

Is  the dramatic increase in variants  ( eg. flu and coronaviruses) and the theorised new RNA viruses  an artefact /  fabricated technological construct ?  Are variants generated  through in silico  genomes   at a faster rate because of the use of NGS technology and errors in technology and procedures?  
Are scientist addressimg the  potential problems? 

Could  ‘ variants’   be part of normal biological processes of constant change that have been redefined by using the theoretical model  construct of  quasispecies? 

In Summary:

(Genetic Virology, In Silico Genome . Manufacturing theoretical viruses and variants, Part 1&2) 

Refuted viral theory , inferred  theories of  existence of RNA viruses , theories and models of quasispecies and variants,  where NGS technology and bioinformatics  is used to  construct theoretical and alleged   ‘pathogenic ‘ viruses and variants . 

What happend to the integrity of science?
Who are the scientists?
Where  is  the scientific debate? 
What are the clinical implications of virology?
Are any vaccines justified and  based on sound science or are they part of a human experiment? What  is the testing and vaccines for?
Why the push for vaccine passports/certificates?

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