Journal of Theoretics Vol.2-3

Mechanisms of Extinction-Viruses

Author: Devaraj M.S.

Abstract: The author formulates the hypothesis viruses are non-living mechanisms which arose as a negatively impact product of abnormal recombination from host cells. The hypothesis and supportive information are explained herein. 

Keywords: extinction mechanisms, recombination, Introns, lysogenic virions, lytic virions, oncogenes, retroviruses, viroids.


What is extinction? A simple question that may possibly answered by the simple statement, “Extinction is a process by which unfit groups or individuals are eliminated in the process of selection and evolution.” This suggests that the same selection process for evolution is also responsible for extinction. That is, in a process of selection, a group can incur any one of two possible outcomes, namely evolution or extinction based on its level of fitness. How does my model predict extinction?

I had provided divisions or means of compartmenting different species based on the ratio of the two types of selection that I had suggested.1 Interpreting the types and effects of selection mechanisms as proposed by the author in the previous article, the following four postulates are drawn.

(1) Organisms with a high level of independent selection and a low level of competitive selection experience tachytelic rates of evolution
(2) Organisms with low levels of both independent and competitive selection experience bradytelic rates of evolution.
(3) Organisms with a balance between the levels of both selection types experience horotelic rates of evolution. (moderate levels of independent and competitive selection)
(4) Organisms with high competitive selection (high dependency) and very low independent selection face extinction.

This model indicates that two possible extremes in the balance between independent and competitive selection in certain life forms can exist. The first are groups where very low or no independent selection takes place and the second where extreme levels of competitive selection take place (which suggests that it is accompanied by a low level of independent selection). It is easy to visualize the method by which a group with high level of competitive selection may become extinct, but it is not easy to understand or explain why a group which does not have any form of adversity should or would become extinct.

Consider a group that does not have very high independent selection factors dictating its survival. Assuming that such a species will not be able to proliferate continually in the same way and thereby being overrunning nature, what could be the methods of population check be? Since the method of check is not made by external independent selection methods, it maybe that the methods inhibiting survival are internal to the organism. 

Unlike the idea of racial senescence2,3, the following idea is based on objective findings and logic. Factors such as behavioral aberration may be a method for population control. Behavioral aberration can definitely be seen in many situations like the lemming and rat where excessive population seems to trigger abnormal behavior like suicide, cannibalism, excessive aggressiveness, and homosexuality. This can be attributed to an increase in stress. Such a behavioral aberration has been seen to occur in most higher organisms that are subject to conditions that lack independent selection and excessive competition (e.g. the guppy fish, Poecilia reticulata and the common rat on which overpopulation experiments have been conducted).

The second possible method is genetic aberration, or the control of the population through genetically arising mechanisms. Just as recombination can produce variations in a species beneficial to it in overcoming selection, it is possible that recombination could also produce lethality to check the population growth.

Apart from the well known “lethal genes,” a term used to describe the homogeneity of characteristics which are unviable (lethal) in the homozygous state (such as sickle cell anemia, cystic fibrosis, and phenylketonuria), my suggestion is that the recombination of genes with varying genetic distances may be able to produce viruses. The lethality or virulence of the virus seems to be proportional to the genetic distance between these recombinant genes, which is usually also proportional to their spatial distance. 

Supporting Evidence

The characteristics of viruses seem to support to this theory of recombination as the basis of viral existence as outlined below:

  • Viruses are host specific and are often tissue or cell specific. 

  • A virus is basically a piece of nucleic material enveloped in a capsid made of capsomeres and sometimes an additional coat of protein.

  • Viruses do not possess a cellular structure. 

  • Viruses cannot reproduce on their own. What is interpreted as viral replication (and the mutation) of viruses is a common misinterpretation of viruses just replacing the natural genetic matter of a cell with their own material, thereby causing the host cell to produce the viral DNA or RNA (in the latter case would be by using reverse transcriptase). This is more than a difference in semantics since a virus can not duplicate itself. 

  • Viruses can “grow” only in living cells. There are clear-cut indications that viruses are incapable of any synthesis or alteration of proteins by themselves. 

  • Viruses do not have any true metabolic activity. They never possess energy in any form at any stage of their cycle. They have no organelles or any kind of cytoplasmic material common to most cell structures. They are the most obligate parasites if they are to be considered as living organisms. 

  • Nucleotide sequence analyses show that the polymorphism in genetic material is significantly greater in those DNA sequences which do not determine amino acid sequences (Introns) compared to that which code for amino acids.4 

  • It is generally accepted that viruses probably evolved after prokaryotic and eukaryotic cells evolved.

  • The base sequence of the viral src gene, which codes for a kinase that phosphorylates proteins, has a base sequence similar to that of a host cell gene, which plays part of the regulatory role in the growth of a normal cell. This has therefore suggested the idea by researchers that the oncogenes of retroviruses are of cellular origin.5 This then lends credence to the suggestion that viruses may also be of cellular origin. 


(a) They are capable of mutation. 

Argument: As suggested above, it is the host cell that produces copies of the viral genetic material and hence any mistake is not because of the genetic coding of the viral template, but rather due to the host cell. 

(b) Viruses are self-replicating as demonstrated by Mills and Eigen. A Qb virus, which is 4,220 nucleotides long upon adding a replicase enzyme and various chemical compounds, started replicating on its own.6

Argument: Such replication, though showing complexity is not necessarily indicative of life. A crystal of sugar suspended in a sugar solution accumulates molecules of sugar and grows. This is not indicative of sugar being a life form. The presence of an enzyme catalyzes the build up. This is supported by inversion, where the same process when initiated in reverse, the Qb replicase starts splicing nucleotides on its own. De novo forms were apparently produced, capable of ‘adapting’ to different environmental conditions. 

(c) Lysogenic cycles. Lysogenic cycles are where the ‘life’ cycle of a virus is interrupted by a long period of dormancy in the host cell. That is, the viral DNA or RNA is copied faithfully by the infected cells but the cycle of the virus does not get completed and cell lysis does not take place for many generations of new infected cells. Such complex cycles may indicate that viruses are living organisms.

Argument: It maybe that lysogenic cycles are precursors of a lytic cycle which could eventually be ‘evolved’ by the virus. That is, a virus that has a lysogenic cycle and is capable of existing in a cell as a prophage, is not sufficiently developed and requires an activation mechanism for it to be able to reach the vegetative state if it does not remain autonomous after infecting the cell. When the host cell makes sufficient ‘mistakes’ in reproducing the lysogenic form, the viral nucleic material is sufficiently distinguished that it is able to start self assembly once the necessary head and tail protein, nucleic material, and capsids are ready. After this stage, the viral DNA is probably incapable of being integrated into the host DNA adequately for it to exist in a lysogenic phase. 

(d) The contractile tail sheaths and insertions of the the DNA in T4 phages, suggests life like motile activity.

Summary of the Model Proposed

(1) Viruses are non-living mechanisms of extinction.
(2) They have “evolved” through the recombination of genes. 
(3) As opposed to the cell organelles which appear to be endo-symbiotic life forms and apparently integrated with Eukaryotic cells after having originated outside initially, probably as some kind of autotropic bacteria, viruses are formed in eukaryotic and prokaryotic cells, that is they evolved in the cell and later existing in the environment.
(4) Their virulence is directly proportional to the genetic distance of their parent genetic material.
(5) Their virulence is directly proportional to the original geographical distance and the level of isolation between the interacting organisms. 
(6) Viruses are incapable of adaptation. Any such ‘adaptation’ is a result of variations that are produced by the host cells. 
(7) It is possible to ‘track’ the origin of viruses to their parental host strains. Host DNA at the probable point of origin (genetic and geographical) will display absolute similarity to the complete sequence or segments. It is likely that Introns will match segments of the viral DNA. 
(8) It is possible to evolve a completely new viral strain by combining genetically distinguished groups under special conditions such as overcrowding at least one group or disseminating the overcrowded group into the second group slowly.
(9) New viruses will keep appearing. 


Since the origin of viruses is the recombination of genes, where particular sequences form, the hypothesis here is that a virus is created only when the recombinant offspring (of the genetically distinguished parents) possesses the necessary replicase enzyme for the virus. This is a suggested evolutionary path that could presumably follow.

(a) Genetically distinguished sub-specific or racial groups may come together after overcoming isolation barriers.
(b) The offspring of this combined gene pool may possess recombinant DNA. The source of the renegade DNA may be from Introns, the intervening sequences. 
(c) This Recombinant DNA will code for enzymes that in turn are responsible for short segments of RNA or DNA encryption. 
(d) Those that catalyze for RNA segments are responsible for viroids which undergo lysis and become pathogenic immediately. Renegade DNA segments exist as a part of the host genetic material. These require an activation mechanism to reach a vegetative state. However unlike the naked virions which cannot exist in a prophage like condition (as they are RNA strands) and hence would probably cause cell lysis. Lysogenic DNA exist in the prophage state until progressive recombination results in further refinements such as capsomeres, capsids, and Protein envelopes. 
(e) Of these, some of the completed virions may “mature” early during their replication in the cell and thereby undergo lysis as RNA retroviruses. Those that retain the DNA genetic structure may take a longer time to evolve a lytic capability. Their initial cycles may be lysogenic cycles where the nucleic material keeps getting inherited and transmitted but without lysis occurring for many generations. Such lytic cycles may be indicators of “mature” DNA viruses. 
(f) Host cell replication may not always be perfect. In the addition of viral nucleic material, oncogenic cytokinins and auxins are liable to cause further “mistakes” to occur which means that the copy may not always be faithful to the original. 
(g) These “mistakes” in replication, supply the necessary variation that allows the virus to exist and replicate despite the adaptation of the host’s defenses. In short, the virus-host conflict is actually a conflict between the renegade infected cells and the host’s defenses. 


It is evident that some retroviruses can cause the development of oncogenes. Using the spectral karyotyping method developed by Tom Reed and Colleagues at the NIH, oncologists know that abnormal chromosomes are composed of as many as six different chromosomes.7 These abnormal chromosomes are often made up of the recombinant genetic material. That is, recombinant DNA can be found in most advanced cancer cells. 

Therefore there can be two situations for the origin of oncogenes. One is the automatic origin consisting of recombinant DNA, where the recombination process is at a very primitive stage and the genetic disposition of the recombinant cells is such that they only code for uncontrolled reproduction. The second origin of oncogenes is that they are a secondary effect of the virus’ infection of the host. Hence in the figure below, oncogenes are represented as being primitive parallel-evolved cells from recombinant DNA along with the basic primitive viroids. While the viroids are spliced as whole nucleotide sequences, oncogenic sequences are probably an active part of the host chromosome.

Suggestions for Verification

(I) Relative mutational rates of the virus should be directly related to the genetic variability of the host. That is, if the different host species and the different types of viruses that infect them are considered. The rate of mutation per 100,000 gametes for a trait such as lysis (as in Strickberger8) is observed for the virus. The ratio between the mutation rates for the virus and that of its host should be similar in all host-virus relationships. In other words, as the host mutation rates increase, so should the mutation rates of the infecting virus. There may need to be allowances made in those with very short nucleotide lengths, as this may perhaps allow for a greater mutational speed.

(II) Intron lengths and the prolificacy of viruses afflicting a species should bedirectly related. An increase in one should correspond to an increase in the other.

(III) Complex virions followed by lytic and lysogenic viruses and viroids should increase the level of difficulty in obtaining a vaccine. That is, complex viruses should be easier to vaccinate against as compared to lytic ones.


This theory concludes what seems to be obvious: viruses are not organisms (life forms) but rather a by-product of recombination, which incidentally acts as a selection and extinction mechanism. 

The most famous extinction event of them all is that which occurred 65 million years ago at the end of the cretaceous period of which the asteroid impact hypothesis has been proposed that is based on findings of relatively large deposits of iridium around the Yucatan Peninsular. I am not aware of any disease epidemic theory that has been actively proposed and investigated which may even be a more probable conclusion.

Considering this hypothesis on the nature of viruses, it is possible to envision a scenario where the larger animals lacking predators and other population control mechanisms may have succumbed to viruses that came from their own recombinated DNA. Such a dinosauridae virus would probably not have affected our mammalian ancestors which could explain the continuation and expansion of mammals thereafter.


1. Devaraj, M. 1999, archived articles, "A New Taxonomy of Selection", Oct/Nov issue in  Journal of Theoretics.

2. Russell, D. A., 1979. The enigma of the extinction of the dinosaurs. Ann. Rev. Earth Planet Sci., 7. 163-182. 

3. Hallam, A., 1987. End-Cretaceous mass extinction event: Argument for terrestrial causation. Science, 238, 1237-1242. 

4. Strickberger, M.W., 1990. Structure and Interactions of populations in Evolution, Jones and Bartlett Publishers, pp 462

5. Fraenkel-Conrat, H., Kimball, P.C. & Levy, J.A. (1988). Virology, 2nd edition. Engelwood Cliffs, NJ: Prentice-Hall.
Luria, S.E., Darnell, J.E., Jr., Baltimore, D. & Campbell, A. (1978) General Virology, 3rd Edition, New York: Wiley.
Martin, S.J. (1978). The Biochemistry of Viruses. Cambridge University Press.

6. Eigen, M. 1983. Self-replication and molecular evolution. In Evolution From Molecules To Man D. S. Bendall (ed.). Cambridge Univ. Press, Cambridge, pp 105-130
Mills, D. R., F. R. Kramer, and S. Spiegelman, 1973. Complete Nucleotide sequence of a replicating RNA molecule. Science, 180, 916-927
Miele, E. A., D. R. Mills and F. R. Kramer, 1983. Autocatalytic recombination of a recombinant RNA. Jour. Mol. Biol., 171, 281-295. 

7. Varmus, Harold E., From the Excerpts of the Foundation Day Lecture at the Centre of DNA Fingerprinting and Diagnostics, Hyderabad, India, on New Perspectives On Medical Research, as published in the Science Supplement of The New Indian Express (Science Express), Page 1, issue dated March 14th, 2000.

8. Strickberger, M.W., 1985. Genetics, 3rd ed. Macmillan, New York.

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