In contrast to other microbes and multi-cellular
organisms, the origin and evolution of viruses is
mostly unknown. Our knowledge concerning their
origin is lost in a sea of conjecture and speculations,
hardly supported at all with precise scientific
evidences. For example, viruses have never been
detected as fossil particles, probably because they
are too small and too fragile to succumb to fossilization
processes. Even in fossilized biological materials such as plant leaves or insects in amber,
preserved nucleic acid sequences of viruses have
never been detected. Hence, evolutionists are limited
in their ability to precisely reconstruct an evolutional
history of viruses. However, in spite of all
the difficulties in understanding their origin and
evolution, several theories more or less successfully
explain the basic observed facts [1–3].
Due to the fact that the genome of viruses
underlies mutation and genetic recombination,
viruses probably evolve according to a form of natural
selection, very similar to that governing other
living things. It seems that this simple fact may
well provide enough support for scientific acceptability
of several commonly discussed hypotheses
on virus origin and evolution. Currently, there are
three such hypotheses. The first hypothesis is the
so-called theory of ‘‘regressive evolution’’, which
proposes that viruses descend from free-living
and more complex parasites. According to this theory,
ancestral viruses developed a growing dependence
on host-cell intracellular ‘‘machinery’’
through evolutionary time, while retaining the ability
to auto-replicate, like mitochondria that have
their own genetic information and replicate on
their own [2–4]. The second hypothesis is the socalled
theory of ‘‘cell origin’’, which assumes that
viruses reflect their origin from cell DNA and/or
messenger RNA, which acquired the ability to
auto-replicate, create extracellular virions, exist
and function independently. Finally, there is the
theory of ‘‘independent’’ or ‘‘parallel’’ evolution
of viruses and other organisms, which assumes that
viruses appeared at the same time as the most
primitive organisms [1,3,4].
Whatever the advantages and disadvantages of
each theory are, the ability of every cell (excluding
cells without a nucleus, e.g., the erythrocytes of
mammals) to release DNA/RNA sequences or de
novo created viruses is unique and amazing. At
the same time, the cell’s ability to release DNA/
RNA sequences shows a high level of evolutionary
conservation. These facts might be well enough
motifs for identification of positive selective pressure
that could be linked with this genome ability,
as well as a highly important thesis for better
understanding of origin and evolution of viruses,
and even life as we know it [3–5]. Several factors
of positive selective pressure could play important
role in development and evolutionary ‘‘symbiotic’’
linking (conservation) of genome and its ‘‘instability’’,
which is probably responsible for cell ability
to emit de novo created viruses: (i) the possibility
of horizontal and vertical dissemination of gene
blocks, and their incorporation into the cell genome
of new hosts; (ii) the possibility of acceleration
of evolutionary processes, which could result
in rapid diversification of species and sometimes
quicker and better adapting to environmental conditions;
(iii) the possibility that de novo created
viruses can act as natural biological weapons
against predator and/or concurrent species.
There are a number of complex molecular life
forms that blur the boundaries between cells and
viruses. Also, there are pieces of self-replicating
genetic material found in bacteria, e.g., episomes,
which evolve independently of their hosts, and can
even move from one host to another – but carry
genetic information that may be toxic or beneficial,
even essential, to their host. In the case of
the beneficial role of episomes, many bacteria
would be unable to reproduce at all without them.
Episomes are, in many ways, quite similar to
viruses – except that they only reproduce themselves
when their hosts do, whereas viruses reproduce
themselves hundreds of times, causing
disease. According to this way of thinking, viruses
probably co-evolve with their hosts, like any ‘‘good
parasite’’. There appears to be quite a lot of justification
for this idea, especially from studies of
viruses such as papilloma viruses, endogenous retrovirus-
like sequences in animal genomes, and herpes
viruses. For example, the divergences of
primates and of birds related to chickens have been
traced by comparing the types and sequences of
retroviral-derived sequences in their genomes. It
has also been repeatedly shown that the closest
relatives of human papillomavirus types infecting
particular tissue types (e.g., cutaneous wart types,
genital mucosal types) are those viruses infecting
similar tissue types in other primates, indicating
that these tissue preferences were well established
before the divergence of humanoid apes from the
primate line [1,3,4].
Answers to all your Biology Questions
