1.9 ORIGIN OF VIRUSES

 

The question of the origin of viruses is a fascinating topic but as so often happens when hard evidence is scarce, discussion can generate more heat than light. There are two popular theories: viruses are either degenerate cells or vagrant genes. Just as fleas are descended from flies by loss of wings, viruses may be derived from pro- or eukaryotic cells that have CHAPTER I TOWARDS A DEFINITION OF A VIRUS 15 dispensed with many of their cellular functions (degeneracy). Alternatively, some nucleic acid might have been transferred accidentally into a cell of a different species (e.g. through a wound or by sexual contact) and, instead of being degraded, as would normally be the case, might have survived and replicated (escape). Although half a century has elapsed since these two theories were first proposed, we still do not have any firm indications if either, or both, are correct. Rapid sequencing of viral and cellular genomes is now providing data for computer analysis that is giving an ever better understanding of the relatedness of different viruses. However, while such analyses may identify the progenitors of a virus, they cannot decide between degeneracy and escape. It is unlikely that all currently known viruses have evolved from a single progenitor. Rather, viruses have probably arisen numerous times in the past by one or both of the mechanisms outlined above. Once formed, viruses are subject to evolutionary pressures, just as are all other organisms, and this has led to the extraordinary diversity of viruses that exist today. Two processes that contribute significantly to virus evolution are recombination and mutation. Recombination takes place infrequently between the single molecule genomes of two related DNA or RNA viruses that are present in the same cell and generates a novel combination of genes. Of far greater significance is the potential for genetic exchange between related viruses with segmented genomes. Here, whole functional genes are exchanged, and this type of recombination is called reassortment. The only restriction is the compatibility between the various individual segments making up the functional genome. Fortunately, this seems to be a real barrier to the unlimited creation of new viruses, although it is not invincible, since pandemic influenza A viruses can be created in this way (see Section 18.7). Mutation is of particular significance to the evolution of RNA genomes as, in contrast to DNA synthesis, there is no molecular proof-reading mechanism during RNA synthesis. Mutations accumulated at a rate of approximately 3 × 10−4 per nucleotide per cycle of replication, whereas with DNA this figure is 10−9 to 10−10 per nucleotide per cycle. In other words, an RNA virus can achieve in one generation the degree of genetic variation which would take an equivalent DNA genome between 300,000 and 3000,000 generations to achieve. Once formed by reassortment, an influenza A virus evolves so rapidly that it takes only 4 years on average to mutate sufficiently to escape recognition by host defences and to reinfect that same individual

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