Throughout history, viruses have been one of the major causes of disease and infection within humans, and have been responsible for a multitude of epidemics, including avian flu, the Spanish flu, and most recently, swine flu (Nicholls 2006). Viruses are unique organisms in that they lack the ability to replicate independently and require a host organism’s proteins to replicate its own genetic material. This has led to the argument that by the strictest definitions, viruses are not living (Moreira 2009). However, viruses have been shown to exhibit evolutionary abilities, and have been reported to become resistant to antiviral drugs (Gilbert & Boivin 2005). The ability of viruses to evolve therefore points to the fact that viruses have an evolutionary history and, by extention, an origin. Many models of the origins of viruses have appeared over time, though there are three prevailing theories that have passed the test of time: the cellular origin, regressive, and coevolution hypotheses.
The cellular origin hypothesis suggests that viruses originated as a product of mobile genetic elements. These mobile genetic elements include plasmids, which are free floating pieces of DNA that can move from cell to cell, and transposons, which are genes that can move around within the genome of an organism (McClintock 1950). As viruses are essential packets of genetic material, this theory is not exceptionally far-fetched. The ability of these mobile genetic elements to remove themselves from the genome could have resulted in free floating DNA or RNA that passed between cells to replicate, eventually evolving to build a body and improved infilration systems (Forterre 2006).
The regressive hypothesis suggests that viruses originated as a product of regression and loss of genetic material. Viruses in this hypothesis would have started off as free-living cells that may have formed symbiotic or commensalistic relationships with other species, but due to environmental or competitive pressures, would have evolved to form a niche by removing essential parts, parts that its symbiote also contains (Andersson et al. 1998). This resultant reduction in body composition in the pre-viral entity would have resulted on a higher dependancy on its symbiote, and over time, develop a parasitic relationship. Further reductions in body composition would have resulted in the inability to replicate independantly, and form the first viruses by today’s definitions. Evidence for this theory can be seen in today’s obligate intracellular parasites, such as chlamydia, which are considered to be living, but cannot self replicate (Forterre 2006). Obligate intracellular parasites serve as an example of a possible intermediate during the evolution of viruses.
The coevoltion hypothesis suggests that viruses originated alongside the origin of cells. As nucleic acids became the method an organism stored information about itself, viroids may have appeared as molecules of RNA which were able to replicate by itself by matching with surrounding nucleic acids floating in the environment (Forterre 2006). This may have led to a shift in replicative processes as cells became more and more complex, and were able to regulate their own replication. These viroids may have then shifted to invading early cells, seeing it as a more effective method of replication. Evidence for this theory can be seen in today’s existing viroids, which do not code for proteins, and only replicate (Tsagris et al. 2008).
As of now, no one theory exists that explains all the complexities of the origins of viruses, but these three theories provide different perspectives on the matter, and can aid in other aspects of virological research. While it is possible that viruses evolved from mobile genes, it is also equally possible that they originated alongside the origin of cells, or evolved from cells in a regressive fashion. Continual research in this area may provide more information that may shed light on the realtionship bewteen viruses and living organisms.
Works Cited:
Andersson, S. G. E. et al. (1998). “The genome sequence of Rickettsia prowazekii and the origin of mitochondria.” Nature 396:133–143.
Forterre P. (2006). “The origin of viruses and their possible role in major envolutionary tarnsitions.” Comparative Genomics and Evolution of Complex Viruses 117(1):5-16.
Gilbert C, Boivin G. (2005). “Human Cytomegalovirus Resistance to Antiviral Drugs.” Antimicrob. Agents Chemother. 49(3):873-883.
McClintock B. (1950). “The origin and behavoior of mutable loci in maize.” PNAS. 36(6):344-355
Moreira D, Lopez-Garcia P. (2009). “Ten reasons to exclude viruses from the tree of life.” Nature Reviews Microbiology 7:306-311.
Nicholls H. (2006). “Pandemic Influenza: The Inside Story.” PLoS Biol 4(2): e50.
Tsagris EM, Martinez de Alba AE, Gozmanova M, Kalantidis K. (2008). “Viroids.” Cellular Microbiology. 10:2168-2179.