The evolution of viruses and how they cause disease.
The origin and evolution of viruses and viral bottlenecks during multiplicity of infection.
How did viruses evolve, where do virus come from. There is no easy or single answer to these questions because there is a great variety of viruses and it is rather difficult or impossible to find a point in the history of viruses where we can relate all viruses. Viruses do not have a common ancestor, they evolved separately (Wessner, 2010). Viruses are pieces of genetic material (DNA or RNA) surrounded by a protein coat. Viruses are not living and they are not cells (they are acellular), they are obligatory parasites and they cannot replicate outside the living host. To trace the origin of viruses is a complicated process due to the fact that viruses have a fragile nucleic acid and do not leave fossils (Emerman and Malik, 2010). Viruses have limited host specificity in terms of which organisms they infect, although other viruses have a broad species specificity and this is achieved through adaptation and evolution. Other viruses evolve to be bacteriophages, in this state they become useful to many medical research studies as they are able to infect bacterial cells, while the host organism remain uninfected.
Up until now scientist don’t really know where do viruses come from, evolution and origin of viruses is but there are many theories and hypothesis presently used to predict the origin of viruses. The great diversity amongst viruses shows that they have multiple origins. Virologist use theories and hypothesis to predict the origin and the evolution of viruses (Wessner, 2010), at the moment there are currently three theories used to predict the origin of viruses, which are: progressive theory, regressive theory and co-evolution (virus-first) theory.
The virus first hypothesis diverts from both the progressive and digressive hypothesis of viral evolution, it states that viruses existed first or co-existed with the cells that they affect (Koonin and Martin, 2005). The genes of the virus seem to share some properties with the host cell and viruses are more related to their host cells than they are to other viruses (Koonin and Martin, 2005). The theory about co-evolution of the virus with their host cells suggest that viruses might have evolved at the same time with their host cells and they might have evolved from complex molecules of proteins and nucleic acids (Katzourakis et al. 2005). Viruses could have co-evolved with their host since they resemble their host cells more than they resemble other viruses, the evolution of both the cells and the viruses influenced the evolution of each other through interactions such as parasitism and mutualistic relationships (Bandin and Dopazo, 2011). The co-evolution theory argues that viruses and host cells evolved in ancient biological interactions that allowed the evolution of viruses to be influenced by the evolution of their host cells and hence viruses are host specific (Connor et al. 1994). The limited host range of viruses when infecting a cell, due to the requirements of certain receptors and the machinery inside the cell needed to support viral replication gives insights to co-evolution theory (Matrosovich et al. 2000).
The progressive hypothesis states that viruses originated through a progressive process. The progressive hypothesis predicts that viruses are pieces of genetic material that escaped the cell and were able to enter another and thus infecting it (Lander et al. 2001), they gained the ability to move between cells. The progressive hypothesis predicts that the viruses might have evolved from pieces of DNA that gained the ability to move out of the cell and as they were out of the cell they developed parasitism in order to replicate their genome (Lander et al. 2001). The progressive theory is largely supported by retrotraspoons as they have the ability to move along the genome. A viral example is retroviruses as they are able to infect a cell and bud out of that cell to infect other cells.
Viruses might have evolved in a regressive way, which states that virus might have been smaller cells that parasitized larger cells and as they gain parasitism the genetic information that was not necessary for replication was lost or it was lost before they develop parasitism and loss of genetic material associated with reproduction might have been a driving force in the adaptation of viruses to be parasitic in nature (Andersson et al. 1998). The regressive hypothesis states that viruses might have been cells that existed independently and overtime they lost their key genes to exist independently, hence they developed parasitism (Andersson et al. 1998). The Smallpox virus and the giant virus Mimivirus are much bigger and very complex than other viruses (La Scola et al, 2003). Their complexity and larger genome has resulted in less dependency to the host cell for replication than compared to other viruses. The pox virus carries enzymes essential for the viral replication inside the cell and this offers evidences suggesting that viruses might have been smaller cells that existed in a symbiotic relationship with the host cell but as they became more dependent to the host cell they became parasites and some of their genes were continuously lost. Since the multiplication of viruses is very rapid and error prone, more strains of the virus evolve overtime (Drummond et al, 2003).
Multiplicity of infection
When different viruses infects the same host cell, competition will take effect between the different viral types, or the different viral types may recombine and complement each other by combining resistance genes and producing a gene that offers high resistance. These viral activities are influenced by the multiplicity of infection of viruses within a host cell. The study of multiplicity of infection offers the opportunity to study the heterogeneous nature of virus populations at different stages of viral infection and the nature of viral populations in different infected organs. It is highly thought that the viral load within a host cell increases continuously in a host cell as a result of the increase in the multiplicity of infection and as more and more cells get infected by the virus (Meunier et al. 2005). However this is not usually the case, the viral load of viruses infecting the same cell may have an equal ratio of viral load since different viral strains can compete equally. The disadvantage of multiplicity infection is the competition for host resources resulting in the exploitation and sudden death of the host cell.
The statistical analysis from the research highlighted that the number of viral genomes with the potential of establishing infections in neighbouring cells after the first cell to cell movement slightly decreases with each movement due to narrow genetic bottlenecks by the host cell. The decrease in the viral population during cell to cell movement suggests that the viral population are using the small rapid bottlenecks as their advantage to select for their most adaptive variants in the changing environment of the host cell, rather than losing their viral fitness and robustness through genetic bottlenecks (Zwart and Elena, 2015). The estimated size of bottlenecks in cell to cell movement is very low in order to select for the fittest strains to survive, if bottleneck sizes were large the transmission of cell to cell would diminish due to the transmission of selfish genomes that are unable to replicate well by themselves. Viral bottlenecks are likely to select for the fittest strains and not always for the most virulent strains, because the host cell population will be wipe out if viruses become more and more virulent. The selection of viral strains by genetic bottlenecks happen both within the host cell and when the virus is transmitted from host to host (Zwart and Elena, 2015). The viral population that survives genetic bottleneck is the founder population and it is genetically less diverse compared to the initial population.
Viral bottlenecks occurring at cellular level influence the bottlenecks that are occurring during transmission within different host cells or colonization of different organs. Multiplicity of infection drives the behaviour of viral population within the host cell as they will experience selection pressures that select for the most adaptive strain. Virus bottlenecks and multiplicity of infection have a huge role in virus evolution and more research directed at how virus infects the host cell will give more insights on virus evolution.
So where do viruses come from? Viruses co-evolved with their host cells and they might have been pieces of naked nucleic acid that were able to escape the cell and gained the ability to move between the cells. Viruses are derived from cellular genetic material that has acquired the capacity to exist outside their cell of origin, even though they later need the cells to replicate their genome. Although these theories might not be correct but they give clues about the origin and evolution of viruses. According to the evidence from different hypothesis, the fact that viruses affect certain cells (specific host), resemble their host cells more than they resemble other viruses and they require specific receptors to affect certain cell, I support that viruses co-evolved with the cells they infect. Viruses must be considered to be polyphyletic in origin, they have multiple independent numbers of origins and if you go down the evolutionary time line you find that they originated independently and at different times. In the three theories proposed for the viral origin, no theory is better than the other and since viruses are polythetic in origin, the three theories might give us clues on the independent evolution of viruses. To date, there is still no clear understanding of how viruses existed. They may have originated from mobile genetic components that developed the ability to move within and between cells. They may have been independent living organisms that lost key reproduction genes and adapted parasitism. Viruses might have also existed before the cell and through evolution gave rise to a cellular life. Further scientific research will shed more light on the evolution of viruses.
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