Virus Evolution Lab Report

Introduction

Viruses are obligate intracellular parasites that are known to harm humans, animals, plants, and bacteria. It is for this reason that research is being devoted to their evolution in hosts. Virus evolution can be microevolution, which is small genetic changes in a population, or macroevolution, which is a large genetic change in a population that may lead to new virus species. Virus evolution is driven by natural selection and genetic drift. Natural selection involves mutations, and is often a rapid process as opposed to genetic drift which is a much slower process involving recombination, complementation, and competition. However, genetic drift can act faster in small populations. Both natural selection and genetic drift can occur

It is the number of viral genomes entering and replicating within a cell. It is also known as the gene copy number. The MOI affects interactions between virus genotypes. For example, recombination cannot occur if only one viral genome (MOI=1) enters a cell. If one viral genome enters a cell there cannot be competition and complementation. In particular, recombination is essential for genetic variation. Therefore the control and regulation of MOI is a strategy the virus uses to achieve colonisation and infection. For example, a study done on lysogenic bacteriophages showed that the bacteriophage multiplies and kills the host if the MOI is 1. However if the MOI is more than 1, the phages tend to integrate into the host genome and not kill the cell. Different viruses have different MOI values depending on their biological properties. In a study by Gonzalez-Jara et al., the MOI of Tobacco mosaic virus in its systemic hosts Nicotiana benthamiana was estimated. This was done by monitoring the progress of infection of two TMV variants using fluorescent proteins GFP and RFP. MOI was high, and during colonisation it decreased from 6 to 1,5-2. At higher MOI levels infection cycles were frequent. The decrease in MOI overtime could have been a result of competition between the two TMV variants, where one variant caused extinction of

During this journey they encounter host defences, limited availability of non-infected cells, and limited availability of surface receptors used to bind and invade the cell or host. A change of host is a selection pressure on the virus population. Selection pressures are genetic bottlenecks. They reduce the population size and genetic diversity. Physical barriers (i.e. cell wall, lack of plasmodesmata) in the host can also impose selection pressures. Genetic bottlenecks lead to founding viruses that generate a new subpopulation. They can occur at different stages in the lifecycle of a virus, and can lead to Muller’s ratchet whereby the virus population becomes dominated by defective mutants as a result of releasing the “wrong guy”. Muller’s ratchet is a mutational meltdown. However, a bottleneck can be used as an adaptive strategy where a fit mutant is released, resulting in a population dominated by best-adapted mutants. A study by Miyashita and Kishino, showed that plant RNA viruses use genetic bottlenecks for rapid selection of adaptive variants in trans-acting genes. Two Soil-borne wheat mosaic virus (SBWMV) RNA2 vectors were used to co-inoculate host plant leaves. It was found that most infected cells had only one of the vectors, suggesting spatial separation. Spatial separation proves further that plant RNA viruses encounter cell-to-cell bottlenecks.