Viral Quasispecies Increased Complexity and Persistence of Replicating Genomes

First formulated by Manfred Eigen, the existence of quasispecies is a fascinating offshoot of the evolutionary theory. A typical species reproduces offspring with the same genotype. Although mutations do occur, they do so relatively infrequently, and the children of mutants will then be born with the same genotype. This is true of most complex organisms.

In contrast a quasispecies is one in which there is a high rate of mutation. The individuals are all highly related, even though the genotypes of the offspring will be different than the parents. The sequences are copied and will show up again and again. It can be visualized as a cloud, with all of the individuals placed somewhere on this cloud. Unlike in a species, those with the greatest reproductive success do not compete and possibly take over, as their children will have yet a different genotype. This effect can be seen in viruses, and research has shown drastic repressions in the complexity and strength of these viruses.

The article Quasispecies Structure and Persistence of RNA Viruses by Esteban Domingo, Eric Baranowski, Carmen M. Ruiz–Jarabo, Ana M. Martín-Hernández, Juan C. Sáiz, and Cristina Escarmís (of various universities) articulated a study on viruses and the mechanisms by which their survival and replication are influenced by their distinction as a quasispecies. They considered how the RNA mutations and replication occurred and how this led to increased strength in viruses as well as the emergence of new types.

The results of this research work are many-fold. Because viruses are a quasispecies, there are many variant genomes in populations. With a random distribution of these mutations, the number of variants increase exponentially with a greater population. These can aid in efficient transmission of the virus and allow it to complete the arbovirus life cycle. These can be seen in infections of HIV-1, hepatitis B virus, hepatitis C virus, influenza virus and more.

The evidence seems to suggest that the way genomes are replicated in quasispecies causes more virulent viruses to emerge, as well as new ones. For instance, some significant human influenza pandemics may be the product of genome reassortment between the influenza viruses of humans and animals. Mutations may create a new virus or make it possible for it to infect an organism once resistant.

With many viruses such as HIV-1, new virions come daily. The immune system may get overwhelmed by all of the different genotypes caused by the mutations, giving more strength to the virus. The RNA viruses are also very adaptable.

The persistence of the virus can also be bolstered by the mechanisms that make it a quasispecies. They can act quickly in both replication and mutations. Virus survival is aided because the constant mutations help them to withstand the host immune response. It can help them escape from antibodies and evade maneuvers that are either natural or through medical intervention.

Studies into viral quasispecies continue. Understanding this complex theory can help scientists to understand how viruses work. With this understanding will hopefully come new ways to combat serious conditions.

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