Larger Mammalian Body Size Leads to Lower Retroviral Activity

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Larger Mammalian Body Size Leads to Lower Retroviral Activity

Biology

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Larger Mammalian Body Size Leads to Lower Retroviral Activity

The retroviruses have affected mammals affected mammals for more than 100 years, leaving the descendants of the hosts in the host genomes to which are referred to as the endogenous retrovirus. The amount of the endogenous retrovirus is to some extent determined by the retrovirus’ mode of replication, but also a suggestion that the host’s life history traits have the possibilities of suppressing or enhancing the retrovirus activity. According to the research results, body size limits the ability of the endogenous retrovirus to replicate due to their adverse effects impacted on the host.

The endogenous retrovirus is favored by lower body size and higher horizontal transmission rates because the retroviral integration is tumorigenic and the negative correlation between body size and the endogenous retrovirus arise from the need to reduce the risk of cancer having the assumptions that the risk scales positively with the body size. It is however contrasted by the research model that indicates that the lifetime risk of cancer tend to be relatively invariant among the mammals regardless of their body size best regarded as the Peto’s Paradox, to which indicates that the larger bodies mammals have as well evolved the mechanisms of limiting the endogenous retrovirus activity.

The fixation of a new endogenous retrovirus insertion is influenced by the fitness consequences of the host. A smaller number of the endogenous retrovirus have been exapted and possess beneficial actions to the host, although the integration of the retrovirus into the host’s genes have a highly deleterious impact, as the consequent alteration of the gene expression has the possibilities of leading to malignant transformations. Also, the illegitimate recombination between the endogenous retrovirus at different loci may also have the deleterious effect, and therefore the uncontrolled proliferation of the endogenous retrovirus would be extremely detrimental to the host. The process of reproduction could only be limited either through cessation replication or by the host-mediated suppression. The vertebrates’ genomes have evolved a variety of responses that tend to act at various stages of their viral life cycle to limit the retroviral replication along with the associated tumorigenic potential.

The mice and the humans are the two mammalian species are among the first to get their genomes sequenced, indicating variations in the in the patterns of the endogenous retrovirus activity. The human endogenous retroviruses are inactive, with a noticeable deceleration in activity over the last 25 million years which is in contrast to that of the mice genome showing no signs of deceleration in the endogenous retrovirus activity having active and unfixed numbers. The number of mates, as well as the type of placenta, have the possibility of influencing the abundance of the endogenous retrovirus through an increased risk of the horizontal or the vertical retroviral transmission. A possible cofounder includes the effective population size of the host; the species with a higher effective population size are expected to be more efficient at purging slightly deleterious mutations such as those incurred by the endogenous retrovirus proliferation. Being a researcher, the next experiment that I could do is based on the Human Tripartite Motif 5α Domains.

Reference

Katzourakis, Aris, et al. “Larger mammalian body size leads to lower retroviral activity.” PLoS pathogens 10.7 (2014): e1004214.

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