Abstract
Endogenous retroviruses (ERV), or the remnants of past retroviral infections that are no longer active, are found in the genomes of most vertebrates, typically constituting approximately 10% of the genome. In some vertebrates, particularly in shorter-lived species like rodents, it is not unusual to find active endogenous retroviruses. In longer-lived species, including humans where substantial effort has been invested in searching for active ERVs, it is unusual to find them; to date none have been found in humans. Presumably the chance of detecting an active ERV infection is a function of the length of an ERV epidemic. Intuitively, given that ERVs or signatures of past ERV infections are passed from parents to offspring, we might expect to detect more active ERVs in species with longer generation times, as it should take more years for an infection to run its course in longer than in shorter lived species. This means the observation of more active ERV infections in shorter compared to longer-lived species is paradoxical. We explore this paradox using a modeling approach to investigate factors that influence ERV epidemic length. Our simple epidemiological model may explain why we find evidence of active ERV infections in shorter rather than longer-lived species.
Highlights
A significant proportion of host genomes are littered with the remnants of past retroviral infections
Our approach of using SIR models to study the multigenerational dynamics of an endogenous retroviral infection is a novel approach, combining methods from demography [35] with epidemiological methods to address the question of Endogenous retroviruses (ERV) epidemic length
We have to consider the possibility that the reverse of endogenisation may occur—exogenous viruses emerging from active ERV lineages
Summary
A significant proportion of host genomes are littered with the remnants of past retroviral infections. Integration into the germline cells and subsequent vertical transmission provides us with a genomic fossil record of multiple, independent, ancient retroviral infections, described from a wide range of vertebrate genomes, including mammals, fish, birds, reptiles and amphibians [3,4]. An ERV consists of 3 genes (gag, pol and env) and two flanking non-coding long terminal repeats (LTRs), which are identical at the time of integration. Over time, these retroviral insertions accumulate mutations and deletions at the same rate as the mutation rate of the host genome [5], rendering them non-functional. ERVs may be inactivated by recombinational deletion between the two flanking
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