The Spread of Endogenous Retroviruses in Populations Infected by Exogenous Viruses

TL;DR

This paper explores how exogenous retroviruses and endogenous retroviruses interact and evolve in populations, focusing on their transmission and impact on host fitness.

Contribution

The study introduces a model showing how maternal transmission affects XRV virulence and ERV spread dynamics.

Findings

XRVs evolve high virulence with low maternal transmission or vice versa.

An ERV with minimal host fitness impact has a high chance of spreading to fixation, especially if it resists XRV.

Non-fixed ERVs can eliminate XRVs, clearing both from the population.

Abstract

Retroviruses insert DNA copies of themselves into the chromosomes of their hosts forming proviruses that can synthesize new transmissible viruses. Exogenous retroviruses (XRVs) insert into the DNA of somatic cells and are transmitted infectiously. Endogenous retroviruses (ERVs) become inserted in the DNA of germline cells and are transmitted genetically. ERVs can spread through the genome by transposition. ERVs originate from an initial copy of an XRV inserted into the genome of an organism infected by the XRV. Many XRVs are transmitted maternally as well as horizontally; therefore, we consider the effect of maternal transmission on the evolution of virulence of an XRV. Our model shows that the XRV either evolves high virulence with low maternal transmission, or vice versa. We then consider the spread of ERV genes in conjunction with the infectious spread of an XRV. Beginning from a single copy of an ERV, we calculate the probability that it spreads to fixation (i.e., the state where all individuals contain ERV genes). This depends on its virulence and transposition rate. If the XRV is present, the fixation probability also depends on the virulence of the XRV and whether the ERV provides resistance to the XRV. An ERV with only a small deleterious effect on host fitness has a high fixation probability, particularly if it provides resistance to the XRV. We also show that, if an ERV does not spread to fixation, it can still cause elimination of the XRV, with the end result that the population is cleared of both XRV and ERV.

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