Pathogen evolution within host individuals as a primary cause of senescence

Abstract

This paper discusses a novel theory of senescence: the community of pathogens within each host individual evolves during the life-time of the host, and in doing so progressively reduces host vigour. I marshal evidence that asymptomatic host individuals maintain persistent populations of viral pathogens; that these pathogens replicate; that they are often extremely variable; that selection within hosts causes the evolution of pathogens better able to exploit the host; that selection is host-specific; and that such evolving infections cause appreciable and progressive deterioration. Experimental approaches to testing the theory are discussed.

The interplay between immunity and aging in Drosophila

“…In the light of gut physiology and tissue homeostasis, the Drosophila microbiome has gained a lot of attention 15 , 16 , 19 , 110 . The evolutionary biologist Graham Bell has proposed that senescence might be caused by infections that outcompete the host immune response in an evolutionary arms race 111 . With the rapid advances in sequencing technology and genomics, it would be very interesting to study pathogen evolution over the course of the Drosophila lifetime.…”

Infection, Polymorphism and Evolution

“…My approach to the problem complements that of Bell (1993), who proposed that persistent infections might be responsible for long-term deterioration of hosts, that is, for senescence. To understand the mutation-prone end of the continuum, we must understand why some viruses generate persistent infections associated with prolonged periods of transmission, and with exposure to strongly activated immune systems during transmission.…”

‘There and back again’: revisiting the pathophysiological roles of human endogenous retroviruses in the post-genomic era

“…The existence of multiple HK2 loci in human genomes means that these loci cannot be strongly deleterious, at least not prior to reproductive age [65]. Population genetics theory predicts that a slightly harmful allele can drift to fixation, especially if the pathogenicity is mainly expressed after the age of reproduction in the same way as a trait associated with senescence [66][67][68][69][70][71][72][73][74][75]. HK2 loci could have slight pathogenic potential especially at the post-reproductive age, which also coincides with the higher incidence of autoimmunity and cancer.…”