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Viral diversity and life cycles are poorly understood in the human gut and other body habitats. Phages and their encoded functions may provide informative signatures of a human microbiota and of microbial community responses to various disturbances, and may indicate whether community health or dysfunction is manifest after apparent recovery from a disease or therapeutic intervention. Here we report sequencing of the viromes (metagenomes) of virus-like particles isolated from faecal samples collected from healthy adult female monozygotic twins and their mothers at three time points over a one-year period. We compared these data sets with data sets of sequenced bacterial 16S ribosomal RNA genes and total-faecal-community DNA. Co-twins and their mothers share a significantly greater degree of similarity in their faecal bacterial communities than do unrelated individuals. In contrast, viromes are unique to individuals regardless of their degree of genetic relatedness. Despite remarkable interpersonal variations in viromes and their encoded functions, intrapersonal diversity is very low, with >95% of virotypes retained over the period surveyed, and with viromes dominated by a few temperate phages that exhibit remarkable genetic stability. These results indicate that a predatory viral-microbial dynamic, manifest in a number of other characterized environmental ecosystems, is notably absent in the very distal intestine.
The diversity of viruses in the gut, and their role in the assembly, maintenance and adaptations of the microbiota and its pool of genes (microbiome), remains unclear. In many environments, the dominant ecological relationship between viruses and their microbial hosts is predatory and follows Lotka-Volterra (or 'kill the winner') dynamics. This dynamic is characterized by top-down control of microbial communities (that is, microbial biomass is significantly below the carrying capacity of the habitat), rapid microbial and viral population shifts, and evidence of Red Queen coevolution (in other words, escape strategies in the prey population are countered by predator adaption). One manifestation of this 'arms race' is positive selection on loci such as bacterial O antigens and clustered regularly interspaced short palindromic repeats (CRISPR) elements1,2, and viral tail fibres3. In contrast to this predator-prey dynamic, there is another viral life cycle where temperate rather than lytic viruses are longertermcontributors to microbial host phenotypes through provision of adaptive genes. This dynamic can change the metabolic capacities of free-living bacteria and obligate intracellular...