Linking internal and external bacterial community control gives mechanistic framework for pelagic virus‐to‐bacteria ratios

Abstract

SummaryFor more than 25 years, virus‐to‐bacteria ratios (VBR) have been measured and interpreted as indicators of the importance of viruses in aquatic ecosystems, yet a generally accepted theory for understanding mechanisms controlling VBR is still lacking. Assuming that the denominator (total bacterial abundance) is primarily predator controlled, while viral lysis compensates for host growth rates exceeding this grazing loss, the numerator (viral abundance) reflects activity differences between prokaryotic hosts. VBR is then a ratio between mechanisms generating structure within the bacterial community and interactions between different plankton functional types controlling bacterial community size. We here show how these arguments can be formalized by combining a recently published model for co‐evolutionary host‐virus interactions, with a previously published “minimum” model for the microbial food web. The result is a framework where viral lysis links bacterial diversity to microbial food web structure and function, creating relationships between different levels of organization that are strongly modified by organism‐level properties such as cost of resistance.

Simple models combining competition, defence and resource availability have broad implications in pelagic microbial food webs

“…Intuitively, expensive defence (large CORs) will generate large between‐strain differences in growth rate, shifting the competition in favour of the viral loop (Våge et al . ). Large interspecies differences in maximum growth rates will, however, also generate large within‐community differences in individual growth rates and thus high virus abundances.…”

The Response of Heterotrophic Prokaryote and Viral Communities to Labile Organic Carbon Inputs Is Controlled by the Predator Food Chain Structure

“…Nutrient availability and predator control have to a large extent been studied using a “black box” approach, treating the heterotrophic prokaryotes as one plankton functional type (PFT), disregarding internal community composition and differences in activity between community members [ 5 , 6 ], and leaving us with a limited understanding of how population dynamics at the two levels of resolution are connected. Top-down control by viruses is believed to be more specific than predatory control, regulating the size of specific host groups, and thus acts more on community composition than on community size [ 7 ]. With host-specific viruses, host–virus interactions must, however, work both ways so that a change in host community composition will be reflected in a subsequent change in viral composition.…”

Viral and bacterial community responses to stimulated Fe(III)‐bioreduction during simulated subsurface bioremediation

“…Higher host abundance and increasing bacterial production may increase the probability of virus–host contact and sustain more viral production in the environment (Brum et al ., ). Våge and colleagues () proposed a framework through integration of a nested virus–host interaction model into the microbial food web model, and the framework indicated that virus abundance increases with increasing host growth rate. Virus‐to‐bacteria ratio was reported to be inversely related with bacterial abundance and production, but positively related with virus abundance, frequency of visibly infected cells, burst size and frequency of lysogenic cells (Parikka et al ., ).…”

“…Our results are consistent with acetate selective growth of Fe(III) reducers, thereby favouring some specific bacterial groups and lowering the overall diversity in the influent section of the acetate‐treated columns. However, as reported in previous studies, significant bacterial community shifts could also be attributed to viral‐mediated cell lysis or ‘top‐down’ controls (Gómez and Buckling ; Koskella and Brockhurst, ; Våge et al ., ; Scanlan, ). Although, some influence was evident through the correlation network analysis, the extent to which viral infection contributed to structuring bacterial communities was not discernable with the data collected in this study.…”