ial populations. An intriguing hypothesis is that heterotrophs and autotrophs may be “primed” (i.e. stimulated) by the lysis of microbes [38,45,47-51]. This includes the release of lysis byproducts that may stimulate the growth of a subset of heterotrophs  as well as eukaryotic auxotrophs . Characterizing priming and its consequences constitutes an important area of future research, as determining the fate of carbon released from lysed cells is critical to understand how it is recycled or removed (i.e. rendered recalcitrant) from marine carbon budgets [44,45,53]. The study of nutrients may also be critical to this goal, as it has been demonstrated that the release of bioavailable nutrient elements, including N and Fe [38,54], may maintain ecosystem productivity under conditions where nutrient availability limits carbon production.
Finally, the infection of microbes also alters host metabolism, often in significant ways. For example, cyanophage-infecting cyanobacteria, such as Prochlorococcus sp. and Synecochoccus sp., increase the overall photosynthetic rate of microbes, presumably changing the fixation rate of carbon from the environment before lysis. Cellular-based studies have confirmed that pathways within cells can be altered at the metabolic level [55-57]. Similarly, persistent infections, such as occurs during lysogeny, can change the rate and type of utilization processes. Hence, infection can alter the behaviour of microbes, as seen from an ecosystem perspective. The net effect of such differential metabolism at the ecosystem level, however, remains largely unknown. Estimates of the contribution of lysogeny production to virus activity in marine systems remain highly variable [21,58,59]. Future work should likely consider changes in cellular biochemistry as well as differences in cellular processes (e.g. growth efficiency, respiration and photosynthesis, etc.) between lysogens and uninfected cells. Quantifying these differences is likely to be an important component of efforts to census the overall rates at which viruses affect ecosystem functions.
Modelling efforts to link viral lysis with carbon and nutrient availability
Dynamic models of viral-host interactions in marine environments have, at their core, the same set of assumptions as were made for dynamics of Escherichia coli and associated phage in chemostats . These now-classic “box” models consider how abundances of hosts, viruses and resources change with time due to the effects of resource uptake, cell division, viral-induced mortality of hosts, and viral reproduction via lysis. Extensions have taken into account a greater complexity of factors, including the possible covariation of bacterial life history traits and viral life history traits [34,35,60]. The most prominent extension to ocean systems is termed “Kill-the-Winner” [28,61], in which viruses specialize in distinct hosts and contribute to the successive decline of host strains that rise to dominance. Kill-the-Winner assumes one-to-one relationships between individual viruses and hosts. The cross-infection of viruses and hosts is more complex. For example, empirical assays of viral-host cross-infectivity reveal that viruses can infect many microbial hosts, and, similarly, microbes can be infected by many viruses [13,24-26]. A reanalysis of phage-bacteria cross-infection assays found a characteristic nested pattern . The nested pattern implies there is a hierarchy of infection ability (amongst viruses) and susceptibility to infection (amongst bacteria) within the re-examined studies. Hence, a major question moving forward is: do the predictions of Kill-the-Winner and other population ecology models change given other cross-infection assumptions? In the context of the first direct effect outlined earlier, it would be important to quantify the relationship between who infects whom and the relative abundance and survival of host and viral strains.
Perhaps the biggest impediment to predictive modelling of direct and indirect effect of viruses of microbes on microbial community composition and ecosyst