em function is the empirical observation that rare genotypes can rise to observable levels rapidly and frequently [62-66]. These changes may be the result of de novo mutation of successful genotypes as well as emergence of pre-existing, yet rare, microbes that experience changes in conditions that dramatically affect fitness. Unifying ecological and evolutionary dynamics in a single model is difficult, and most models of host-viral dynamics neglect evolution entirely. A few models are available that have begun to assess how such evolutionary details matter. First, it has been proposed that evolutionary changes in allocation of phytoplankton to virus resistance vs. growth would lead to the evolution of co-limitation by hosts rather than the maximization of host productivity in a given environment . However, the cost of resistance to viral infection remains largely uncharacterized in natural communities (see  for a laboratory study using marine cyanobacteria). Second, an evolutionary Kill-the-Winner model predicts that constant total diversity can emerge at the community level even if the identities of strains are in constant flux . This model predicts that at the community scale there may be invariants for which fine-scale evolutionary details do not matter. Some empirical support for this idea comes from one study in which changes in system nutrient levels were buffered despite rapid changes in strains coevolving over a multi-month experiment . Third, multiple coevolutionary models of viral-host interactions mediated by receptor resistance [71,72] and CRISPR immune defense  demonstrate principles under which coevolutionary-induced diversification may arise. Linking models to data and understanding when and which details matter is an issue relevant to the study of viruses of microbes and to problems in microbial ecology more generally .
Viruses are everywhere, but what are they doing and how important are they?
The potential role of viruses in marine biogeochemical cycles [75,76] and the viral shunt  has been discussed for nearly two decades now, yet the quantitative impact viruses have on regional and global scale processes remains generally unresolved apart from estimates from a few marine virus production surveys [e.g. 32,38,40,41,77-81]. This uncertainty with respect to quantifying viral effects manifests itself in two critical ways. First, there are a number of global earth systems and climate models that integrate geophysical processes with the biology of microbes to metazoans to predict the dynamics of carbon nutrients and biodiversity [82-84]. However, the smallest biotic agents on the planet – viruses – are rarely, if ever, included in such models. Second, the most recent Intergovernmental Panel on Climate Change released its last report in 2007 noting: “The overall reaction of marine biological carbon cycling (including processes such as nutrient cycling as well as ecosystem changes including the role of bacteria and viruses) to a warm and high-CO2 world is not yet well understood. Several small feedback mechanisms may add up to a significant one” . The emphasis is ours. The assessment of quantitative effects of viruses on populations, communities and ecosystems in a form that can be integrated into large-scale models and climate change scenarios should be a major research goal.
There are many challenges to reach this goal. First, data on the quantitative effects of viruses on ecosystem processes are highly variable, and may reflect differences in collection and estimation methods in addition to natural biological variation. There is a need for increased standardization of methods (e.g. ) as well as the integration of existing data to relate viral interaction and effect data to environmental and geographic drivers. Second, new methods are being developed to characterize the genomes of viruses of microbes and the microbes they infect (e.g. ). Yet, how much do these details matter? That is, are there particular host-viral interactions, and even particular lineages or ecotypes, that are key to the flux of particula