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Notes on “Viruses in the sea” by Suttle (2005) and “Marine viruses – Major players in the global ecosystem” by Suttle (2007)

Suttle (2005)

Three most abundant types of viruses that affect prokaryotes: * myovirus: contractile tails, typically lytic and borad host ranges, can take advantage quickly of a rising host population (r-selection: short generation times and high reproductive rates) * podoviruses: small non-contractile tails, typically lytic and narrow host ranges * siphovirus: long non-contractile tails, capable of integrating the host genome (in which case their production rate is tied to that of the host until an environmental cue triggers the lytic cycle) (K-selection: longer generation times and lower reproductive rate) and broad host range

Virus diversity is high even over small spatial scales but common genes can be found in very different places (in other words, we could speculate that diversity is constant over all the oceans).

I don’t understand this: “The communities have an uneven distribution, with the most abundant genotypes making up less than 5% of the communities, whereas the majority of genotypes comprise <0.01 of the communities.”

A cool thing: “viruses capture genes of host origin and exchange them among viral progeny, resulting in photosynthetic genes that are now clearly viral.”

Estimates of virus-mediated mortality rate are poorly constrained and vary a lot depending on the method used: “accurate estimates of virus-mediated mortality remain elusive, and we are not much further ahead than a decade ago when viruses were estimated to kill ~20–40 % of marine bacteria on a daily basis and contribute to microbial mortality at a level similar to that of grazing by zooplankton.”

Importance of virus to the biochemical cycles:

“Viruses short circuit the flow of carbon and nutrients from phytoplankton and bacteria to higher trophic levels by causing the lysis of cells and shunting the flux to the pool of dissolved and particulate organic matter (D-P-OM). The result is that more of the carbon is respired, thereby decreasing the trophic transfer efficiency of nutrients and energy through the marine foodweb.”

Why is carbon more respired? Because of virus killing plankton, less plankton sink into the deep ocean and is instead transformed back into particulate and dissolved organic carbon that stays near the surface and participate in the air-sea flux of carbon. In cases where plankton is quickly killed, however, the sink of plankton is increased.

See ref. 4 (Wihlem and Suttle 1999) and ref. 5 (Fuhrman 1999) for simple models of viruses and ref. 77 (Middelboe et al. 2003) experimental testing of hypothesis concerning viral dynamics.

Suttle (2007)


Wommack, K. E. & Colwell, R. R. Virioplankton: viruses in aquatic ecosystems. Microbiol. Mol. Biol. Rev. 64, 69–114 (2000).


Weinbauer, M. G. Ecology of prokaryotic viruses. FEMS Microbiol. Rev. 28, 127–181 (2004).

for two other reviews of viruses.

“the total viral abundance generally varies along with the prokaryotic abundance and productivity”

“Such observations might help us to understand some of the emergent properties of viral infection. For example, most models that try to estimate the impact of viral infection on marine microbial mortality assume that every member of the prokaryotic community is equally affected by viral infection (ref. 2,36–38). However, if viruses preferentially infect cells that are growing more rapidly this will, in turn, affect nutrient cycling and, potentially, the efficiency with which carbon is transported from where it is fixed in surface waters to the deep ocean.”

“Although over long time periods viral-mediated mortality must approach a steady state, in which mortality and production are balanced, this is frequently not the case for the timescales over which experiments are conducted.”

“The fact that virus replication rates increase in conjunction with increases in host growth rates emphasizes that viralmediated mortality is not in a steady state, and that some subsets of the host community will be disproportionately affected. An increase in the rate of viral reproduction in response to an increase in the growth rate of host cells is a strong feedback mechanism that would probably prevent dominance by the fastest growing taxa. Reports that bacteriophage abundance is most strongly correlated with the most active subset of the prokaryotic community (J.P. Payet and C.A.S., unpublished observations) is further evidence that it should not be assumed that the effects of viral infection are spread evenly across the microbial community.”

“The lack of straightforward and reliable approaches for estimating the rates of mortality that are imposed by viruses on marine prokaryotic and eukaryotic heterotrophic and autotrophic communities remains one of the biggest obstacles for incorporating viral-mediated processes into global models of nutrient and energy cycling.”

“By the simplest approximation, the viral shunt moves material from living organisms into the particulate and dissolved pools of organic matter, where much of it is converted to carbon dioxide by respiration and photodegradation. However, the effects can also be more profound and potentially include the release of dimethyl sulphide5, a gas that affects the Earth’s climate, and the remobilization of the organically complexed iron that limits primary production in much of the world’s oceans. For example, the viral lysis of prokaryotes liberates sufficient amounts of biologically available iron to support the needs of phytoplankton62. Ultimately, it is both the quantity and composition of the material that is released by viral lysis that affects microbial communities and global geochemical cycles.”

“The efficiency of the biological pump (BP) increases as the ratio of carbon relative to the amount of the limiting resource (or resources) increases. Viruses can increase the efficiency of the BP if they increase the export of carbon relative to the export of the limiting resource (or resources).”

Viruses are also responsible for the high diversity of plankton. See

Thingstad, T. F. & Lignell, R. Theoretical models for the control of bacterial growth rate, abundance, diversity and carbon demand. Aquat. Microb. Ecol. 13, 19–27 (1997).


Thingstad, T. F. Elements of a theory for the mechanisms controlling abundance, diversity, and biogeochemical role of lytic bacterial viruses in aquatic systems. Limnol. Oceanogr. 45, 1320–1328 (2000).

for models of virus-mediated diversity of microbes (the “killing-the-winner” scenario).

See also

Murray, A. G. & Jackson, G. A. Viral dynamics: a model of the effects size, shape, motion and abundance of single-celled planktonic organisms and other particles. Mar. Ecol. Prog. Ser 89, 103–116 (1992).

[A Google search “model diversity virus prokaryote killing the winner” provided these interesting papers: Hoffman et al. (2007), Rodriguez-Valera et al. (2009), Sandaa (2008), Jessup and Forde (2008)]

“a high host abundance does not necessarily lead to the collapse of a taxon, even when the concentrations of infectious virus are high. In the case of the cyanobacterium Synechococcus spp., even though virus titres increase dramatically when the host-cell abundance exceeds ~103 per ml, high numbers that are resistant to virus infection persist.”

“A less obvious direct effect [of viruses on microbial diversity] is the introduction of new genetic traits by the horizontal gene transfer that can be acted upon by natural selection. Potentially important indirect effects include the release of predation pressure by the lysis of grazers and the stimulation of the growth of subsets of the microbial community by the recycling of organic substrates.”

Finally, “[i]n nature, there are strong temporal and spatial gradients that have the potential to affect the influence of viruses on microbial diversity.”

Two types of evolutionary selections for microbial communities:

  1. K-selection: abundant, slow growth rate but resistant to viruses and grazing
  2. r-selection: rare, high growth rate but highly susceptible to viruses and grazing.

Question: why is there not a species that has a high growth rate and would be resistant to viruses and grazing?

In contrast to marine microbes, the most abundant are r-selected and the rarest are K-selected. Furthermore, the host of the r-selected viruses are r-selected prokaryotes and similarly for K-selected viruses and hosts.

Proposition: Could we demonstrate these speculations in a model? (see Weinbauer, M. G. Ecology of prokaryotic viruses. FEMS Microbiol. Rev. 28, 127–181 (2004)?) At least, the motivation is there:

“Whether or not the scenarios outlined above are responsible for the highly uneven population structures that are characteristic of marine microbial communities, in which few taxa are numerically dominant, requires further exploration.”