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Review
. 2000 Mar;64(1):69-114.
doi: 10.1128/MMBR.64.1.69-114.2000.

Virioplankton: viruses in aquatic ecosystems

K E Wommack  1 , R R Colwell
Affiliations
Review

Virioplankton: viruses in aquatic ecosystems

K E Wommack et al. Microbiol Mol Biol Rev. 2000 Mar.

Abstract

The discovery that viruses may be the most abundant organisms in natural waters, surpassing the number of bacteria by an order of magnitude, has inspired a resurgence of interest in viruses in the aquatic environment. Surprisingly little was known of the interaction of viruses and their hosts in nature. In the decade since the reports of extraordinarily large virus populations were published, enumeration of viruses in aquatic environments has demonstrated that the virioplankton are dynamic components of the plankton, changing dramatically in number with geographical location and season. The evidence to date suggests that virioplankton communities are composed principally of bacteriophages and, to a lesser extent, eukaryotic algal viruses. The influence of viral infection and lysis on bacterial and phytoplankton host communities was measurable after new methods were developed and prior knowledge of bacteriophage biology was incorporated into concepts of parasite and host community interactions. The new methods have yielded data showing that viral infection can have a significant impact on bacteria and unicellular algae populations and supporting the hypothesis that viruses play a significant role in microbial food webs. Besides predation limiting bacteria and phytoplankton populations, the specific nature of virus-host interaction raises the intriguing possibility that viral infection influences the structure and diversity of aquatic microbial communities. Novel applications of molecular genetic techniques have provided good evidence that viral infection can significantly influence the composition and diversity of aquatic microbial communities.

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Figures

FIG. 1
FIG. 1
Transmission electron micrograph of an unfiltered Chesapeake Bay water sample (magnification, ca. ×36,000). a, short-tailed or nontailed virus-like particle; b, tailed virus-like particle; c, bacterium, coccal morphotype; d, bacterium, vibrio morphotype.
FIG. 2
FIG. 2
CB 7Φ inactivation (lines) and viral capsid loss (bars). Symbols: ○, PFU per milliliter for microcosms under surface sunlight conditions; ■, PFU per milliliter for microcosms under low light and dark conditions; open bars, VDC per milliliter under surface light conditions; shaded bars, VDC per milliliter under low light and dark conditions. Alternating light and dark boxes represent day and night periods, respectively. Error bars are standard errors of duplicate determinations. Adapted from reference .
FIG. 3
FIG. 3
CB 38Φ inactivation (lines) and viral capsid loss (bars). Symbols: ○, PFU per milliliter for microcosms under surface sunlight conditions; ■, PFU per milliliter for microcosms under low light and dark conditions; open bars: VDC per milliliter under surface light conditions; shaded bars, VDC per milliliter under low light and dark conditions. Alternating light and dark boxes represent day and night periods, respectively. Error bars are standard errors of duplicate determinations. Adapted from reference .
FIG. 4
FIG. 4
Frequency of bacterial strains within a species or genus which are lysogens. Adapted from reference .
FIG. 5
FIG. 5
Viruses and the microbial loop. A schematic diagram highlights the potential role of viral infection and lysis in the production of DOM in aquatic ecosystems.
FIG. 6
FIG. 6
Model of virioplankton control of host community diversity. For each PHS, a selective factor stimulates the growth of a specific host. An epidemic of phage infection begins at a critical host cell density, and the abundance of a specific phage increases. Phage lysis causes the abundance of host cells to decline to baseline levels and thus prevents excessive dominance of a single host species. At the end of the epidemic, numbers of infective phage decline to a baseline level at a decay rate specific for each phage. It is also possible that the PHS shown are temperate. Stimulation of host growth, from a selective event, causes curing of lysogeny and thus a release of phage. While the abundances of specific hosts and phages change rapidly, the overall abundance of virioplankton and bacterioplankton is stable over longer, seasonal scales. A and D, moderate burst size (10 to 50); B and C, large burst size (100 to 500); A and B, slow decay; C and D, fast decay. Adapted from reference .
FIG. 7
FIG. 7
PFGE of virioplankton genomes from Chesapeake Bay water samples. August 1995 water samples (I) from stations 858, 845, 818, 744, and 724 are shown in lanes A to E, respectively. The May 1996 (II), June 1996 (III), and July 1996 (IV) water sample station lane designations are identical: 908 (A), 858 (B), 845 (C), 818 (D), 744 (E), and 724 (F). Molecular size markers (in kilobases) specific for each pulsed-field gel are shown in lanes λ Adapted from reference .
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