FIG. 6.

Conceptual model of virioplankton regulation of host community diversity. For each phage-host system, a selective factor stimulates growth of a specific host. An epidemic of phage infection begins at a critical threshold host cell density, and the abundance of a specific phage increases; thereafter, phage lysis causes the abundance of host cells to decline to background levels, preventing overdominance 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 phage-host systems are temperate. Stimulation of host growth by a selective event causes curing of lysogeny and thus a release of phage. While abundances of specific hosts and phages change rapidly, the overall abundance of virio- and bacterioplankton is stable over longer, seasonal scales. A and D, moderate burst size of 10 to 50; B and C, large burst size of 100 to 500; A and B, low decay rate; C and D, high decay rate.