Microscopic analyses (TEM, Weinbauer et al. 2002) suggest that 2–24% of
bacterial cells are infected by viruses and that viral lysis removes 20–40% of the
prokaryotic standing stock per day (Suttle 2007). Rates of production are 12 × 10^9 to
230 × 10^9 viruses per ml per day in coastal waters (Weinbauer 2004). Viruses are
subject to mortality from non-biotic factors such as solar radiation, and temperature
and biotic factors like inhibitory compounds released by bacteria (Weinbauer 2004).
Decay rates (loss of infectivity) can be measured experimentally, and rates range from
−0.05 to −0.11 h−1. The turnover times for viral populations are 1.6 days in coastal
water and 6.1 days in oceanic waters.
(^) Most, or all, viruses are host-specific, so the effect of viruses on bacterial
populations depends on abundance and activity of the host population and on host-
virus contact rates. Infection rates depend on contact rates, so the more abundant
components of bacterial communities are more likely to be controlled by viruses. This
leads to a “kill the winner” hypothesis: viruses infect and lyse the fastest-growing
bacteria, and then the less-abundant bacteria become dominant. Thingstad (2000)
developed a model showing how non-selective grazing by heterotrophic protists and
host-selective viral lysis of fast-growing bacteria could account for the co-existence of
many bacterial species and also for the 1 : 10 ratio of bacterial to viral abundance.
Possibly, abundances of host bacterial species and their viruses could oscillate in a
predator–prey relationship, yet maintain relatively constant total levels of bacteria and
viruses (Fig. 5.14). Experimental and field data provide some support for this concept;
however, the oscillations of specific host bacteria and their viruses have not been