The Lysis-Lysogeny Decision

Image of influenza virus. Copyright Linda M. Stannard, Department of Medical Microbiology, University of Cape Town, 1995.

A well-known case of phenotypic plasticity in viruses is the lysis-lysogeny decision, whereby parasitic lambda-phage viruses adopt a bet-hedging strategy in order to cope with fluctuations in the availability of their hosts (E. coli bacteria). Preuss (2000) describes the process thus:

When a bacteriophage ("bacteria eater") virus injects its own dna (sic) into a microorganism such as Escherichia coli, the host cell apparatus rapidly expresses the program on the viral dna (sic) that decides whether or not to kill the host immediately. Under conditions that are less than optimal for replication, the phage may actually confer immunity to further infection upon the host (lysogeny). But if conditions are good, the virus produces so many copies of itself that the cell walls burst - a state known as lysis - and the infection spreads.

Two independently produced regulatory proteins compete to control whether the invading genes will remain quiescent or be expressed. Because of inescapable thermal noise, the outcome in any given case is random, and the proportion of the population in either state changes according to conditions such as cell nutrition and the number of invading particles per cell...

Arkin and his colleagues have found that the underlying stochastic [i.e. random - V.J.T] mechanisms of the lysis-lysogeny decision circuit... depend entirely upon the chance timing and concentrations of bursts of competing proteins that act to reinforce or inhibit one another.

"...Thermal fluctuation at the molecular level makes for diversity in cells that start out under identical conditions," says Arkin. "The phage actually makes use of noise as a survival mechanism: sometimes it pays to multiply and infect as many hosts as possible, sometimes it pays to lie low. Either way, the viral population is prepared to cope with changing conditions" (italics mine).