For many bacterial viruses, the choice of whether to kill host cells or enter a latent state depends on the multiplicity of coinfection. Here, we present a mathematical theory of how bacterial viruses can make collective decisions concerning the fate of infected cells. We base our theory on mechanistic models of gene regulatory dynamics. Unlike most previous work, we treat the copy number of viral genes as variable. Increasing the viral copy number increases the rate of transcription of viral mRNAs. When viral regulation of cell fate includes nonlinear feedback loops, very small changes in transcriptional rates can lead to dramatic changes in steady state gene expression. Hence, we prove that deterministic decisions can be reached, e.g., lysis or latency, depending on the cellular multiplicity of infection within a broad class of gene regulatory models of viral decision making. Comparisons of a parametrized version of the model with molecular studies of the decision structure in the temperate bacteriophage {lambda} are consistent with our conclusions. Because the model is general, it suggests that bacterial viruses can respond adaptively to changes in population dynamics, and that features of collective decision making in viruses are evolvable life history traits.

Viruses found in the River Cam in Cambridge, famous as a haunt of students in their punts on long, lazy summer days, could become the next generation of antibiotics, according to scientists speaking today (Monday 3 September 2007) at the Society for General Microbiology’s 161st Meeting at the University of Edinburgh, UK, which runs from 3-6 September 2007.

An old-fashioned treatment for bacterial infections which was once found in every Red Army soldier's kit bag is being touted as a new weapon against hospital superbug MRSA. In the 1930s, a war was on. A new treatment for bacterial infections - antibiotics - was seeking to assert its supremacy over another fledgling therapy - a bacteria-devouring virus called a bacteriophage. Even today, the bacteriophage is used as standard treatment in parts of Eastern Europe for bacterial infections from gangrene to strep throat.

Most invasive bacterial infections are caused by species that more commonly colonize the human host with minimal symptoms. Although phenotypic or genetic correlates underlying a bacterium's shift to enhanced virulence have been studied, the in vivo selection pressures governing such shifts are poorly understood. The globally disseminated M1T1 clone of group A Streptococcus (GAS) is linked with the rare but life-threatening syndromes of necrotizing fasciitis and toxic shock syndrome1. Mutations in the GAS control of virulence regulatory sensor kinase (covRS) operon are associated with severe invasive disease, abolishing expression of a broad-spectrum cysteine protease (SpeB)2, 3 and allowing the recruitment and activation of host plasminogen on the bacterial surface4. Here we describe how bacteriophage-encoded GAS DNase (Sda1), which facilitates the pathogen's escape from neutrophil extracellular traps5, 6, serves as a selective force for covRS mutation. The results provide a paradigm whereby natural selection exerted by the innate immune system generates hypervirulent bacterial variants with increased risk of systemic dissemination.