In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of external cues.
In some cases, the genes encoded by prophages can alter the phenotype of the infected bacterium, a process known as lysogenic conversion. Some phages encode proteins or toxins called virulence factors that can facilitate bacterial infections. Through lysogenic conversion, normally non-pathogenic bacteria can become highly virulent via infection by a phage carrying virulence factors.
For example, such phages are largely responsible for the pathogenicity of the bacterial species that cause botulism (Clostridium botulinum), diphtheria (Corynebacterium diphtheriae), and cholera (Vibrio cholerae). Without lysogenic conversion, these bacteria do not usually cause disease.
A particularly well-studied example of lysogenic conversion is that of the Escherichia coli strain O157:H7. Several massive food recalls have stemmed from contamination by E. coli O157:H7. This strain of E. coli has been infected by a phage that encodes Shiga-like toxin (Stx), which can cause intestinal bleeding and kidney failure. In the lysogenic cycle, Stx is not produced, and the bacteria do not cause disease. The phage must re-enter the lytic cycle for Stx to be produced. Unfortunately, certain antibiotics can trigger the induction of the prophage and consequent Stx production, making treatment of these infections difficult. Current research is investigating novel therapies that prevent initiation of the prophage.
