Bacteriophages are viruses that specifically infect and replicate within bacterial cells. Often called phages, these viruses are the most abundant biological entities on Earth, playing a massive role in microbial ecosystems. Phages reproduce using two primary methods: the lytic cycle, which immediately destroys the host, and the lysogenic cycle, which allows for a period of coexistence. The lysogenic infection is a mechanism of viral propagation that avoids immediate cell death.
What Defines the Lysogenic Cycle
The lysogenic cycle is characterized by a temporary, non-destructive relationship between the virus and the bacterium. Phages capable of this dual lifestyle are known as “temperate phages,” distinguishing them from “virulent phages” that only use the destructive lytic pathway.
The integrated viral genome is termed a “prophage” once it becomes part of the host’s genetic material. This arrangement is a form of passive replication, where the bacterium, now called a lysogen, continues to live and divide normally. The prophage is replicated along with the bacterial chromosome and passed down to every subsequent daughter cell, allowing the virus to spread without immediate replication and lysis.
How the Temperate Phage Integrates and Remains Dormant
The process of establishing a lysogenic infection begins when the temperate phage attaches to the bacterial surface and injects its nucleic acid, typically DNA, into the host cytoplasm. Once inside, the linear phage DNA circularizes. The phage must then decide between the lytic and lysogenic pathways; factors like a high concentration of phages can favor the lysogenic decision.
To achieve integration, the circular viral DNA utilizes a specialized enzyme called integrase, which is encoded by the phage itself. Integrase facilitates a site-specific recombination event, inserting the phage genome into a specific location within the host’s bacterial chromosome. This integration point is where the viral DNA transitions into the dormant prophage state.
Maintaining dormancy is an active process governed by repressor proteins, such as the cI repressor in the lambda phage. These proteins bind to the prophage DNA and block the transcription of viral genes required for the lytic cycle and the production of new viral particles. As long as these repressors are active and bind effectively, the prophage remains quiescent, replicating passively every time the bacterial cell divides. This process propagates the viral genome without harming the host.
The Switch: When Lysogeny Transitions to the Lytic Cycle
The stable coexistence of the lysogenic state is not permanent and can be broken through a process known as induction. Induction involves the prophage excising itself from the host chromosome to initiate the destructive lytic cycle. This switch is typically triggered by environmental stressors that signal damage or a threat to the host cell’s survival.
Inducing factors include DNA-damaging agents like ultraviolet (UV) radiation or exposure to certain chemicals. These stresses activate the host bacterium’s emergency DNA repair system, known as the SOS response, which destabilizes the prophage’s repressor proteins. The loss of the repressor then allows the viral genes to be transcribed, starting with those that encode excision enzymes.
These excision enzymes cut the prophage DNA out of the bacterial chromosome, reversing the integration process. Once free, the viral genome begins to hijack the host’s cellular machinery to actively replicate its DNA and synthesize new viral structural proteins. The culmination of this process is the assembly of new phage particles, followed by the synthesis of lytic enzymes that burst, or lyse, the host cell, releasing the infectious progeny.
Why Lysogeny Matters: Impact on Bacterial Hosts
The presence of a prophage alters the characteristics of the host bacterium, a phenomenon called lysogenic conversion. This conversion occurs because the integrated viral genome carries genes that provide a survival or fitness advantage to the bacterium, even if they are not necessary for the phage life cycle. These new genes can change the host’s phenotype, such as its surface properties or its ability to produce toxins.
A major consequence of lysogenic conversion is the acquisition of virulence factors, turning a harmless bacterial strain into a pathogen. For instance, the bacteria that cause diseases like cholera (Vibrio cholerae) and diphtheria (Corynebacterium diphtheriae) only become virulent when they are lysogenized by a specific phage that carries the gene for the toxin. The prophage-encoded toxins are often responsible for the severe symptoms of the resulting infection. This interaction highlights how the lysogenic lifestyle drives the evolution of bacterial pathogenicity.