The lysogenic cycle is a replication strategy employed by bacteriophages, viruses that infect bacteria. This process is a non-destructive method for viral genetic material to persist and multiply within the host cell. The cycle begins when the virus introduces its DNA into a bacterial cell, integrating it directly into the host’s chromosome. Once integrated, the viral genome enters a dormant state, replicating passively every time the bacterium divides, ensuring the virus’s survival across multiple generations.
The Choice: Comparing Lysogenic and Lytic Cycles
Viruses that can undergo the lysogenic cycle are called temperate phages, and they face a choice between two replication pathways upon infecting a host cell. The lytic cycle is the alternative strategy, characterized by the immediate takeover of the host cell’s machinery to rapidly produce new viral particles. This pathway culminates in the bursting, or lysis, of the host cell, releasing hundreds of new viruses.
The lysogenic cycle prioritizes long-term persistence over rapid reproduction. The decision between these two paths is influenced by conditions external to the virus itself. High numbers of phages infecting a single bacterium, known as a high multiplicity of infection, often bias the decision toward lysogeny, suggesting that the environment is saturated and immediate replication is less favorable.
The availability of nutrients and the overall health of the host cell also factor into the viral decision. When the host environment is poor or resources are scarce, the virus often chooses the dormant lysogenic path until conditions improve. This allows the virus to conserve resources and spread its genome vertically through bacterial division rather than risking immediate release into an unsupportive environment.
Steps of Viral Integration and Prophage Formation
The lysogenic cycle begins with adsorption, where the bacteriophage recognizes and binds to specific receptor sites on the bacterial cell surface. Following this attachment, the virus performs penetration, injecting its nucleic acid—typically double-stranded DNA—into the bacterial cytoplasm, leaving the empty protein coat outside. The injected viral DNA then circularizes, preparing for the next step.
The defining event is integration, a process mediated by a specific viral enzyme called integrase. This enzyme facilitates the physical insertion of the circular viral DNA into a specific location on the host bacterium’s chromosome. The integrated viral genome is no longer referred to as phage DNA but is now termed a prophage.
Once the prophage is formed, the vast majority of its genes are repressed, maintaining a state of dormancy. A specialized repressor protein, encoded by a viral gene, is responsible for silencing the genes necessary for the lytic cycle. The prophage remains a silent part of the bacterial chromosome. This physical integration distinguishes the lysogenic cycle from other forms of viral latency.
The State of Dormancy: Consequences for the Host Cell
While the prophage is dormant, the host bacterium, now called a lysogen, continues to live and reproduce normally. The viral DNA is passively replicated every time the host cell’s chromosome duplicates before cell division. The prophage is thus inherited by all daughter cells, allowing the viral genome to spread rapidly throughout the bacterial population without killing the host.
The presence of the prophage can also alter the host bacterium’s characteristics through a phenomenon known as lysogenic conversion. This occurs when the viral genes that remain active confer new traits to the bacterium. A notable example is the acquisition of virulence factors, such as the genes for the toxins that cause diseases like diphtheria, botulism, and cholera.
The integrated prophage also provides the lysogen with superinfection immunity, protecting it from subsequent infection by the same type of phage. The repressor protein that keeps the prophage dormant binds to the regulatory regions of any newly introduced phage DNA, preventing it from integrating or initiating a lytic cycle.
Induction: Triggering the Lytic Exit
The state of lysogeny is stable but not permanent; the virus can transition back to the lytic cycle through a process called induction. This switch is triggered by signs of environmental stress, which indicate that the host cell’s survival is threatened. Common stressors include exposure to ultraviolet (UV) radiation, chemical mutagens, or nutrient deprivation.
The environmental stress signals activate a bacterial stress response system, such as the SOS response, which involves the RecA protein. This protein initiates the cleavage of the viral repressor protein that maintained the dormant state. With the repressor destroyed, the lytic genes of the prophage are expressed.
The newly activated viral genes direct the synthesis of an excision enzyme, which precisely cuts the prophage DNA out of the host chromosome. Once excised, the viral genome is free in the cytoplasm and immediately begins the rapid replication and assembly phase characteristic of the lytic cycle, leading to the production of new phages and the eventual lysis of the host cell.