What Is the Lysogenic Cycle of a Virus?

The lysogenic cycle is a strategy utilized by certain viruses to replicate their genetic material without immediately destroying the host cell. This mode of reproduction is distinct from the lytic cycle, which results in the rapid production of new viral particles and the prompt rupture of the cell. The lysogenic pathway allows the viral genome to lie dormant within the host’s own genetic material. This process is best understood in temperate bacteriophages, which are viruses that infect bacteria. Temperate phages use this cycle as a long-term propagation method, ensuring the virus’s survival across multiple generations of host cells.

How Viral DNA Integrates into the Host Genome

The initial phase of the lysogenic cycle involves the bacteriophage recognizing and attaching itself to specific receptor sites on the bacterial cell surface. Following this attachment, the phage injects its nucleic acid, typically double-stranded DNA, directly into the host cell’s cytoplasm. If the injected DNA is linear, it must first undergo a circularization process.

The defining event of this cycle is the splicing of the viral genome into the host’s chromosome. This integration occurs at a specific location, often referred to as an attachment site. A specialized viral enzyme, integrase, mediates this site-specific recombination, covalently linking the viral DNA into the bacterial genome. For example, in the lambda phage, the integrase facilitates recombination at the attB site on the E. coli chromosome.

This precise enzymatic action ensures that the viral genetic instructions become a permanent, latent part of the host cell’s DNA. By becoming part of the host chromosome, the viral genome is indistinguishable from the bacterium’s own genes. This successful integration marks the transition into the dormant stage of the cycle.

The Dormant Prophage State

Once the viral DNA is incorporated into the host chromosome, it is referred to as a prophage. The infected bacterial cell is called a lysogen, and it continues to live and divide normally without immediate signs of viral infection. This state of latency is maintained by a genetic mechanism that suppresses the expression of most viral genes.

The key component maintaining this dormancy is a repressor protein, such as the cI repressor found in lambda phage. This protein binds to specific operator regions on the prophage DNA, blocking the transcription of genes required for the lytic cycle, including those for viral replication and capsid assembly. The presence of this repressor protein ensures that the prophage remains transcriptionally silent.

The characteristic of the dormant prophage state is passive replication, also known as vertical transmission. Every time the host lysogen cell undergoes binary fission, it replicates its entire chromosome, including the integrated prophage. The viral genome is thus silently copied and passed on to all daughter cells, allowing the virus to propagate through the bacterial population for many generations.

Triggering the Viral Replication Switch

The lysogenic cycle is not a permanent state and can transition back to the active lytic cycle through a process called induction. This switch is triggered by environmental stressors that signal damage or instability in the host cell, indicating the environment is no longer favorable for passive propagation. Triggers include exposure to ultraviolet (UV) radiation, chemical mutagens, or nutrient deprivation.

These stressors activate the host cell’s DNA damage response system, known as the SOS response. Activation of the SOS system leads to the cleavage and degradation of the repressor protein that maintained the dormant state. The destruction of the repressor removes the block on the lytic genes.

With the repressor protein gone, the viral genes necessary for excision and replication are immediately transcribed. The prophage DNA excises itself from the host chromosome through a recombination event that is the reverse of the integration step. Once excised, the viral DNA hijacks the cell’s machinery to synthesize new viral components, initiating the final stages of the lytic cycle.