Bacteriophages, viruses that infect bacteria, follow two distinct life cycles: the lytic cycle or the lysogenic cycle. The lytic cycle is the aggressive approach, where the virus hijacks the host cell’s machinery to rapidly produce new viral particles before bursting and killing the cell. In contrast, the lysogenic cycle is a subtle strategy where the viral genetic material integrates directly into the host bacterium’s chromosome, lying dormant. This temporary state of coexistence allows the virus to spread its genes without immediately sacrificing its host, offering advantages related to persistence, survival, and host cell enhancement.
Persistence Through Silent Replication
When a bacteriophage enters the lysogenic cycle, its DNA integrates into the bacterial genome, forming a prophage. The viral genes that cause the host to lyse are actively kept silent by a repressor protein produced by the virus.
This dormancy is beneficial because the viral genome is replicated every time the host bacterium divides. Since bacteria reproduce through binary fission, the number of cells carrying the viral DNA increases exponentially without the virus expending energy on new infections. This passive replication allows the virus to build a large, distributed population silently.
The virus leverages the host’s reproductive success for its own propagation, effectively hitchhiking along the bacterial family tree. This mechanism ensures that the viral lineage persists across numerous generations of host cells. The prophage remains a stable part of the bacterial chromosome, guaranteeing its transmission to all daughter cells.
Strategic Timing for Survival
The choice between the lytic and lysogenic cycles is dictated by the environmental conditions the host is experiencing. If the environment is poor, immediate lysis risks the rapid death of newly released progeny. When resources are scarce or bacterial population density is low, released virions would quickly run out of healthy new host cells to infect.
By entering the lysogenic cycle, the virus waits out unfavorable conditions, treating the host as a secure vessel until the environment improves. The prophage is sensitive to signals that indicate host cell stress, such as DNA damage caused by UV radiation or exposure to certain chemicals. These stressors signal that the host cell is unlikely to survive much longer, making the dormant state disadvantageous.
This sensing of host distress triggers a process called induction, where the prophage DNA excises itself from the bacterial chromosome. The virus then switches to the aggressive lytic cycle, rapidly producing new virions and bursting the now-doomed host cell to escape. This allows the virus to salvage its genetic material from a dying host and release a new generation of viral particles into a potentially healthier environment, maximizing the chance of finding new, viable hosts.
Modifying the Host (Lysogenic Conversion)
A powerful, secondary advantage of the lysogenic cycle is the ability of the integrated prophage to alter the characteristics of the host bacterium, a phenomenon known as lysogenic conversion. The prophage carries genes that are expressed by the host, providing a new function that the bacterium did not possess before the infection. This new trait often makes the host more competitive or enhances its ability to spread.
A high-profile example of this is the bacterium Vibrio cholerae, which is harmless until it is infected by a specific bacteriophage. The prophage carries the gene that codes for the cholera toxin, transforming the benign bacterium into the pathogen that causes severe disease in humans. Similarly, the bacteria responsible for diphtheria and botulism acquire their toxin-producing capabilities from integrated prophages.
The advantage to the virus is indirect yet substantial: by making the host cell more virulent or more resistant to environmental threats, the prophage increases the overall fitness and survival of the host population carrying its genes. For instance, the expression of prophage genes can confer resistance to other phages, known as superinfection immunity, protecting the lysogen from further viral attack. Ultimately, anything that helps the host survive and spread also ensures the continued, silent propagation of the viral genome integrated within it.