Viruses are microscopic entities requiring a host to reproduce. As obligate intracellular parasites, they must invade a living cell and hijack its processes to create more viral particles. This need means viruses employ various strategies, leading to different outcomes for the infected cell.
The Lytic Cycle
One common strategy viruses employ is the lytic cycle, a destructive infection pathway. This cycle begins when a virus attaches to the host cell’s surface, a process called attachment. Following attachment, the virus injects its genetic material, either DNA or RNA, into the host cell. Once inside, the viral genetic material takes control, degrading the host’s DNA and redirecting the cell’s machinery to replicate viral components.
These newly synthesized components then self-assemble into new viral particles, known as virions. The host cell becomes filled with these new virions, and eventually, the cell’s membrane or wall ruptures in a process called lysis, releasing new viral particles into the environment. This destruction of the host cell allows for rapid viral spread to new cells.
The Lysogenic Cycle
In contrast to the destructive lytic pathway, some viruses can enter a lysogenic cycle, characterized as an integrative infection. Similar to the lytic cycle, it begins with the virus attaching to and injecting its genetic material into the host cell. However, instead of immediately taking over the cell’s machinery, the viral DNA integrates into the host cell’s genome.
In this integrated state, the viral DNA is known as a prophage in bacteria, or a provirus in eukaryotic cells, and it remains latent. As the host cell divides, the integrated viral DNA is replicated along with the host’s own genetic material and passed to all daughter cells. The host cell continues to live and function normally. However, under specific conditions, this prophage can excise itself from the host genome and initiate a lytic cycle, leading to the production of new virions and host cell destruction.
Key Distinctions Between Cycles
The fate of the host cell differs fundamentally. Lytic infection destroys the host cell through lysis, releasing new viral particles. Conversely, lysogenic infection allows the host cell to survive and continue dividing, carrying the integrated viral DNA.
Regarding viral replication, the lytic cycle involves immediate, rapid replication of new virions. The lysogenic cycle features a dormant period where viral DNA replicates only with the host cell, meaning new viral particles are not immediately produced.
The state of the viral DNA also differs. In the lytic cycle, viral DNA exists as an independent, free-floating molecule within the host cell’s cytoplasm. During the lysogenic cycle, it integrates into the host cell’s chromosome, forming a prophage or provirus.
The outcome for the host population varies. Lytic infections cause rapid viral spread and host cell death. Lysogenic infections result in a latent spread of viral genetic material through host cell division, potentially affecting many generations without immediate harm.
Symptoms and disease progression often differ. Lytic infections typically result in acute, symptomatic diseases due to rapid cell destruction. In contrast, lysogenic infections can be latent or asymptomatic for extended periods, with disease onset delayed until the virus switches to the lytic cycle.
Factors Influencing Viral Choice and Real-World Examples
Several factors influence whether a virus enters a lytic or lysogenic cycle, including environmental conditions and host cell health. For example, stressors like ultraviolet (UV) radiation, certain chemicals, or nutrient deprivation can trigger a prophage to excise from the host genome and enter the lytic cycle. Host cell physiological state and viral concentration also play a role.
Bacteriophages, viruses that infect bacteria, are classic examples. The lambda phage is a temperate phage known for its ability to switch between lytic and lysogenic pathways depending on environmental cues. Human viruses like herpesviruses (e.g., herpes simplex virus) demonstrate similar latency, where viral DNA remains dormant in host cells for long periods before reactivating and causing outbreaks. Human immunodeficiency virus (HIV) also integrates its genetic material into host cells before active replication.