lytic cycle
Summary
The lytic cycle is a viral replication pathway in which a virus (or bacteriophage) infects a host cell, hijacks its machinery to replicate, and then lyses the cell to release progeny virions. It contrasts with the lysogenic cycle, in which viral genome integrates into the host genome as a dormant prophage/provirus. Virulent phages only undergo lytic cycle; temperate phages can do either.
Detail
**Stages (bacteriophage model):** 1. Attachment (adsorption) – phage binds specific host receptors. 2. Penetration – phage injects its genome (tail contraction/lysozyme degrades peptidoglycan). 3. Biosynthesis – host RNA polymerase/ribosomes transcribe and translate phage genes (early genes: nucleases, DNA replication proteins; late genes: capsid and tail proteins, lysozyme). Host DNA is degraded. 4. Maturation (assembly) – capsids and genomes are packaged into virions. 5. Release – holins and endolysins (lysozyme) lyse the cell wall, releasing progeny phages.
**Lytic vs. lysogenic:** - Lytic: active replication, host cell death, no genome integration. Virulent phages are exclusively lytic. - Lysogenic: temperate phage (e.g., lambda) integrates as a prophage and replicates passively with host chromosome. Repressor (cI in lambda) maintains latency. Stressors such as UV light or DNA damage (SOS response, RecA cleaves the repressor) trigger induction, switching to the lytic cycle.
**Clinical/board relevance:** - Lysogenic conversion: prophage genes encode toxins in some bacteria. Mnemonic **ABCD'S** – **A**-B toxin of Shiga toxin-producing E. coli (Shiga-like toxin), **B**otulinum toxin (C. botulinum), **C**holera toxin (V. cholerae), **D**iphtheria toxin (C. diphtheriae), **S**treptococcus pyogenes erythrogenic toxin (scarlet fever), plus staphylococcal enterotoxin A/TSST-1 and PVL in some strains. (Note: tetanus toxin is plasmid-encoded, not phage-encoded.) - Transduction: Generalized transduction occurs from errors during the lytic cycle (host DNA mistakenly packaged into a phage head). Specialized transduction occurs from imprecise excision of a prophage in the lysogenic-to-lytic switch (carries adjacent host genes, e.g., gal or bio for lambda). - Animal viruses: most acute infections (influenza, enteroviruses such as poliovirus, rhinovirus, adenovirus, rotavirus) follow lytic-type replication with cytopathic effects, in contrast with latent infections (HSV, VZV, EBV, CMV) and integrating viruses (HIV provirus, HBV). Herpesviruses switch between latent and lytic (reactivation) phases, which is clinically relevant (e.g., EBV lytic reactivation in immunosuppression, HSV recurrences). - Phage therapy uses virulent (strictly lytic) phages against multidrug-resistant bacteria, because temperate phages can transfer virulence or resistance genes. - Enveloped viruses often exit by budding without immediate cell lysis; naked (non-enveloped) viruses typically exit by cell lysis, so lysis is characteristic of non-enveloped viruses.
**High-yield pearls:** Lytic = cell death and burst; lysogenic = latent integration; induction by DNA damage; toxin genes via lysogenic conversion; generalized transduction arises from the lytic cycle.
Sources
- First Aid for the USMLE Step 1 (Microbiology: Bacterial genetics; Virology)
- Sketchy Medical – Microbiology: Bacterial Genetics and Virology
- Murray's Medical Microbiology
- Brock Biology of Microorganisms
- Pathoma/Boards and Beyond – Microbiology
Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.