lysogeny
Summary
Lysogeny is the bacteriophage life cycle in which phage DNA integrates into the host bacterial chromosome as a prophage and replicates passively with the host without lysing the cell. Induction (e.g., by SOS response/UV) can switch it to the lytic cycle. Clinically important because prophages encode toxins in several pathogens (lysogenic conversion).
Detail
**Definition:** Lysogeny (lysogenic cycle) is a temperate bacteriophage life cycle in which the viral genome integrates into the bacterial chromosome (or persists as a plasmid-like element) as a **prophage**. The host cell, now a "lysogen," survives and replicates the prophage along with its own DNA. The prophage is vertically transmitted to daughter cells.
**Mechanism (lambda phage model):** - Phage attaches, injects DNA, which circularizes. - The **cI repressor** is expressed and blocks lytic gene transcription. It also confers immunity to superinfection by the same phage. - Integrase (Int) mediates site-specific recombination at the attachment sites (attP/attB), integrating the genome. - **Induction:** DNA damage (UV, mitomycin C) activates the SOS response, where RecA-mediated autoproteolysis cleaves the repressor. The prophage excises (integrase plus excisionase), and the lytic cycle begins, ending in cell lysis and release of progeny phage.
**Lytic vs lysogenic:** - Lytic (virulent phages): phage takes over the cell, makes progeny, and lyses the cell. - Lysogenic (temperate phages): the genome is integrated and dormant, with no cell lysis until induction.
**Lysogenic (phage) conversion:** Prophage genes can change the phenotype of the host bacterium. This is a high-yield Step 1 topic. Toxins encoded by prophages include: - **Corynebacterium diphtheriae**: diphtheria toxin (β-prophage), which inactivates EF-2. - **Clostridium botulinum**: botulinum toxin (types C and D). - **Vibrio cholerae**: cholera toxin (CTXφ, a filamentous phage that integrates). - **Streptococcus pyogenes**: erythrogenic (pyrogenic exotoxin) toxin, which causes scarlet fever. - **Shiga toxin** of EHEC (STEC), encoded by a lambdoid phage. - **Staphylococcus aureus**: Panton-Valentine leukocidin, and toxic shock syndrome toxin (TSST-1) on a pathogenicity island, which is mobilized by phages.
Mnemonic: **"ABCDE"** for phage-encoded toxins: **A**-B toxin Shiga (and Shiga-like), **B**otulinum, **C**holera, **D**iphtheria, **E**rythrogenic toxin of *S. pyogenes*.
**Transduction link:** - **Specialized transduction** results from imprecise excision of a lysogenic phage. It carries adjacent bacterial genes (e.g., gal or bio for lambda) and is restricted to genes near the integration site. - **Generalized transduction** occurs in the lytic cycle, when a packaging error places random host DNA into the phage head.
**Clinical significance:** Prophage-carried virulence genes explain why only toxigenic strains of some bacteria cause disease (e.g., non-toxigenic *C. diphtheriae* is harmless). Phage therapy usually uses strictly lytic phages, since temperate phages can transfer virulence or resistance genes. Some antibiotics (e.g., fluoroquinolones) can trigger the SOS response and phage induction, which can increase Shiga toxin release in EHEC. This is one reason antibiotics are avoided in EHEC infection (risk of HUS).
**Note:** Retroviral proviral integration (HIV) is analogous conceptually but is not termed lysogeny.
Sources
- First Aid for the USMLE Step 1 (Microbiology: Bacterial genetics, transduction, toxins)
- Sketchy Medical – Microbiology (Bacterial Genetics)
- Murray: Medical Microbiology
- Brooks: Jawetz, Melnick & Adelberg's Medical Microbiology
- Levinson: Review of Medical Microbiology and Immunology
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.