Bacteriophage Calculators
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Phage Structure
Tail phages (e.g., T4): head (icosahedral capsid containing dsDNA) + tail (hollow tube for DNA injection) + tail fibers (host recognition). Filamentous phages (e.g., M13): single-stranded DNA in a helical protein coat. Icosahedral RNA phages (e.g., MS2, Qβ): ssRNA in icosahedral capsid. Phage size: typically 25–200 nm. Phage genome: 5 kb–700 kb; encodes structural proteins, replication enzymes, and lysis proteins.
Lytic Cycle
1. Adsorption: tail fibers bind specific bacterial surface receptors (host-range determinism). 2. Injection: DNA injected into host; protein coat remains outside. 3. Takeover: phage enzymes degrade host chromosome; phage DNA replicated; phage proteins synthesized. 4. Assembly: new phage particles assembled from components. 5. Lysis: phage-encoded lysins lyse cell wall; ~100–300 new phages released (burst size). Latent period: ~25–35 min for T4 at 37°C. Eclipse period (within latent period): no infective phage detectable inside cell.
Lysogenic Cycle
Phage DNA integrates into host chromosome (prophage) via site-specific recombination (integrase enzyme). Prophage replicates with host; genes silenced by CI repressor. Induction: UV light, DNA damage → SOS response → excision → lytic cycle.
Phage Therapy
Uses phages to treat antibiotic-resistant bacterial infections; personalized (phage must match the pathogen); FDA-regulated as biologics; compassionate use cases growing; ongoing clinical trials.
Glossary
Frequently Asked Questions
A bacteriophage is a virus that specifically infects bacteria. Basic structure varies by phage family: Tailed phages (Caudovirales, ~96% of all described phages): icosahedral capsid (head) containing double-stranded DNA; a tail structure for DNA injection; and tail fibers for specific host recognition. These are further divided by tail morphology: Myoviridae (contractile tail, like T4); Siphoviridae (long flexible tail, like lambda); Podoviridae (short tail). Non-tailed phages: filamentous (M13) or icosahedral RNA phages. Phages do not have their own metabolism — they are obligate intracellular parasites that hijack bacterial machinery for replication.
Lytic cycle: phage DNA is immediately transcribed; host chromosome degraded; phage components synthesized; ~100–300 new phage particles assembled; host cell lysed; new phages released. Rapid — ~30 minutes for T4. Outcome: bacterial death, phage amplification. Lysogenic cycle: phage DNA integrates into the bacterial chromosome (as prophage); silenced by CI repressor protein; replicates with the bacterium through binary fission; no host killing. Can maintain for many generations. Induction: DNA damage triggers SOS response → CI repressor inactivated → prophage excised → enters lytic cycle. Phages capable of both cycles are called temperate phages (example: bacteriophage lambda). Phages that can only undergo lytic cycle are called virulent phages (example: T4).
The one-step growth experiment (Ellis and Delbruck, 1939) demonstrated that phages replicate by a burst rather than continuous budding. Protocol: infect bacteria synchronously with phage at low MOI; dilute immediately to prevent secondary infection; plate samples over time to count infective centers. Results: latent period: no increase in phage titer (phage multiplying inside cells); rise period: sharp increase as cells lyse; plateau: maximum titer reached (all infected cells lysed). Key measurements: latent period (time from infection to first lysis); burst size = (final titer / initial infective centers) ≈ 100–300 phage/cell for T4. The experiment proved phages replicate intracellularly, demolishing the earlier view of continuous phage growth.
Phage therapy uses bacteriophages to treat bacterial infections, particularly antibiotic-resistant ones (MRSA, MDR-Pseudomonas, carbapenem-resistant Klebsiella). How it works: lytic phages specifically infect and kill target bacteria; host cells (human) are not infected (phages are bacteria-specific); phages may replicate at infection sites (self-amplifying treatment). Advantages: highly specific (minimal dysbiosis of normal flora); can evolve to overcome resistance; can penetrate biofilms. Challenges: narrow host range (phage must exactly match the bacterial strain); immune response against phages; regulatory uncertainty; personalized medicine approach required. Status: not FDA-approved for general use; available under expanded access (compassionate use) in life-threatening cases; multiple clinical trials ongoing in US and Europe.