Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.
Attachment and DNA Injection
The infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage specifically interact with receptor molecules on the bacterial outer membrane, ensuring host specificity. Upon attachment, the baseplate of the phage releases gp5, an enzyme that locally degrades the peptidoglycan layer of the bacterial cell wall, weakening its structure and facilitating DNA entry. As the tail sheath contracts like a spring, the tail tube punctures the weakened cell wall, creating a direct pathway for viral DNA entry into the bacterial cytoplasm. The empty protein capsid remains outside the cell.
Hijacking Host Machinery
Once inside the host, the phage DNA rapidly takes control of cellular functions. Early viral genes are transcribed first, producing enzymes that degrade bacterial DNA and modify transcription factors to favor viral replication. This prevents interference with viral gene expression and allows for the efficient synthesis of new viral proteins and genomic DNA using the host’s ribosomes and nucleotides. The phage redirects the host's transcription and translation machinery entirely toward viral replication.
Assembly of New Virions
After the production of viral components, a highly coordinated process organizes structural proteins into new phage particles. Self-assembly of viral components follows a precise order, assisted by scaffolding proteins and chaperones, ensuring the correct attachment of capsids, tails, and fibers. Fully assembled, infectious virions form within the bacterial cytoplasm, ready to infect new hosts.
Cell Lysis and Virion Release
To release progeny virions, the phage produces holin proteins that create membrane pores, facilitating the action of lysozyme in degrading the bacterial cell wall. As the enzymatic degradation progresses, the bacterial cell swells before bursting due to osmotic lysis. Within approximately 25–30 minutes of initial infection, the bacterial cell ruptures, releasing dozens to hundreds of new phage particles. These virions then disperse to infect other susceptible E. coli cells, perpetuating the lytic cycle.
A T-even bacteriophage, such as T4, infects E. coli to replicate.
The phage first attaches to specific receptors on the E. coli cell wall using its tail fibers, ensuring host specificity.
Lysozyme released from the phage’s baseplate weakens the bacterial cell wall, creating an entry point.
The phage then contracts its tail sheath, injecting its DNA into the bacterial cytoplasm while leaving the empty capsid outside.
Inside the host cell, bacterial transcription and translation are shut down, the host DNA is degraded, and cellular resources, such as RNA and DNA polymerases, are redirected toward viral protein synthesis and genome replication.
Newly synthesized viral components self-assemble into complete phages.
Once enough virions have formed, they release holin proteins to create pores in the host membrane, and together with lysozyme degrade the bacterial cell wall.
Within 25–30 minutes, the bacterial cell lyses, releasing new virions to infect other E. coli, thereby repeating the lytic cycle.
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