For the sake of comparison, we now turn to multiplication in bacterial viruses—the bacteriophages. When Frederick Twort and Felix d’Herelle discovered these viruses in 1915, they first thought that the bacterial host cells were being eaten by some unseen parasite, which they called a bacteriophage.
So far as is known, all bacteria are parasitized by various specific viruses. Most bacteriophages (often shortened to phage) contain double-stranded DNA, though single-stranded DNA and RNA types exist as well. Bacteriophages are of great interest to medical microbiologists because they can make the bacteria they infect more virulent for humans.
Probably the most widely studied bacteriophages are those of the intestinal bacterium Escherichia coli—especially the T-even phages and the lambda phages. They are complex in structure, with an icosahedral capsid head containing DNA, a central tube (surrounded by a sheath), collar, base plate, tail pins, and fibers.
Bacteriophages go through stages similar to those of the animal viruses described earlier (process figure 1). First, they adsorb to host bacteria using specific receptors on the bacterial surface. Although the entire phage cannot enter the host cell, the nucleic acid is injected through a rigid tube the phage inserts through the bacterial membrane and wall (figure2). The empty capsid remains attached to the cell surface. Entry of the nucleic acid stops host cell DNA replication and protein synthesis, and it soon prepares the cell machinery for viral replication and synthesis of viral proteins. As the host cell produces new phage parts, the parts spontaneously assemble into bacteriophages.
Process Fig1. Events in the multiplication cycle of lambda bacteriophages. The lytic cycle (1–7) involves full completion of viral infection through lysis and release of virions. Occasionally the virus enters a reversible state of lysogeny (left), and its DNA is incorporated into the host’s genetic material.
Fig2. Penetration of a bacterial cell by a bacteriophage. After adsorption, the phage plate becomes embedded in the cell wall, and the sheath contracts, pushing the tube through the cell wall and membrane and releasing the nucleic acid into the interior of the cell.
An average-size Escherichia coli cell can contain up to 200 new phage units at the end of this period. Eventually, the host cell becomes so packed with viruses that it undergoes lysis and splits open, thereby releasing the mature virions (figure 3). This process is hastened by viral enzymes produced late in the infection cycle that weaken the cell envelope. Upon release, the virulent phages can spread to other susceptible bacterial cells and begin a new cycle of infection.
Fig3. A weakened bacterial cell, crowded with viruses. The cell has ruptured and released numerous virions that can then attack nearby susceptible host cells. Note the empty heads of “spent” phages lined up around the ruptured wall. Lee D. Simon/Science Source
Lysogeny: The Silent Virus Infection
The lethal effects of a virulent phage on the host cell present a dramatic view of virus–host interaction. However, not all bacteriophages go immediately into a lytic cycle. Depending upon the conditions in the bacterial host, some special DNA viruses, called temperate phages, undergo adsorption and penetration into the bacterial host but are not replicated or released immediately. Instead, the viral DNA enters an inactive prophage state, during which it is usually inserted into the bacterial chromosome. This viral DNA will be retained by the bacterial cell and copied during its normal cell division so that the cell’s progeny will also have the phage DNA. This condition, in which the host chromosome carries bacteriophage DNA, is termed lysogeny. Because viral particles are not produced, the bacterial cells carrying temperate phages do not lyse, and they appear entirely normal. Later, in a process called induction, the prophage in a lysogenic cell will be activated and progress directly into viral replication and the lytic cycle. The lysogenic phase is depicted in the green section of process figure 1. Lysogeny is a less deadly form of infection than the full lytic cycle and is thought to be an advancement that allows the virus to spread without killing the host.
Because of the close association between the genetic material of the virus and host, phages occasionally serve as transporters of bacterial genes from one bacterium to another; consequently, they can play a profound role in bacterial genetics. This phenomenon, called trans duction, is one way that genes for toxin production and drug resistance are transferred between bacteria.
Phages have profound effects on the infectiousness and virulence of pathogenic bacteria. Viral genomes often encode toxins, enzymes, and other factors that can alter the course and outcome of infections. When a bacterium acquires genes from its temperate phage, it is called lysogenic conversion (see process figure 1). The phenomenon was first discovered in the 1950s in Corynebacterium diphtheriae, the pathogen that causes diphtheria. The diphtheria toxin responsible for the severe nature of the disease is a bacteriophage product. C. diphtheriae cells without the phage are less pathogenic. Other bacteria that are made virulent by their prophages are Vibrio cholerae, the agent of cholera, and Clostridium botulinum, the cause of botulism.
The cycles of bacterial and animal viruses illustrate different patterns of viral multiplication, which are summarized in table1.
Table1. Comparison of Bacteriophage and Animal Viral Multiplication
