ECOLOGICAL BIOCHEMISTRY - Study Guide - V. M. Isaienko 2005

Chapter I. VIRAL INFECTIONS AND ORGANISMAL RESPONSES (General Concepts)

1.1. Virus-Bacteria Interactions

Viruses that infect Bacteria are called Bacteriophages, or simply phages (from Gr. phagos meaning devourer). To date, bacteriophages capable of infecting over 100 bacterial species have been identified.

The Morphology of tadpole-shaped phages has been studied in the greatest detail; their main structural components are a protein-encased HEAD (capsid) and a tail. The Structure/83.html">Structural elements of the tail include an outer sheath, an inner core, tail fibers, and a base plate with spikes.

The presence of a rigid Cell wall in most prokaryotes requires specialized mechanisms for bacteriophage entry and exit. In terms of population dynamics, prokaryotes resemble Cells that continue to multiply as long as a suitable nutrient medium is available. The interaction between phage virions and bacteria occurs cyclically within a bacterial culture until an equilibrium state is established,

which is determined by the number of host cells, Viral Particles, and their Replication rates. A different scenario unfolds when bacteria are capable of differentiation, such as in response to environmental shifts.

In terms of chemical composition, bacteriophages are relatively simple structures containing genomic nucleic acid, protein, and minor amounts of Lipids and CARBOHYDRATES. The nucleic acid in most bacteriophages is double-stranded DNA, though single-stranded DNA or RNA, as well as double-stranded RNA, can also occur.

Bacteriophages possess several Proteins, predominantly structural ones that form the head capsid and tail elements (sheath, core, base plate, and fibers). The head of tadpole-shaped bacteriophages also contains an internal protein (accounting for 3–7% of the total protein content). Certain phages have additionally been found to contain Enzymes such as Lysozyme and phosphatase, among others.

The process of bacterial infection by phages consists of several stages. The first of these is the specific recognition of particular receptor-containing sites on the host cell surface by the tail fibers (fibrils), to which the phage attaches. This is followed by the attachment of the base plate spikes. Subsequently, the tail core detaches from the base plate, and the tail sheath contracts, forcefully driving the tail core through the "soft" layers of the bacterial envelope, which consist of Lipoproteins and glycopolysaccharides. Further penetration of the core is facilitated by a lysozyme-like enzyme. Through the resulting opening, the genomic nucleic acid is injected from the phage head into the bacterium via tail contraction (an ATP-dependent process).

In addition to genomic nucleic acid, a small amount of protein and certain other substances, including oligopeptides and Polyamines, are also injected into the bacterial cell.

From the moment the nucleic acid enters the bacterium, its interaction with The Cell begins—marking the latent period of intracellular bacteriophage reproduction. During this stage, the nucleic acid triggers rapid restructuring of intracellular processes within the bacterial cell, directing them entirely toward the synthesis of new phage virions. At the beginning of this stage, The production of enzymes is initiated that catalyze phage Nucleic Acid Replication utilizing the host's own Nucleic Acids. Shortly thereafter, the synthesis of phage proteins commences within the bacterial cell. Aggregation of these proteins results in the assembly of individual phage virion components. Another product of this process is the synthesis of phage lysozyme. Once all phage components are synthesized, the complete virion is assembled.

The lytic enzymes produced, encoded by the phage nucleic acid, are capable of degrading the dense peptidoglycan layer of the Introduction/37.html">Bacterial cell wall. This process results in the lysis of the bacterial cell and the release of newly formed phage virions.

In addition to the lytic interaction between a phage and a bacterium, which culminates in the lysis of the infected cell, a lysogenic interaction also exists. In this case, the phage genome is transmitted in a non-infectious form by bacterial cells from generation to generation, with corresponding virions being synthesized from time to time in a fraction of the cells, which then lyse those cells and are released into the external environment. Lysogenic cells that are reinfected by these virions do not undergo lysis (owing to their Immunity to this phage), allowing the lysogenic culture to continue growing normally. The presence of free virions can be detected by exposing other, non-lysogenic bacterial strains that are susceptible to lysis by the given phage. Phages capable of lysogenizing the bacteria they infect are termed temperate. It should be noted, however, that even temperate phages induce a productive infection in many or even all cells during the initial infection of susceptible bacteria.

The Emergence of lysogenic, or lysogenized, cells requires a specific sequence of events. The probability of such cells appearing varies among phages and depends on cultivation conditions. For a stable lysogenic cell line to be established, two conditions must be met. First, the prophage must reside within the cell in such a state that upon Cell Division, each daughter cell receives at least one copy. In the case of this phage, this is achieved by integrating its DNA into the bacterial chromosome, allowing the prophage DNA to replicate passively and segregate via the host cell apparatus. Second, those viral genes whose products are potentially capable of disrupting cell integrity must be regulated so that the cells can grow and multiply unimpeded. This is achieved through the repression of Gene METABOLISM/31.html">Transcription. In cells lysogenic for a given phage, none of the viral genes required for infection production should be transcribed. However, under The Influence of various factors or spontaneously, bacteriophages in lysogenic cells can undergo induction, becoming aggressive toward the bacterial cell.