Virus, coat protein

The bacteriophage T4 is a complex virus capable of infecting certain bacteria. The virus protein coat (head, tail and tail fibers) contains 40 structural proteins. T4 illustrates well the spatial and temporal control of the stepwise assembly process and the role of external input in regulating that process. A further 13 proteins are required for assembly but do not appear in the completed virus particle. Three of these act as a transient template to promote the formation of the tail baseplate (Fig. 5-3). Another one is a protease which cleaves the major protein of the head (from 55 kDa to 45 kDa) but only after the head has been partially assembled. It is only when the tail reaches its correct length that the cap protein is placed on top allowing the completed head to become attached (Fig. 5-3). Finally, the intact tail fibers are added at the baseplate, and this requires an enzyme-catalyzed reaction to occur. 

Vibrio (i) Curved, rod-shaped bacterial cell, (ii) Bacterium of the genus Vibrio. Virion Virus particle the virus nucleic acid surrounded by protein coat and in some cases other material. 

Virus Any of a large group of submicroscopic infective agents that typically contain a protein coat sunounding a nucleic acid core and are capable of growth only in a living cell. 

FIGURE 1.25 The virus life cycle. Viruses are mobile bits of genetic iuformatiou encapsulated in a protein coat. The genetic material can be either DNA or RNA. Once this genetic material gains entry to its host cell, it takes over the host machinery for macromolecular synthesis and subverts it to the synthesis of viral-specific nucleic acids and proteins. These virus components are then assembled into mature virus particles that are released from the cell. Often, this parasitic cycle of virus infection leads to cell death and disease. 

Tannic acid is a strong inhibitor of virus particles in vitro. It inactivated both TMV and TMV-RNA by forming noninfectious complexes (1). TMV-RNA was much more sensitive to inactivation than was whole TMV. It would thus appear that tannic acid could possibly inactivate TMV by reacting with either the protein coat or the RNA core. 

The eclipse is the period during which the stages of virus multiplication occur. This is called the latent period, because no infectious virus particles are evident. Finally, maturation begins as the newly synthesized nucleic acid molecules become assembled inside protein coats. During the maturation phase, the titer of active virus particles inside the cell rises dramatically. At the end of maturation, release of mature virus particles occurs, either as a result of cell lysis or because of some budding or excretion process. The number of virus particles released, called the burst size, will vary with the particular virus and the particular host cell, and can range from a few to a few thousand. The timing of this overall virus replication cycle varies from 20-30 minutes in many bacterial viruses to 8-40 hours in most animal viruses. We now consider each of the steps of the virus multiplication cycle in more detail. 

As we have noted, the outcome of a virus infection is the synthesis of viral nucleic acid and viral protein coats. In effect, the virus takes over the biosynthetic machinery of the host and uses it for its own synthesis. A few enzymes needed for virus replication may be present in the virus particle and may be introduced into the cell during the infection process, but the host supplies everything else energy-generating system, ribosomes, amino-acid activating enzymes, transfer RNA (with a few exceptions), and all soluble factors. The virus genome codes for all new proteins. Such proteins would include the coat protein subunits (of which there are generally more than one kind) plus any new virus-specific enzymes. 

We might also note another important difference between animal and bacterial cells. Bacterial cells have rigid cell walls containing peptidoglycan and associated substances. Animal cells, on the other hand, lack cell walls. This difference is important for the way by which the virus genome enters and exits the cell. In bacteria, the protein coat of the virus remains on the outside of the cell and only the nucleic acid enters. In animal viruses, on the other hand, uptake of the virus often occurs by endocytosis (pinocytosis or phagocytosis), processes which are characteristic of animal cells, so that the whole virus particle enters the cell. The separation of animal virus genomes from their protein coats then occurs inside the cell. 

Subsequently, similar experiments were done with viral nucleic acids. The pure viral nucleic acid, when added to cells, led to the synthesis of complete virus particles the protein coat was not required. This process is called transfection. More recently, DNA has been used in cell-free extracts to program the synthesis of RNA that functions as the template for the synthesis of proteins characteristic of the DNA... 

Fig. 5.21 Cryoelectron micrograph of a single virus-like particle showing the well-defined protein coating of the 12 nm diameter Au nanoparticle (black disk). (Reprinted with permission from [98]. Copyright (2006) American Chemical Society).

Virus Any of various submicroscopic pathogens consisting essentially of a core of a single nucleic acid surrounded by a protein coat, having the ability to replicate only inside a living cell. 

One of the most intriguing recent examples of disordered structure is in tomato bushy stunt virus (Harrison et ah, 1978), where at least 33 N-terminal residues from subunit types A and B, and probably an additional 50 or 60 N-terminal residues from all three subunit types (as judged from the molecular weight), project into the central cavity of the virus particle and are completely invisible in the electron density map, as is the RNA inside. Neutron scattering (Chauvin et ah, 1978) shows an inner shell of protein separated from the main coat by a 30-A shell containing mainly RNA. The most likely presumption is that the N-terminal arms interact with the RNA, probably in a quite definite local conformation, but that they are flexibly hinged and can take up many different orientations relative to the 180 subunits forming the outer shell of the virus particle. The disorder of the arms is a necessary condition for their specific interaction with the RNA, which cannot pack with the icosahedral symmetry of the protein coat subunits. 

Redox Fe-S proteins High-potential iron protein Ferredoxin Viral coat proteins f Tomato bushy stunt virus protein I Southern bean mosaic virus protein Tobacco mosaic virus protein... 

Viruses are parasitic nucleoprotein complexes. They often consist of only a single nucleic acid molecule (DNA or RNA, never both) and a protein coat. Viruses have no metabolism of their own, and can therefore only replicate themselves with the help of host cells. They are therefore not regarded as independent organisms. Viruses that damage the host cell when they replicate are pathogens. Diseases caused by viruses include AIDS, rabies, poliomyelitis, measles, German measles, smallpox, influenza, and the common cold. 

Viruses are genetic materials enclosed in a protein coat. They show a very high specificity for a particular host cell, infecting and multiplying only within those cells. Viral genetic... 

Viruses are composed of one or more strands of a nucleic acid (core) enclosed by a protein coat (capsid). Many viruses possess an outer envelope of protein or... 

Unlike in bacteria and fungi, viruses do not have a protective coat that separates essential proteins and nucleic acids from the environment. The majority of viruses consist of nucleic acid polymers (DNA or RNA) enclosed within a protein coat (capsid). Sometimes, viruses pick up a lipid membrane (envelope) from the host cell that surroimds the capsid. The average size of viral particles is in the range 10-300 nm. The most common... 

Another complex macromolecular aggregate that can reassemble from its components is the bacterial ribosome. These ribosomes are composed of 55 different proteins and by 3 different RNA molecules, and if the individual components are incubated under appropriate conditions in a test tube, they spontaneously form the original structure (Alberts et al., 1989). It is also known that even certain viruses, e.g., tobacco mosaic virus, can reassemble from the components this virus consists of a single RNA molecule contained in a protein coat composed by an array of identical protein subunits. Infective virus particles can self-assemble in a test tube from the purified components. 

The question of the criteria of autopoiesis is formalized at length, but not always clearly, in the primary literature on autopoiesis. Varela, in his latest book (2000), has simplified these criteria into three basic ones, which can he expressed as follows Verify (1) whether the system has a semi-permeable boundary that (2) is produced from within the system and (3) that encompasses reactions that regenerate the components of the system. Thus, a virus is not an autopoietic system, as it does not produce the protein coat of its boundary or the nucleic acids (the host cell does this, and it is living). A computer virus is also not autopoietic, as it needs a computer system that is not produced hy the virus itself. A growing crystal is not autopoietic, as the components are not generated from an internalized network of reactions. 

Viruses have no cell wall and made up of nucleic acid core enclosed in a protein coat which consists of identical subunits. Viruses are of two types, DNA (deoxyribonucleic acid) viruses and RNA (ribonucleic acid) viruses. DNA viruses are herpes simplex, small pox, hepatitis B, varicellazoster etc. and RNA viruses are rabies, measles, dengue, rubella, yellow fever, poliomyelitis and HIV etc. 

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