Virus particles protein coat

Synthesis of proteins for virus particles. Proteins that make the virus coat as well as those in the viral envelope are synthesized from instructions in the viral genetic information. Once these proteins are synthesized, all the components necessary for formation of new vims particle are present within the infected cell. 

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. 

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. 

In another rather different application, ROA data indicated that the coat protein subunits of intact tobacco rattle virus contain a significant amount of PPII structure, which is possibly associated with sequences previously suggested to be mobile and to be exposed externally in the intact virus particle and which may be associated with its transmission by nematodes (Blanch et al., 2001b). 

The virus genome consists of either RNA or DNA. The genome is surrounded by a coat of protein (and occasionally other material). When the virus genome is inside the coat it is called a virus particle or virion. 

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. 

The bacterial RNA viruses are all of quite small size, about 26 nm in size, and they are all icosahedral, with 180 copies of coat protein per virus particle. The complete nucleotide sequence of several RNA phages are known. In the RNA phage MS2, which infects Escherichia coli, the viral RNA is 3,569 nucleotides long. The virus RNA, although single stranded, has extensive regions of secondary and tertiary structure. The RNA strand in the virion has the plus (+) sense, acting directly as mRNA upon entry into the cell. 

As seen in the genetic map, the genes after gene 1.1, transcribed by the T7 RNA polymerase, code for proteins that are involved in T7 DNA synthesis, the formation of virus coat proteins, and assembly. Three classes of T7 proteins are formed class I, made 4-8 minutes after infection, which use the cell RNA polymerase class II, made 6-15 minutes after infection, which are made from T7 RNA polymerase and are involved in DNA metabolism class III, made from 6 minutes to lysis, which are transcribed by T7 RNA polymerase and which code for phage assembly and coat protein. This sort of sequential pattern, commonly seen in many large double-stranded DNA phages, results in an efficient channeling of host resources, first toward DNA metabolism and replication, then on to formation of virus particles and release of virus by cell lysis. 

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).

The possibility to use the YI sensor for virus detection was explored by monitoring the interaction between a-HSV-1 gG antibody and HSV-1 virus particles. To this end, channel 1 was coated with protein pA as described in Sect. 10.4.2 followed by the immobilization of a a-HSV-1 gG layer on the sensing surface of channel 1. Channel 4 was used as a reference channel. Finally a solution with HSV-1 virus particles at a concentration of 105 particles/ml was added to channel 1. Figure 10.2 shows the phase change measured between channel 1 and reference channel 4, clearly demonstrating the detection of virus particles by the YI sensor (Fig. 10.15). 

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. 

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. 

Viruses Viruses are not free-living organisms rather, they are infectious parasites that use the resources of a host cell to carry out many of the processes they require to propagate. Many viral particles consist of no more than a genome (usually a single RNA or DNA molecule) surrounded by a protein coat. 

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