Viruses must replicate in living cells. The most basic molecular requirement for virus replication is for virus to induce either profound or subtle changes in the cell so that viral genes in the genome are replicated and viral proteins are expressed. This will result in the formation of new viruses — usually many more than the number of viruses infecting the cell in the first place. When reproducing, viruses use at least part of the cell's equipment for replication of viral nucleic acids and expression of viral genes. They also use the cell's protein synthetic machinery, and the cell's metabolic energy resources.
The dimensions and organization of "typical" animal, plant, and bacterial cells are shown in Fig. 2.1. The size of a typical virus falls in the range between the diameters of a ribosome and of a centriolar filament. With most viruses, infection of a cell with a single virus particle will result in the synthesis of more than one (often by a factor of several powers of 10) infectious virus. Any infection that results in the production of more infectious virus at the end than at the start is classified as a productive infection. The actual number of infectious viruses produced in an infected cell is called the burst size, and this number can range from less than 10 to over 10,000, depending on the type of cell infected, the nature of the virus, and many other factors.
Infections with many viruses completely convert the cell into a factory for replication of new viruses. Under certain circumstances and/or in particular cells, however, virus infection leads
Rough endoplasmic reticulum
Nuclear pore Nucleus
Smooth endoplasmic reticulum
Respiratory enzymes tRNA molecule
Cytoplasmic membrane Peptidoglycan layer Outer lipopolysaccharide laminar cell wall
to a state of coexistence between the cell and infecting virus, which can persist for as long as the life of the host. This process can be a dynamic one in which there is a small amount of virus produced constantly, or it can be passive where the viral genome is carried as a "passenger" in the cell with little or no evidence of viral gene expression. Often in such a case the virus induces some type of change in the cell so that the viral and cellular genomes are replicated in synchrony. Such coexistence usually results in accompanying changes to the protein composition of the cell's surface — the immune "signature" of the cell — and often there are functional changes as well. This process is called lysogeny in bacterial cells and transformation in animal and plant cells.
In animal cells, the process of transformation often results in altered growth properties of the cell and can result in the generation of cells that have some or many properties of cancer cells. There are instances, however, where the coexistence of a cell and an infecting virus leads to few or no detectable changes in the cell. For example, herpes simplex virus (HSV) can establish a latent infection in terminally differentiated sensory neurons. In such cells there is absolutely no evidence for expression of any viral protein at all. Periods of viral latency are interspersed with periods of reactivation (recrudescence) where virus replication is reestablished from the latently infected tissue for varying periods of time.
Some viral infections of plant cells also result in stable association between virus and cell. Indeed, the variegation of tulip colors, which led to economic booms in Holland during the sixteenth century, is the result of such associations. Many other examples of mosaicism resulting from persisting virus infections of floral or leaf tissue have been observed in plants. However, many specific details of the association are not as well characterized in plants as in animal and bacterial cells.
Various patterns of replication as applied to specific viruses, as well as the effect of viral infections on the host cell and organism, are the subject of many of the following chapters in this book. The best way to begin to understand patterns of virus replication is to consider a simple general case: the productive infection cycle — this is shown schematically in Fig. 2.2. A number of critical events are involved in this cycle. The basic pattern of replication is as follows:
1 The virus specifically interacts with the host cell surface, and the viral genome is introduced into the cell. This involves specific recognition between virus surface proteins and specific proteins on the cell surface (receptors) in animal and bacterial virus infections.
2 Viral genes are expressed using host cell processes. This viral gene expression results in synthesis of a few or many viral proteins involved in the replication process.
3 Viral proteins modify the host cell and allow the viral genome to replicate using host and viral enzymes. While this is a simple statement, the actual mechanisms by which viral enzymes and proteins can subvert a cell are manifold and complex. This is often the stage at which the cell is irreversibly modified and eventually killed. Much modern research in the molecular biology of virus replication is directed toward understanding these mechanisms.
4 New viral coat proteins assemble into capsids and viral genomes are included.
The process of assembly of new virions is relatively well understood for many viruses. The successful description of the process has resulted in a profound linkage of knowledge about the principles of macromolecular structures, the biochemistry of protein—protein and protein-nucleic acid interactions, and an understanding of the thermodynamics of large macromolecule structure.
Fig. 2.2 The virus replication cycle. Most generally, virus replication can be broken into the stages shown: (a) initial recognition between virus and cell and introduction of viral genetic material into the host cell; (b) virus gene expression and induction of virus-induced modification of host allowing; (c) virus genome replication. Following this, (d) virus-associated proteins are expressed, and (e) new virus is assembled and released, often resulting in cell death.
5 Virus is released where it can infect new cells and repeat the process. This is the basis of virus spread, whether from cell to cell or from individual to individual. Understanding the process of virus release requires knowledge of the biochemical interactions between cellular organelles and viral structures. Understanding the process of virus spread between members of a population requires knowledge of the principles of epidemiology and public health.
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