one virus species preventing multiplicastion of another called
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The pathologic effects of viral diseases result from (a) toxic effect of viral genes products on the metabolism of infected cells, (b) reactions of the host to infected cells expressing virus genes, and (c) modifications of cellular functions by the interaction of cellular DNA or proteins with viral gene products (see chapter 44.) In many instances, the symptoms and signs of acute viral diseases can be directly related to the destruction of cells by the infecting virus. The keys to understanding how viruses multiply are a set of concepts and definitions.
To multiply, a virus must first infect a cell. Susceptibility defines the capacity of a cell or animal to become infected. The host range of a virus defines both the kinds of tissue cells and the animal species which it can infect and in which it can multiply. Viruses differ considerably with respect to their host range. Some viruses (e.g. St. Louis encephalitis) have a wide host range whereas the host range of others (e.g. human papillomaviruses) may be a specific set of differentiated cells of one species (e.g human keratinocytes). Determinants of the host range and susceptibility are discussed in the next section.
When an individual becomes exposed to a virus with a human host range, the cells that become immediately infected are the susceptible cells at the portal of entry (see chapter 45.) Infection of these cells may not be sufficient to cause clinically demonstrable disease. All too frequently the disease is the consequence of infection of target cells (e.g., central nervous system) by virus introduced into the body directly (e.g. the bite of a mosquito) or made in the susceptible cells at the portal of entry. In many instances (e.g., respiratory infections, genital herpes simplex infections), the target cells are at the portal of entry.
In the course of infection, the virus introduces into the cell its genetic material — RNA or DNA — accompanied in many instances by essential proteins. The sizes, compositions, and gene organizations of viral genomes vary enormously. Viruses appear to have evolved by different routes and while no single pattern of replication has prevailed, two concepts are key to the understanding of how viruses multiply. First, the ability of a virus to multiply and the fate of an infected cell hinge on the synthesis and function of virus gene products — the proteins. Nowhere is the correlation between structure and function, between the sequence and arrangement of genetic material and the mechanism of expression of genes more apparent than in viruses. The diversity of mechanisms by which viruses ensure that their proteins are made is reflected but, unfortunately, not always deduced from their genomic structure. Second, although viruses differ considerably in the number of genes they contain, all viruses encode a minimum of three sets of functions which are expressed by the proteins they specify. Viral proteins (a) ensure the replication of the viral genomes, (b) package the genome into virus particles - the virions — and, (c) alter the structure and/or function of the infected cell. The capacity to remain latent, a feature essential for the survival of some viruses in the human population, is an additional function expressed by the gene products of some viruses.
The strategy employed by viruses to ensure the execution of these functions varies. In a few instances (papovaviruses), viral proteins merely assist host enzymes to replicate the viral genome. In most instances (e.g., picornaviruses, reoviruses, herpesviruses), it is the viral proteins that replicate the virus genome , but even the most self-dependent virus utilizes at least some host proteins in this process. In all instances, it is the viral proteins which package the genome into virions even though host proteins or polyamines may complex with viral genomes (e.g., papovaviruses) before or during the biogenesis of the virus particle. The effects of viral multiplication may range from cel
To multiply, a virus must first infect a cell. Susceptibility defines the capacity of a cell or animal to become infected. The host range of a virus defines both the kinds of tissue cells and the animal species which it can infect and in which it can multiply. Viruses differ considerably with respect to their host range. Some viruses (e.g. St. Louis encephalitis) have a wide host range whereas the host range of others (e.g. human papillomaviruses) may be a specific set of differentiated cells of one species (e.g human keratinocytes). Determinants of the host range and susceptibility are discussed in the next section.
When an individual becomes exposed to a virus with a human host range, the cells that become immediately infected are the susceptible cells at the portal of entry (see chapter 45.) Infection of these cells may not be sufficient to cause clinically demonstrable disease. All too frequently the disease is the consequence of infection of target cells (e.g., central nervous system) by virus introduced into the body directly (e.g. the bite of a mosquito) or made in the susceptible cells at the portal of entry. In many instances (e.g., respiratory infections, genital herpes simplex infections), the target cells are at the portal of entry.
In the course of infection, the virus introduces into the cell its genetic material — RNA or DNA — accompanied in many instances by essential proteins. The sizes, compositions, and gene organizations of viral genomes vary enormously. Viruses appear to have evolved by different routes and while no single pattern of replication has prevailed, two concepts are key to the understanding of how viruses multiply. First, the ability of a virus to multiply and the fate of an infected cell hinge on the synthesis and function of virus gene products — the proteins. Nowhere is the correlation between structure and function, between the sequence and arrangement of genetic material and the mechanism of expression of genes more apparent than in viruses. The diversity of mechanisms by which viruses ensure that their proteins are made is reflected but, unfortunately, not always deduced from their genomic structure. Second, although viruses differ considerably in the number of genes they contain, all viruses encode a minimum of three sets of functions which are expressed by the proteins they specify. Viral proteins (a) ensure the replication of the viral genomes, (b) package the genome into virus particles - the virions — and, (c) alter the structure and/or function of the infected cell. The capacity to remain latent, a feature essential for the survival of some viruses in the human population, is an additional function expressed by the gene products of some viruses.
The strategy employed by viruses to ensure the execution of these functions varies. In a few instances (papovaviruses), viral proteins merely assist host enzymes to replicate the viral genome. In most instances (e.g., picornaviruses, reoviruses, herpesviruses), it is the viral proteins that replicate the virus genome , but even the most self-dependent virus utilizes at least some host proteins in this process. In all instances, it is the viral proteins which package the genome into virions even though host proteins or polyamines may complex with viral genomes (e.g., papovaviruses) before or during the biogenesis of the virus particle. The effects of viral multiplication may range from cel
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