why can a virus not multiply on its own until it enter the host cell
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General Concepts
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 spectrum of antigens expressed on the cell surface.
A few years ago, our knowledge concerning reproductive cycles of viruses stemmed mainly from analyses of the events occurring in synchronously infected cells in culture; we knew little concerning viruses that had not yet been grown in cultured cells. Recently, molecular cloning and expression of viral genes enriched enormously our knowledge concerning viruses which grow poorly if at all (e.g., human hepadnaviruses, human papillomaviruses) in cells in culture.
The reproductive cycles of all viruses exhibit several common features (Figure 42-1). First, shortly after gratuitous; its significance stems from the observation that cytolytic viruses which normally destroy the permissive cell during productive infection may merely injure, but not destroy, abortively infected, permissive or non-permissive cells. The consequences of this injury may be the expression of host functions which transform the cell from normal to malignant. Persistence of the viral genomes is a more common consequence of restrictive and abortive infections.
Initiation of Infection
To infect a cell, the virus must attach to the cell surface, penetrate into the cell, and become sufficiently uncoated to make its genome accessible to viral or host machinery for transcription or translation.
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