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You are watching: Cell in which a virus multiplies itself

Baron S, editor. Clinical Microbiology. Fourth edition. Galveston (TX): college of Texas clinical Branch in ~ Galveston; 1996.


General Concepts

The pathologic impacts of famous diseases result from (a) toxic result of viral genesproducts top top the metabolism of infected cells, (b) reactions of the host to infectedcells express virus genes, and also (c) modifications of cellular functions by theinteraction of moving DNA or proteins with viral gene products (see chapter 44.) In many instances, thesymptoms and signs the acute viral illness can be directly related come thedestruction of cell by the infecting virus. The keys to understanding how virusesmultiply room a set of concepts and also definitions.

To multiply, a virus must very first infect a cell. Susceptibility defines the volume ofa cell or animal to come to be infected. The host selection of a virus defines both thekinds of tissue cells and also the animal varieties which it can infect and in which it canmultiply. Viruses differ substantially with respect to their organize range. Part viruses(e.g. St. Luigi encephalitis) have actually a broad host selection whereas the host variety ofothers (e.g. Person papillomaviruses) may be a specific collection of differentiated cellsof one varieties (e.g human keratinocytes). Determinants of the host range andsusceptibility are questioned in the following section.

When one individual becomes exposed come a virus v a human host range, the cells thatbecome instantly infected are the vulnerable cells at the portal of entry (seechapter 45.) epidemic of thesecells might not be enough to cause clinically demonstrable disease. Every toofrequently the condition is the consequence of epidemic of target cell (e.g.,central worried system) by virus introduced into the body straight (e.g. The bite ofa mosquito) or do in the vulnerable cells in ~ the portal of entry. In manyinstances (e.g., respiratory infections, genital herpes simplex infections), thetarget cells space at the portal of entry.

In the food of infection, the virus introduces into the cabinet its genetic material— RNA or DNA — add in countless instances through essentialproteins. The sizes, compositions, and also gene establishments of famous genomes varyenormously. Viruses appear to have developed by different routes and also while no singlepattern of replication has prevailed, two concepts are crucial to the understanding ofhow viruses multiply. First, the capacity of a virus to multiply and also the fate of aninfected cabinet hinge top top the synthetic and duty of virus gene commodities —the proteins. I do not have anything is the correlation in between structure and also function, between thesequence and arrangement of hereditary material and also the system of expression ofgenes an ext apparent 보다 in viruses. The diversity of mechanisms by which virusesensure that their proteins space made is reflected but, unfortunately, not alwaysdeduced from their genomic structure. Second, back viruses differ considerablyin the number of genes castle contain, all viruses encode a minimum of 3 sets offunctions which room expressed by the proteins they specify. Viral proteins (a)ensure the replication that the famous genomes, (b) package the genome right into virusparticles - the virions — and, (c) transform the structure and/or duty ofthe infected cell. The capacity to remain latent, a feature crucial for thesurvival of some viruses in the human population, is an additional functionexpressed by the gene products of part viruses.

The strategy to work by viruses to ensure the execution that these functions varies.In a few instances (papovaviruses), viral proteins merely help host enzyme toreplicate the famous genome. In many instances (e.g., picornaviruses, reoviruses,herpesviruses), it is the famous proteins that replicate the virus genome , yet eventhe many self-dependent virus utilizes at the very least some organize proteins in this process.In all instances, it is the famous proteins which package the genome right into virionseven though host proteins or polyamines may facility with viral genomes (e.g.,papovaviruses) before or throughout the biogenesis that the virus particle. The effects ofviral multiplication may variety from cell fatality to subtle, yet potentially verysignificant, transforms in cell duty and in the spectrum that antigens to express onthe cabinet surface.

A couple of years ago, ours knowledge concerning reproductive cycles of viruses stemmedmainly from analyses the the events developing in synchronously infected cells inculture; us knew little concerning viruses that had not however been grown in culturedcells. Recently, molecule cloning and expression of viral genes enriched enormouslyour knowledge concerning viruses which prosper poorly if at all (e.g., humanhepadnaviruses, human papillomaviruses) in cells in culture.

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The reproductive cycles of all viruses exhibition several usual features (Figure 42-1). First, quickly after infectionand for approximately several hours thereafter, only small amounts the parental infectiousvirus have the right to be detected. This expression is well-known as the eclipse phase; it signals thefact that the famous genomes have been exposed to hold or viral machinery necessaryfor their expression, but that progeny virus production has not yet increased to adetectable level. There adheres to the tires phase, an interval in i beg your pardon progenyvirions accumulate in the cell or in the extracellular setting at exponentialrates. After several hours (e.g., picornaviruses) or days (cytomegalovirus), cellsinfected with lytic viruses cease all your metabolic activity and shed theirstructural integrity. Cells infected through non-lytic viruses may continue tosynthesize viruses indefinitely. The reproductive bike of viruses arrays from 8 hrs(picornaviruses) to more than 72 hrs (some herpesviruses). The virus returns per cellrange from much more than 100,000 poliovirus corpuscle to number of thousand poxvirusparticles.