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I would like to apologise to the authors of many of the important original studies that have not been cited owing to space limitations. You can also search for this author in PubMed Google Scholar. Correspondence to J M Flanagan.
From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3. Reprints and Permissions. Flanagan, J. Host epigenetic modifications by oncogenic viruses. Br J Cancer 96, — Download citation.
Received : 14 September Revised : 06 November Accepted : 09 November Published : 19 December Issue Date : 29 January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.
Advanced search. Skip to main content Thank you for visiting nature. Download PDF. This article has been updated. Abstract Epigenetic alterations represent an important step in the initiation and progression of most human cancers, but it is difficult to differentiate the early cancer causing alterations from later consequences. Main Epigenetics describes the regulation of gene expression and genomic stability by heritable, but potentially reversible, changes in DNA methylation and chromatin structure.
Host epigenetic changes owing to viruses and virus-associated cancers The cause or consequence conundrum in cancer epigenetics is equally relevant to the epigenetics of viral infection. Table 1 Epigenetic interactions of oncogenic viral proteins Full size table. Figure 1. Full size image. Change history 16 November This paper was modified 12 months after initial publication to switch to Creative Commons licence terms, as noted at publication.
Acknowledgements I would like to apologise to the authors of many of the important original studies that have not been cited owing to space limitations. Rights and permissions From twelve months after its original publication, this work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3. About this article Cite this article Flanagan, J. Copy to clipboard.
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This can be illustrated by thinking of several keys and several locks, where each key will fit only one specific lock. Watch this video to learn how influenza attacks the body. Viruses may enter a host cell either with or without the viral capsid. Plant and animal viruses can enter through endocytosis as you may recall, the cell membrane surrounds and engulfs the entire virus. Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane.
Once inside the cell, the viral capsid degrades, and then the viral nucleic acid is released and becomes available for replication and transcription. The replication mechanism depends on the viral genome. DNA viruses usually use host-cell proteins and enzymes to replicate the viral DNA and to transcribe viral mRNA, which is then used to direct viral protein synthesis. The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and assemble new virions.
Of course, there are exceptions to this pattern. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the information to direct synthesis of the missing proteins. Reverse transcription never occurs in uninfected host cells—the enzyme reverse transcriptase is only derived from the expression of viral genes within the infected host cells.
This approach has led to the development of a variety of drugs used to treat HIV and has been effective at reducing the number of infectious virions copies of viral RNA in the blood to non-detectable levels in many HIV-infected individuals. The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to infect adjacent cells and repeat the replication cycle.
Influenza virus is packaged in a viral envelope that fuses with the plasma membrane. This way, the virus can exit the host cell without killing it. What advantage does the virus gain by keeping the host cell alive? Watch this video on viruses, identifying structures, modes of transmission, replication, and more.
This feature of a virus makes it specific to one or a few species of life on Earth. On the other hand, so many different types of viruses exist on Earth that nearly every living organism has its own set of viruses trying to infect its cells.
Even prokaryotes, the smallest and simplest of cells, may be attacked by specific types of viruses. In the following section, we will look at some of the features of viral infection of prokaryotic cells.
As we have learned, viruses that infect bacteria are called bacteriophages Figure 2. Archaea have their own similar viruses. Phage particles must bind to specific surface receptors and actively insert the genome into the host cell.
The complex tail structures seen in many bacteriophages are actively involved in getting the viral genome across the prokaryotic cell wall. When infection of a cell by a bacteriophage results in the production of new virions, the infection is said to be productive.
If the virions are released by bursting the cell, the virus replicates by means of a lytic cycle Figure 3. An example of a lytic bacteriophage is T4, which infects Escherichia coli found in the human intestinal tract. Sometimes, however, a virus can remain within the cell without being released.
For example, when a temperate bacteriophage infects a bacterial cell, it replicates by means of a lysogenic cycle Figure 3 , and the viral genome is incorporated into the genome of the host cell.
When the phage DNA is incorporated into the host-cell genome, it is called a prophage.
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