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Chapter 14 : Genome Plasticity of Papillomaviruses

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Genome Plasticity of Papillomaviruses, Page 1 of 2

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Abstract:

The human papillomavirus type 16 (HPV-16) genome is typical for the vast majority of all papillomaviruses. In contrast to RNA viruses, papillomaviruses replicate based on the same mechanisms and enzymes that support replication of the chromosomes of the host cell. Humans are presently known to carry at least 125 different human papillomavirus types, i.e., virus genomes differing by more than 10% from one another. In phylogenetic trees, these 125 human papillomaviruses form minor and major clusters that, under present taxonomic rules, are identified as species and genera. On the higher taxonomic level of the genus, the human papillomaviruses belong to five remotely related genera: , , , , and . The most extreme examples of papillomavirus-host linkage are the three and two papillomaviruses which have so far been identified in birds and reptiles, respectively, and which form phylogenetic out-groups to all mammalian papillomaviruses and to one another. The molecular strategies encoded in the replication initiator E1, the transcription/replication regulator E2, the major capsid protein L1, and the minor capsid protein L2, with its important role in the infection process, are apparently very successful and indispensable to the papillomavirus life cycle. The majority of papillomaviruses have these genes, but one or two of the genes are lacking in many animals and even three human papillomavirus types. The stability of the HPV-16 and HPV-18 genomes makes it unlikely that new viral variants will emerge in response to vaccination.

Citation: Bernard H. 2012. Genome Plasticity of Papillomaviruses, p 242-247. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch14

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Circular Double-Stranded DNA
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The genome of human papillomavirus type 16 (HPV-16) represents a genetic organization that is typical for all papillomaviruses. The function of early (E) and late (L) genes is described elsewhere in this chapter. doi:10.1128/9781555817213.ch14f01

Citation: Bernard H. 2012. Genome Plasticity of Papillomaviruses, p 242-247. In Hacker J, Dobrindt U, Kurth R (ed), Genome Plasticity and Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817213.ch14
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References

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