Quote:
Originally Posted by graciegirl
(Post 1045551)
Read it again. It would not have been developed without recent genetic research and the unlocking of the human genome..
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Gracie - you are correct as usual. I am including some of the genetic work done on HPV prior to the development of the vaccine. I have included the abstract and conclusions. Please read the last sentence of the conclusions. A link to the paper is found at the end of this post.
Public Health Genomics
Karger Publishers
Human Papillomaviruses: Genetic Basis of Carcinogenicity
Robert D. Burk, Zigui Chen, and Koenraad Van Doorslaer
Additional article information
Abstract
Persistent infection by specific oncogenic human papillomaviruses (HPVs) is established as the necessary cause of cervix cancer. DNA sequence differences between HPV genomes determine whether an HPV has the potential to cause cancer. Of the more than 100 HPV genotypes characterized at the genetic level, at least 15 are associated, to varying degrees, with cervical cancer. Classification based on nucleotide similarity places nearly all HPVs that infect the cervicovaginal area within the α-PV genus. Within this genus, phylogenetic trees inferred from the entire viral genome cluster all cancer-causing types together, suggesting the existence of a common ancestor for the oncogenic HPVs. However, in separate trees built from the early open reading frames (ORFs; i.e. E1, E2, E6, E7) or the late ORFs (i.e. L1, L2), the carcinogenic potential sorts with the early region of the genome, but not the late region. Thus, genetic differences within the early region specify the pathogenic potential of α-HPV infections. Since the HPV genomes are monophyletic and sites are highly correlated across the genome, diagnosis of oncogenic types and non-oncogenic types can be accomplished using any region across the genome. Here we review our current understanding of the evolutionary history of the oncogenic HPVs, in particular, we focus on the importance of viral genome heterogeneity and discuss the genetic basis for the oncogenic phenotype in some but not all α-PVs.
Key Words: Human papillomavirus, Cervix cancer, Evolution, Phylogeny
Evolution of the Association between Human Papillomavirus and Cervix Cancer
Although an infectious cause of genital warts was suspected in ancient times, interest in ‘wart virus’ research was only galvanized by the suggestion that human papillomavirus (HPV) was the long-sought sexually transmitted etiological agent of cervical cancer. In 2009, Prof. Harold zur Hausen was awarded the Nobel Prize for this innovative idea [1] and demonstrating HPV genomes in cervical cancer tissues [2, 3]. Confluence of idea and technology was enabled by recombinant DNA methods, the cloning of HPV genomes [4] and the use of molecular hybridization. This quantum advance was critical, since standard virologic methods such as serology were not readily available for HPV molecular epidemiological investigations. The free and widespread distribution of cloned HPV genomes by the Heidelberg group and the commencement of an annual international papillomavirus conference accelerated discovery and fostered a collaborative culture within the PV scientific community. Breakthroughs in understanding the molecular pathogenesis have and continue to revolutionize the screening, diagnosis, treatment and prevention of HPV-associated diseases. From a public health viewpoint, HPV has become the model for molecular medicine and how technology can be readily applied to global health problems.
Conclusion and Perspectives
HPVs are a major cause of morbidity and mortality. Characterization and classification of the large group of HPV types contributing to disease has provided important molecular tools for the medical community, resulting in novel diagnostic, screening and prevention strategies. Current studies demonstrate a viral genetic basis of pathogenicity derived from evolution of a common ancestor of all oncogenic HPV types. Nevertheless, understanding the exact genetic basis of HPV oncogenicity is highly complex and will require innovative analytic methods. Study of α-HPV genomics can serve as a model for non-recombinant genome evolution, genetic determinants of pathogenicity and application of genomics for therapeutics.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835381/