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Rev Electron Biomed / Electron J Biomed 2010;2:8-11

Editorial:

HUMAN PAPILLOMAVIRUS: CURRENT ASPECTS.

Prof. José María Eirós Bouza MD, PhD.

Microbiology Department. Faculty of Medicine
University of Valladolid. Spain

eiros @ med.uva.es


Version española

Human papillomavirus (HPV) are a necessary cause for development of cervical cancer^1,2. To the present moment, more than 120 HPV genotypes have been described, at least 80 genotypes have been completely sequenced, and a greater number of possible new types have been identified based on amplification of subgenomic regions³. Papillomavirus are perfectly adapted to the mucosal and skin cells undergoing differentiation, using the cellular maturation cycle for replication purposes⁴.

Anogenital HPV can be divided in two groups depending on the risk of inducing cervical cancer: high-risk (hrHPV) and low-risk virus group (lrHPV) which involves genotypes that have been widely referred. Furthermore, these groups differ in the molecular composition of some viral oncoproteins. Epidemiological and clinical studies based on high sensitivity molecular diagnostic methods detect oncogenic HPV genotypes in the vast majority of the cases of cervical cancer⁵. There is thus a strong evidence on HPV infection as a necessary cause to develop cervical cancer^5-7. In spite of this evidence, diagnostic of HPV is not an extended practice neither in Spain not in other Western European countries.

The prevalence of HPV infection in women ranges from 2% to 44%, with large variations depending on geographical and social or epidemiological differences⁷. Up to 70% of sexually active women will suffer a HPV infection throughout their life⁸. Sub-clinic infection in young age groups could involve up to 40% of female population depending on their sexual behaviour.

The highest prevalence is found in young women and tends to decrease with age. A second peak is observed in perimenopausic women, which could be due to reactivation of previous silent infections or new infections during this period⁹. HPV infections use to be transitory, showing a spontaneous resolution in most cases. Cronification is observed only in 10-20% of the cases, being these cases those with the highest risk for evolution to cervical cancer¹⁰. Molecular diagnosis of HPV has emerged as a new tool for the eradication and epidemiological surveillance of cervical cancer^11,12.

Introduction of the new vaccines against some serotypes of HPV represents a revolution in the prevention of cervical cancer. It is expected that the implementation of the HPV vaccine in the vaccination programs of developed countries will translate into a decrease in the incidence of cervical cancer. In this scenario HPV diagnosis will become more and more important.

Detection of HPV allows evaluating in advance the risk to develop cancerous and precancerous lesions in the infected women¹³. First step of molecular diagnostic screening of HPV infection is the detection of viral genome, in order to differentiate between infected and no infected individuals. Different studies tend to demonstrate that HPV diagnosis along with cytology could differed gynaecologic revisions and could help to evaluate vaccine efficiency^14-20.

In our criterion two essential priorities exist in the area of the infection for VPH. Of a part to describe with brightness the profile of the diagnostic tests used in the welfare area that must serve to the demand generated by the clinical ones who attend to pathology related to the infection for VPH. Of other one establishing by means of sifted of population samples the prevalence of the infection and his protagonism in the precocious detection of cervical pathology. They must be evaluated both under the prism of the efficiency with a suitable weighting of the value that they suppose for the sanitary systems in the whiteness of the 21st century.



REFERENCES

1.- Kurman R, editor. Blaustein's Pathology of the female genital tract. New York: Springer-Verlag, 1994.

2.- Beutner KR, Tyring S. Human papillomavirus and human disease. Am J Med 1997;102:9-15.

3.- Muñoz N, Bosch FX, de Sanjosé S, Herrero R, Castellsagué X, Shah KV, et al. Epidemiologic classification of human Papillomavirus types associated with cervical cancer. N Engl J Med 2003;348:518-527.

4.- Knipe DM, Howley PM. Papillomaviruses. En: Fields BN, Knipe DM, Howley PM, Griffin DE, editors. Fields virology. Philadelphia: Lippincott Williams & Wilkins, 2001; p. 2231-64.

5.- Castellsagué X, Díaz M, de Sanjosé S, Muñoz N, Herrero R, Franceschi S, et al. Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. J Natl Cancer Inst 2006;98:303-15.

6.- Bosch FX, Lorincz A, Muñoz N, Meijer CJ, Shah KV. The causal relation between human papillomavirus and cervical cancer. J Clin Pathol 2002;55:244-65.

7.- Bosch FX, de Sanjosé S. Chapter 1: Human papillomavirus and cervical cancer-burden and assessment of causality. J Natl Cancer Inst Monogr 2003;(31):3-13.

8.- Muñoz N, Bosch FX, Castellsagué X, Díaz M, de Sanjose S, Hammouda D, et al. Against which human papillomavirus types shall we vaccinate and screen? The international perspective. Int J Cancer 2004;111:278-85.

9.- Clifford GM, Gallus S, Herrero R, Muñoz N, Snijders PJ, Vaccarella S, et al. Worldwide distribution of human papillomavirus types in cytologically normal women in the International Agency for Research on Cancer HPV prevalence surveys: a pooled analysis. Lancet 2005;366:991-8.

10.- Walboomers JM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol 1999;189:12-9.

11.- Cuzick J. Human papillomavirus testing for primary cervical cancer screening. JAMA. 2000;283:108-9.

12.- Bosch FX, de Sanjosé S, Castellsagué X. Virus del Papiloma Humano: riesgo oncogénico y nuevas oportunidades para la prevención. An Sist Sanit Navar 2001;24:7-14.

13.- Schiffman M, Herrero R, Hildesheim A, Sherman ME, Bratti M, Wacholder S, et al. HPV DNA testing in cervical cancer screening: results from women in a high-risk province of Costa Rica. JAMA 2000;283:87-93.

14.- Safaeian M, Herrero R, Hildesheim A, Quint W, Freer E, Van Doorn LJ, et al. Comparison of the SPF10-LiPA system to the Hybrid Capture 2 Assay for detection of carcinogenic human papillomavirus genotypes among 5,683 young women in Guanacaste, Costa Rica. J Clin Microbiol 2007;45:1447-54.

15.- González C, Canals J, Ortiz M, Muñoz L, Torres M, García-Saiz A, et al. Prevalence and determinants of high-risk human papillomavirus (HPV) infection and cervical cytological abnormalities in imprisoned women. Epidemiol Infect 2008;136:215-21.

16.- Ortiz M, Torres M, Muñoz L, Fernández-García E, Canals J, Cabornero AI, et al. Oncogenic human papillomavirus (HPV) type distribution and HPV type 16 E6 variants in two Spanish population groups with different levels of HPV infection risk. J Clin Microbiol 2006;44:1428-34.

17.- Solis MT, Aguayo F, Vargas M, Olcay F, Puschel K, Corvalán A, et al. [Risk factors associated with abnormal cervical cytology among Chilean women: A case control study.]. Rev Med Chil. 2010;138:174-80.

18.- Castle PE, Fetterman B, Thomas Cox J, Shaber R, Poitras N, Lorey T et al. The age-specific relationships of abnormal cytology and human papillomavirus DNA results to the risk of cervical precancer and cancer. Obstet Gynecol. 2010;116:76-84

19.- Filipi K, Tedeschini A, Paolini F, Celicu S, Morici S, Kota M, et al. Genital human papillomavirus infection and genotype prevalence among Albanian women: a cross-sectional study. J Med Virol. 2010 ;82:1192-6.

20.- Hamlin-Douglas LK, Coutlée F, Roger M, Hanley J, Franco EL, Brassard P. Determinants of human papillomavirus infection among inuit women of northern Quebec, Canada. Sex Transm Dis. 2010 ;37:377-81.


CORRESPONDENCE:
JM Eiros Bouza.
Area de Microbiología. Facultad de Medicina de Valladolid.
Avda. Ramón y Cajal, 7.
47005, Valladolid.
eiros @ med.uva.es

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