covid
Buscar en
Revista Colombiana de Cancerología
Toda la web
Inicio Revista Colombiana de Cancerología Presencia y persistencia de variantes moleculares del ORF E6 y ORF E7 del VPH 58...
Información de la revista
Vol. 16. Núm. 1.
Páginas 40-48 (enero 2011)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 16. Núm. 1.
Páginas 40-48 (enero 2011)
Acceso a texto completo
Presencia y persistencia de variantes moleculares del ORF E6 y ORF E7 del VPH 58 en mujeres con citología normal que pertenecen a la cohorte de Bogotá, Colombia
Presence and Persistence of HPV 58 Molecular Variations ORF E6 and ORF E7 Among Women With Normal Cytology in the Bogotá, Colombia Cohort
Visitas
2653
Óscar Buitrago1, Nicolás Morales1, Carolina Martín1, Antonio Huertas1, Pablo Moreno1, Teresa Martínez2, Mónica Molano1,
Autor para correspondencia
mmolano@cancer.gov.co

Correspondencia: Instituto Nacional de Cancerología, Avenida 1a No. 9-85, Bogotá, Colombia. Tel.:éfono (571) 334 1111 ext. 4205.
, Grupo de Estudio VPH 3
1 Grupo de Investigación en Biología del Cáncer, Instituto Nacional de Cancerología, Bogotá D. C., Colombia
2 Grupo de Investigación Epidemiológica, Instituto Nacional de Cancerología, Bogotá D. C., Colombia
3 Grupo de Estudio VPH: Héctor Posso, Margarita Ronderos, Raúl Murillo, Joaquín Luna, Natasha Ortiz, Gilberto Martínez, Edmundo Mora, Gonzalo Pérez, José María Fuentes, Constanza Gómez, Eva Klaus, Constanza Camargo, Cecilia Tabón, Teodolinda Palacio, Carolina Suárez, Claudia Molina
Este artículo ha recibido
Información del artículo
Resumen
Objetivo

Analizar la presencia y persistencia de variantes en E6/E7/VPH 58 en muestras de mujeres con infecciones prevalentes por VPH 58, con citología normal, que pertenecen a la cohorte de Bogotá, Colombia.

Métodos

Se utilizaron cepillados cervicales de 34 mujeres VPH 58, con citología normal, pertenecientes a la línea de base de la cohorte, con su respectivo seguimiento. Se amplificó la región E6/E7 del VPH 58 usando los iniciadores E6F1-E7R1 y los iniciadores E7P1-E7P2. Para el análisis de las variantes se utilizó la técnica de secuencia automática directa. La secuencia referencia del VPH 58 se utilizó para comparar las secuencias obtenidas.

Resultados

En 27/34 muestras se lograron detectar variantes de E6/E7 de VPH 58. En total, se detectaron cinco variantes diferentes, dos de ellas nunca antes reportadas (A169/T307/A694/G744/A761 y T307/A694/G744/A761/G763). Los análisis de eliminación mostraron que el 75% de las variantes se habían eliminado antes de los dos años de seguimiento, y todas las variantes ya se habían eliminado a los seis años de seguimiento.

Conclusiones

Dos nuevas variantes se reportaron a escala mundial de gran relevancia en los ámbitos filogenético y epidemiológico.

Palabras clave:
virus del papiloma humano
estudios de seguimientos
variación estructural del genoma
Abstract
Objective

To analyze the presence and persistence of E6/E7 HPV58 variations in women with prevalent HPV 58 infection, with normal cytology, who belong to the Bogotá, Colombia cohort.

Methods

Cervical cytobrush was used on 34 HPV58 women, with normal cytology, who are part of the cohort base line; respective follow was performed. The HPV58 E67/E7 region was broadened by using E6F1-E7R1 and E7P1-E7P2 indicators. Variation analysis was carried out with automatic direct sequencing. HPV58 sequence reference was used to compare the sequences that had been obtained.

Results

In 27/34 samples, E6/E7 variations of HPV58 were successfully detected. A total of five different variations were detected, two of which had never been reported before (A169/T307/A694/G744/A761 and T307/A694/G744/A761/G763). Elimination analysis revealed that 75% of variations had been eliminated within two years of follow up, and that all variation had been eliminated at the end of six years of follow up.

Conclusions

Two new variations of universal phylogenetic and epidemiologic noteworthiness were reported

Key words:
Papilloma human virus
follow-up studies
genomic structural variants
El Texto completo está disponible en PDF
Referencias
[1.]
J. Ferlay, H.R. Shin, F. Bray, et al.
Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008.
Int J Cancer, 127 (2010), pp. 2893-2917
[2.]
C. Pardo, R. Cendales.
Incidencia estimada y mortalidad por cancer en Colombia 2002-2006.
Instituto Nacional de Cancerologia, (2010),
[3.]
G.M. Clifford, S. Gallus, R. Herrero, 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.
[4.]
M. Molano, H. Posso, E. Weiderpass, et al.
Prevalence and determinants of HPV infection among Colombian women with normal cytology.
Br J Cancer, 87 (2002), pp. 324-333
[5.]
M. Molano, A.J. Van den Brule, M. Plummer, et al.
Determinants of clearance of human papillomavirus infections in Colombian women with normal cytology: a population- based, 5-year follow-up study.
Am J Epidemiol, 158 (2003), pp. 486-494
[6.]
N. Munoz, F. Méndez, H. Posso, et al.
Incidence, duration, and determinants of cervical human papillomavirus infection in a cohort of Colombian women with normal cytological results.
J Infect Dis, 190 (2004), pp. 2077-2087
[7.]
F. Méndez, N. Muñoz, H. Posso, et al.
Cervical coinfection with human papillomavirus (HPV) types and possible implications for the prevention of cervical cancer by HPV vaccines.
J Infect Dis, 192 (2005), pp. 1158-1165
[8.]
M. Almonte, G. Albero, M. Molano, et al.
Risk factors for human papillomavirus exposure and co-factors for cervical cancer in Latin America and the Caribbean.
[9.]
L. Villa, L. Sichero, P. Rahal, et al.
Molecular variants of human papillomavirus types 16 and 18 preferentially associated with cervical neoplasia.
J Gen Virol, 81 (2000), pp. 2959-2968
[10.]
H. zur Hausen.
Human papillomaviruses in the pathogenesis of anogenital cancer.
Virology, 184 (1991), pp. 9-13
[11.]
V.S. Veras, D.M. Cerqueira, C.R. Martins.
L1 sequence of a new human papillomavirus type-58 variant associated with cervical intraepithelial neoplasia.
Braz J Med Biol Res, 38 (2005), pp. 1-4
[12.]
I.E. Calleja-Macias, L.L. Villa, J.C. Prado, et al.
Worldwide genomic diversity of the high-risk human papillomavirus types 31, 35, 52, and 58, four close relatives of human papillomavirus type 16.
[13.]
P.K. Chan, C.W. Lam, T.H. Cheung, et al.
Association of human papillomavirus type 58 variant with the risk of cervical cancer.
J Natl Cancer Inst, 94 (2002), pp. 1249-1253
[14.]
C.Y. Xin, K. Matsumoto, H. Yoshikawa, et al.
Analysis of E6 variants of human papillomavirus type 33, 52 and 58 in Japanese women with cervical intraepithelial neoplasia/cervical cancer in relation to their oncogenic potential.
Cancer Lett, 170 (2001), pp. 19-24
[15.]
Y. Kirii, S. Iwamoto, T. Matsukura.
Human papillomavirus type 58 ADN sequence.
Virology, 185 (1991), pp. 424-427
[16.]
M.V. Jacobs, A.J. van den Brule, P.J. Snijders, et al.
A nonradioactive PCR enzyme-immunoassay enables a rapid identification of HPV 16 and 18 in cervical scrapes after GP5+/6+ PCR.
[17.]
A.J. van den Brule, C.J. Meijer, V. Bakels, et al.
Rapid detection of human papillomavirus in cervical scrapes by combined general primer-mediated and type-specific polymerase chain reaction.
J Clin Microbiol, 28 (1990), pp. 2739-2743
[18.]
E.Q. Wu, X. Zha, X.H. Yu, et al.
Profile of physical status and gene variation of human papillomavirus 58 genome in cervical cancer.
J Gen Virol, 90 (2009), pp. 1229-1237
[19.]
Y.J. Chang, H.C. Chen, B.H. Lee, et al.
Unique variants of human papillomavirus genotypes 52 and 58 and risk of cervical neoplasia.
Int J Cancer, 129 (2011), pp. 965-973
[20.]
T. Raiol, P.S. Wyant, R.M. de Amorim, et al.
Genetic variability and phylogeny of the high-risk HPV-31, -33, -35, -52, and -58 in central Brazil.
J Med Virol, 81 (2009), pp. 685-692
[21.]
P.K. Chan, A.C. Luk, J.S. Park, et al.
Identification of human papillomavirus type 58 lineages and the distribution worldwide.
Infect Dis, 203 (2011), pp. 1565-1573
[22.]
M.H. Mayrand, F. Coutlee, C. Hankins, et al.
Detection of human papillomavirus type 16 ADN in consecutive genital samples does not always represent persistent infection as determined by molecular variant analysis.
J Clin Microbiol, 38 (2000), pp. 3388-3393
[23.]
N.F. Schlecht, R.D. Burk, J.M. Palefsky, et al.
Variants of human papillomaviruses 16 and 18 and their natural history in human immunodeficiency virus-positive women.
J Gen Virol, 86 (2005), pp. 2709-2720
[24.]
M.M. Da Costa, C.J. Hogeboom, E.A. Holly, et al.
Increased risk of high-grade anal neoplasia associated with a human papillomavirus type 16 E6 sequence variant.
J Infect Dis, 185 (2002), pp. 1229-1237
Copyright © 2012. Instituto Nacional de Cancerología
Descargar PDF
Opciones de artículo