Human papillomavirus type 18 variant lineages in United States populations characterized by sequence analysis of LCR-E6, E2, and L1 regions

被引:52
作者
Arias-Pulido, H [1 ]
Peyton, CL [1 ]
Torrez-Martínez, N [1 ]
Anderson, DN [1 ]
Wheeler, CM [1 ]
机构
[1] Univ New Mexico, Hlth Sci Ctr, Sch Med, Dept Mol Genet & Microbiol, Albuquerque, NM 87111 USA
关键词
papillornavirus; HPV; 18; variants; oncogenic potential; vaccine; ethnicity;
D O I
10.1016/j.virol.2005.04.022
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
While HPV 16 variant lineages have been well characterized, the knowledge about HPV 18 variants is limited. In this study, HPV IS nucleotide variations in the E2 hinge region were characterized by sequence analysis in 47 control and 51 tumor specimens. Fifty of these specimens were randomly selected for sequencing of an LCR-E6 segment and 20 samples representative of LCR-E6 and E2 sequence variants were examined across the L I region. A total of 2770 nucleotides per HPV 18 variant genome were considered in this study. HPV 18 variant nucleotides were linked among all gene segments analyzed and grouped into three main branches: Asian-American (AA), European (E), and African (Af). These three branches were equally distributed among controls and cases and when stratified by Hispanic and non-Hispanic etlinicities. Among invasive cervical cancer cases, no significant differences in the three HPV variant branches were observed among ethnic groups or when stratified by histopathology (squamous vs. adenocarcinoma). The Af branch showed the greatest nucleotide variability when compared to the HPV 18 reference sequence and was more closely related to HPV 45 than either AA or E branches. Our data also characterize nucleotide and amino acid variations in the L1 capsid gene among HPV 18 variants, which may be relevant to vaccine strategies and subsequent studies of naturally occurring HPV 18 variants. Several novel HPV 18 nucleotide variations were identified in this study. (C) 2005 Elsevier Inc. All rights reserved.
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页码:22 / 34
页数:13
相关论文
共 86 条
[1]  
ACS (American Cancer Society), 2002, CANC FACTS FIG 2002
[2]   Genomic polymorphism of human papillomavirus type 52 predisposes toward persistent infection in sexually active women [J].
Aho, J ;
Hankins, C ;
Tremblay, C ;
Forest, P ;
Pourreaux, K ;
Rouah, F ;
Coutlée, F .
JOURNAL OF INFECTIOUS DISEASES, 2004, 190 (01) :46-52
[3]   CCAAT displacement protein binds to and negatively regulates human papillomavirus type 6 E6, E7, and E1 promoters [J].
Ai, WD ;
Toussaint, E ;
Roman, A .
JOURNAL OF VIROLOGY, 1999, 73 (05) :4220-4229
[4]  
[Anonymous], HUMAN PAPILLOMAVIRUS
[5]   HUMAN PAPILLOMAVIRUS TYPE-18 ASSOCIATES WITH MORE ADVANCED CERVICAL NEOPLASIA THAN HUMAN PAPILLOMAVIRUS TYPE-16 [J].
ARENDS, MJ ;
DONALDSON, YK ;
DUVALL, E ;
WYLLIE, AH ;
BIRD, CC .
HUMAN PATHOLOGY, 1993, 24 (04) :432-437
[6]  
BARBOSA MS, 1989, ONCOGENE, V4, P1529
[7]   POSSIBLE PROGNOSTIC-SIGNIFICANCE OF HUMAN PAPILLOMAVIRUS TYPE IN CERVICAL-CANCER [J].
BARNES, W ;
DELGADO, G ;
KURMAN, RJ ;
PETRILLI, ES ;
SMITH, DM ;
AHMED, S ;
LORINCZ, AT ;
TEMPLE, GF ;
JENSON, AB ;
LANCASTER, WD .
GYNECOLOGIC ONCOLOGY, 1988, 29 (03) :267-273
[8]  
Bernard H.U., 2000, PAPILLOMAVIRUS REP, V11, P73
[9]   GENOME AMPLIFICATION OF HUMAN PAPILLOMAVIRUS TYPES 16 AND 18 IN CERVICAL CARCINOMAS IS RELATED TO THE RETENTION OF E1/E2 GENES [J].
BERUMEN, J ;
CASAS, L ;
SEGURA, E ;
AMEZCUA, JL ;
GARCIACARRANCA, A .
INTERNATIONAL JOURNAL OF CANCER, 1994, 56 (05) :640-645
[10]   PREVALENCE OF HUMAN PAPILLOMAVIRUS IN CERVICAL-CANCER - A WORLDWIDE PERSPECTIVE [J].
BOSCH, FX ;
MANOS, MM ;
MUNOZ, N ;
SHERMAN, M ;
JANSEN, AM ;
PETO, J ;
SCHIFFMAN, MH ;
MORENO, V ;
KURMAN, R ;
SHAH, KV ;
ALIHONOU, E ;
BAYO, S ;
MOKHTAR, HC ;
CHICAREON, S ;
DAUDT, A ;
DELOSRIOS, E ;
GHADIRIAN, P ;
KITINYA, JN ;
KOULIBALY, M ;
NGELANGEL, C ;
TINTORE, LMP ;
RIOSDALENZ, JL ;
SARJADI ;
SCHNEIDER, A ;
TAFUR, L ;
TEYSSIE, AR ;
ROLON, PA ;
TORROELLA, M ;
TAPIA, AV ;
WABINGA, HR ;
ZATONSKI, W ;
SYLLA, B ;
VIZCAINO, P ;
MAGNIN, D ;
KALDOR, J ;
GREER, C ;
WHEELER, C .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1995, 87 (11) :796-802