新疆汉族、维吾尔族HPV16E6基因变异与子宫颈癌及宫颈病变的关系

目的探讨新疆地区汉族、维吾尔族宫颈癌及宫颈病变中HPV16型E6基因变异分布及频率,比较两个民族之间的差异。方法对140例HPV16阳性标本,设计E6基因特异性引物,通过PCR扩增HPV16E6全长基因,PCR产物直接测序,进行序列分析并与德国标准株对比,筛选突变位点。结果 123例汉族、维吾尔族妇女宫颈癌及宫颈病变标本中均存在HPV16E6变异株,其中突变率分别为:47.37%(27/57)和50%(33/66),E6突变位点主要是L83V、D25E、D64E、I73V、H78Y、D113E,其中L83V变异株在两个民族突变中占的比例均最高,汉族L83V突变频率为29.82%(17/57)显著低于维吾尔族的40.90%(27/66)(P0.05)。而汉族D25E突变频率为19.30%(11/57)显著高于维吾尔族的7.58%(5/66)(P0.05),D64E变异株在维族突变株中占的比例为6.1%,而汉族标本中未检出。结论两个民族HPV16 E6基因变异发生的位置和变异发生的频率存在差异,维吾尔族人群中HPV16E6基因D64E变异株可能与该地区维吾尔族宫颈癌高发存在一定的关系。     

子宫颈组织中人乳头瘤病毒16型E6基因片段的定量PCR检测

目的探讨子宫颈组织中人乳头瘤病毒(HPV)16型E6基因的含量与疾病严重程度的关系.方法用定量聚合酶链反应(PCR)检测20例慢性宫颈炎,6例宫颈非典型增生,18例宫颈癌组织中HPV16E6基因的拷贝数.结果HPV16E6基因在慢性宫颈炎,宫颈非典型增生及宫颈癌组织中的平均拷贝数(拷贝/μgDNA)分别为6.16×104,5.33×106和6.45×106.统计学处理表明,宫颈非典型增生及宫颈癌组织中E6基因的拷贝数显著高于慢性宫颈炎(P<0.01),宫颈癌组织中E6基因的拷贝数高于宫颈非典型增生组织,但差异无显著性(P>0.05).结论HPV16E6基因的拷贝数与宫颈疾病程度呈正相关,定量检测HPV16E6基因可作为监测宫颈癌高危人群的一种方法.     

新疆南部地区维吾尔族妇女宫颈癌组织中HPV-16型L2基因多态性分析

目的探讨新疆南部地区维吾尔族妇女宫颈癌组织中人乳头瘤病毒16型(humanpapillomavirus16,HPV16)L2基因的变异,并预测L2蛋白的功能变化。方法从19份中国新疆南部地区维吾尔族妇女宫颈癌活检组织标本中提取DNA,以此DNA为模板,PCR扩增HPV16L2全长基因,PCR产物直接测序或克隆后测序,分析新疆维吾尔族妇女宫颈癌组织HPV16L2基因多态性及HPV16L2蛋白功能的变化。结果PCR检测结果显示宫颈癌组织中HPV16L2阳性率为84.21%(1619);测序和序列分析表明L2基因核苷酸多处发生变异,并引起编码氨基酸的变异;L2基因在核苷酸水平上形成7种突变模式(XJL21～XJL27),各模式与HPV16原型比较,同源性在99.37%～99.79%之间;在氨基酸水平上形成5种突变模式,其中XJL1123突变模式占66.67%(812),是突变的主流模式,各模式与HPV16原型比较,同源性在98.31%～99.58%之间;以上突变引起HPV16L2蛋白疏水性和抗原性的改变,继而改变了L1蛋白的结构及功能。结论中国新疆南部地区维吾尔族妇女宫颈癌组织中HPV16L2基因发生多位点变异,并形成多种突变模式和突变主流模式;这些突变引起HPV16L2蛋白疏水性和抗原性的改变,提示HPV16L2基因突变可能与HPV16的系统发生以及病毒逃避机体免疫识别有关。     

新鲜和石蜡包埋宫颈癌组织中HPV l6/18检测

目的为了了解宫颈癌新鲜组织和石蜡包埋宫颈癌组织中HPV检测的差异。方法FQ-PCR技术用于77例宫颈新鲜组织和44例石蜡包埋的宫颈组织中HPVl6/18的检测。结果宫颈癌新鲜组织HPV的检出率为51.43%(36/70),石蜡包埋的櫖颈癌组织检出率为22.72%(10/44)P=0.0024)。两组病毒拷贝对三值分别为5.75±2.36和3.21±1.98(P=-0.000317)。结论宫颈癌新鲜组织HPV的检出率显著高于石蜡包埋的宫颈癌组织,病毒拷贝数有极显著差异。     

HPV16/18和HPV16E6/E7DNA在宫颈癌组织中的表达

目的检测HPV16/18和HPV16E6/E7 DNA在宫颈癌组织中的表达,探讨其在宫颈癌发病中的作用.方法应用PCR和琼脂糖凝胶电泳方法检测46例宫颈癌组织中HPV16/18和HPV16E6/E7DNA.结果 46例宫颈癌中56.5%(26/46)扩增HPV16/18 DNA,其中宫颈鳞癌25例,宫颈腺癌1例.正常对照组20例HPV16/18DNA均为阴性,与宫颈癌组相比差异有显著性(P<0.01).HPV16/18 DNA阳性拷贝对数值为4.32±2.45.HPV16E6,E7DNA分别有53.8%(14/26)、46.2%(12/26)扩增.结论 HPV16/18和HPV16E6/E7 DNA与宫颈癌的发生密切相关,是宫颈癌恶性转化的关键之一,预示着宫颈癌有较强的增殖能力和转移能力.     

子宫颈癌中MHC-Ⅰ类分子抗原呈递相关蛋白GRP78、CRT、ERP57表达及意义

目的 探讨子宫颈炎组织和子宫颈癌组织中GRP78、CRT、ERP57蛋白与HPV16型感染在维吾尔族和汉族妇女中的表达及相关关系.方法 采用免疫组化SP法和PCR技术检测子宫颈炎组织69例(汉族38例,维吾尔族31例)以及子宫颈癌组织124例(汉族36例,维吾尔族88例)中GRP78、CRT、ERP57蛋白的表达和HPV16的感染情况.结果 HPV16型感染在子宫颈癌中的阳性表达率(31.45%)高于宫颈炎组(11.59%),差异有统计学意义(P<0.05).GRP78、CRT、ERP57 3种蛋白在宫颈癌中的表达(95.16%、90.32%、90.32%)均高于与其各自在宫颈炎中的表达(89.96%、50.72%、49.28%),差异均有统计学意义(P<0.05).GRP78和CRT在汉族妇女宫颈癌中的表达(100.00%、97.22%)均高于各自在汉族妇女宫颈炎中的表达(81.58%、39.47%),并且差异均有统计学意义(P<0.05).CRT和ERP57在维吾尔族妇女宫颈癌中的表达(87.50%、94.32%)均高于各自在维吾尔族妇女宫颈炎中的表达(64.51%、35.48%),并且差异均有统计学意义(P<0.05).除此之外,仅ERP57在维吾尔族妇女宫颈癌中的表达(94.32%)高于其在汉族宫颈癌中的表达(80.56%),差异有统计学意义(P<0.05).而通过对GRP78、CRT、ERP57蛋白与HPV16的相关性分析发现:GRP78、CRT、ERP57蛋白在维吾尔族妇女宫颈癌中的阳性表达率与HPV16型感染均存在正相关关系(r=0.278,P<0.05;r=0.429,P<0.05;r=0.222,P<0.05).结论 通过对GRP78、CRT、ERP57 3种蛋白和HPV16联合检测,可能作为检查子宫颈癌的标记物,提高宫颈癌的检出率;ERP57蛋白在宫颈癌中的表达存在民族间差异.     

不同宫颈病变组织中人乳头瘤病毒16型E5基因的研究

目的:探讨人乳头瘤病毒(Human papillomavirus type,HPV)16型E5早期基因在临床宫颈炎、宫颈上皮内瘤变(Cervical intraepithelial neoplasia,CIN)Ⅰ、Ⅱ、Ⅲ型及宫颈癌患者中的存在情况,判断HPV16E5是否能作为临床宫颈癌的早期诊断治疗靶点,以利进一步研究HPV16的致癌机制。方法:从临床标本中筛选出HPV16阳性标本61例,根据病理诊断分为5组(宫颈炎组、CINⅠ级、CINⅡ级、CINⅢ级及宫颈癌组),再应用PCR的方法分别测定各组组织中HPV16E5DNA的表达情况。结果:宫颈炎组E5DNA阳性率为58.33%,CINⅠ级为63.64%,CINⅡ级为70.00%,CINⅢ级为44.44%,宫颈癌为77.78%,各组间阳性率差异无统计学意义。结论:E5DNA不仅仅在宫颈癌早期存在,因而E5不能作为临床宫颈癌的早期诊断靶点,但可作为宫颈癌疫苗研究的靶点。     

98例宫颈癌人乳头状瘤病毒16型E6基因突变及多态性分析

目的 研究湖北地区宫颈癌患者人乳头状瘤病毒16型(HPV16)E6基因点突变分布及频率,与国内外其他研究人员发现的E6突变进行对比,分析E6突变在宫颈癌发生中的意义.方法 从宫颈癌患者手术切除标本中提取组织DNA,用HPV16 E6特异性引物进行PCR扩增,对扩增的E6基因片段进行测序分析.结果 在35例宫颈癌组织DNA中有18例发生E6基因178位核苷酸的突变,变突频率为51.43%,相应核苷酸改变为Asp→Glu,442位核苷酸有4例发生核苷酸序列的改变,突变频率为11.43%,另有10例发生1～2个核苷酸序列的改变.结论 湖北地区98例宫颈癌患者人乳头状瘤病毒E6基因存在高频率的178和442位核苷酸突变,一些为新发现的核苷酸序列的突变,这些突变在宫颈癌发生中的作用有待于进一步研究.     

维吾尔族妇女宫颈癌人乳头状瘤病毒感染与人类白细胞抗原Ⅰ类基因表达缺失的关系及其意义

目的 研究维吾尔族妇女宫颈癌中人乳头状瘤病毒(HPV)感染和人类白细胞抗原Ⅰ类(HLA-Ⅰ)家族基因HLA-A、B和C表达的关系,探讨HPV感染和HLA-Ⅰ类家族基因表达缺失在宫颈癌演进过程中的作用.方法 收集维吾尔族妇女宫颈炎、宫颈上皮内瘤样病变(CIN)Ⅰ/Ⅱ/Ⅲ和宫颈鳞癌患者的新鲜组织标本共78例,提取总RNA,采用半定量RT-PCR方法鉴定HLA-A、B和C基因的mRNA表达水平.提取组织DNA,采用HPV通用引物和HPV分型芯片确定HPV亚型.结果 HLA-A、B和C基因的总体mRNA表达缺失率随着宫颈病变的加重而增加,在宫颈炎组织内为1/12,在CIN及宫颈鳞癌分别占70.0%(14/20)和84.8%(39/46),在恶性程度高的低分化癌组织中高达90.6%(29/32),并与高危型HPV16感染呈正相关(r=0.803,P＜0.01).结论 HLA-Ⅰ类基因的表达缺失是维吾尔族妇女宫颈癌发生的重要标志,而HPV16感染可能是HLA-Ⅰ分子表达缺失的前提条件.     

宫颈癌组织APOBEC3A蛋白的表达与高危型HPV感染的相关性研究

 目的： 探讨宫颈癌组织中载脂蛋白 B mRNA 编辑酶催化多肽样蛋白3A（APOBEC3A）表达与高危型人乳头瘤病毒（HPV）感染的关系。方法： 采用免疫组化法检测26例宫颈癌、27例宫颈上皮内瘤变（CIN）I～III和22例正常宫颈组织APOBEC3A蛋白的表达,同时使用凯普分型检测试剂盒对3组样品分别进行高危HPV16/HPV18分型检测。以脂质体法转染APOBEC3A质粒进入HeLa细胞,RT-qPCR与Western blotting验证APOBEC3A对高危型HPV18 E6 mRNA以及蛋白表达的影响。结果：宫颈癌组织、CIN组织以及正常宫颈组织中APOBEC3A蛋白表达的阳性率分别为46.2%、92.6%和86.4%,宫颈癌组织中APOBEC3A蛋白表达较正常宫颈组织明显下降（P<0.01）。宫颈癌组织、CIN及正常宫颈组织中HPV16感染阳性率分别为92.3%、77.8%和54.5%; HPV18感染阳性率分别为80.8%、51.8%和68.2%;APOBEC3A蛋白表达与HPV18感染阳性率呈负相关(P<0.05)。增加HeLa细胞中APOBEC3A的表达明显降低了HPV18 E6 mRNA以及蛋白的表达。结论：在宫颈癌组织中APOBEC3A高表达可以对抗HPV18感染,并抑制HPV18 E6的转录和表达。     

Distinctive distribution of HPV16 E6 D25E and E7 N29S intratypic Asian variants in Korean commercial sex workers

The distribution of HPV16 sequence variations differs geographically and specific HPV16 E6 and E7 variants might carry a high risk for development of invasive cervical cancer and cervical intraepithelial neoplasia in a given population. To investigate the genetic variation of HPV 16 E6 and E7 genes, genomic DNAs from 56 HPV16-infected commercial sex workers were extracted from their cervical swabs by using DNA isolation kit. The E6 and E7 coding region (34-880) with HPV16 E6/E7 specific PCR were amplified and analyzed by using the DNAstar software. At the nucleotide level, 26 variants of the HPV16 E6 and E7 genes were identified including 12 silent mutations. At the amino acid level, the isolates showed 14 variants including E6 Q14H, E6 D25E, E6 I27R, E6 H78Y, E6 L83V, and E7 N29S. The dominant HPV16 E6 and E7 variants were HPV16 E6 D25E (68%) and HPV16 E7 N29S (73%), respectively, which belong to Asian lineage. Although this study has some limitations such as a small sample size and not enough clinical data, these finding suggests that the distinctive distribution of HPV 16 As-variant E6 D25E and E7 N29S might be associated with geographical dependence rather than disease progression. Further study is needed to determine the clinical and biological effects of these variants.     

Molecular variants of human papillomavirus type 16 and 18 and risk for cervical neoplasia in Portugal

Persistent high-risk human papillomavirus (HPV) infection is considered as the central cause of invasive cervical cancer. Specific HPV 16 and 18 sequence variations were associated with an increased risk for progression. The purpose of this study was to analyze intratypic variations of HPV 16 and 18 within the E6 gene, MY09/11 and LCR regions, and to evaluate the risk of these variants for cervical neoplasia among Portuguese women. Cervical samples from 187 HPV 16-positive and 41 HPV 18-positive women with normal epithelium, cervical intraepithelial neoplasia, or invasive cervical cancer were amplified by type-specific PCR, followed by sequence and phylogenetic analysis. Sixteen new HPV 16 and 18 patterns are described in this paper. European HPV 16 variants were the most frequent (74.3%), particularly Ep-T350 (44.4%), followed by African (16.1%), and Asian-American (9.6%). Non-European HPV 16 variants were more frequent in pre-invasive lesions than in normal tissue and low-grade lesions. However, when analyzed separately, only African variants were associated significantly with an increased risk for cervical cancer. For HPV 18, the AsAi variant showed a trend, which was not statistically significant to an enhanced oncogenicity. European variants seemed to be significantly associated with a lower risk for cervical cancer development. The distribution of HPV 16 and 18 variants was not related to age or race among women living in the same geographical region. Knowledge of variants will be important for risk determination as well as for designing primers or probes for HPV detection methods, and for appropriate cervical cancer prevention strategies.     

The prevalence of HPV-18 and variants of E6 gene isolated from cervical cancer patients in Taiwan.

BACKGROUND: Cervical cancer is the second most common cancer in women worldwide. It has been considered that human papillomavirus (HPV) is associated with cervical cancer. Currently, more than 80 different serotypes of HPV have been characterized and they are divided into low- and high-risk groups. The most common types that lead to cervical cancer are HPV-16 and -18. The viral oncogenes E6 and E7 are associated with the development of cervical cancer. In previous study, the variants of HPV-16 E6 gene have been reported. It suggests that variants may influence the morbidity of carcinogenesis, but the variant study on HPV-18 remains unknown. OBJECTIVES: To identify the variants of integrated HPV-18 E6 gene in the prevalent infection of HPV-18 of cervical cancer patients. STUDY DESIGN: 25 cervical cancer patients were clinically identified and the biopsies were obtained. The infectious HPV types were identified by PCR and Southern blotting analysis. The DNA fragments of the integrated HPV-18 E6 were amplified by PCR and cloned. The nucleotide sequences were obtained by sequencing. RESULTS: The prevalence of HPV infection in our 25 cases was HPV-18 (100%) and 7 out of these 25 cases (28%) were co-infected with HPV-16. The most dominant mutation among 25 tested patients was a silence mutation C183G of the E6 coding region. CONCLUSIONS: The prevalent HPV infectious serotype is HPV-18, which differs from the worldwide prevalent type. The identified HPV-18 E6 variants had a unique silence mutation located on C183G in E6 coding region.     

Genetic diversity of human papillomavirus type 16 E6, E7, and L1 genes in Italian women with different grades of cervical lesions

High‐risk human papillomaviruses (HPVs) are risk factors for the development of cervical cancer. HPV 16 is the most common type, being present in about 60% of cervical cancers worldwide. Previous studies have reported upon the association between HPV 16 E6 variants and increased risk of cervical intraepithelial neoplasia and invasive cervical cancer. In this study, the presence of HPV 16 polymorphisms in the E6, E7, and L1 genes was investigated in relation to the presence of high‐grade lesions. Sequencing of the E6 gene revealed the presence of nucleotide mutations resulting in 15 amino acid changes. Of these, the G134D and C136R fall within the CXXC zinger finger domain important for p53 binding. In the E7 gene, four nucleotide variations were identified with two leading to the amino acid substitutions L15V and S31R. The L1 gene showed 13 nucleotide changes leading to 11 amino acid substitutions. Among these, the R364C and N367D are located at the base of the HI‐loop of the L1 protein, considered to be the immunodominant epitope of HPV 16. No significant relationship between HPV 16 variants and high‐grade lesions was found. Phylogenetic analysis showed that all the HPV 16 variants identified belonged to the European lineage, except one which was of the Asian‐American lineage. The European‐350G variant was detected most frequently (22 of 34, 64.7%). The study provides some new data on the genetic diversity of HPV 16 which may help to understand the oncogenic potential of the virus and to improve management of patients. J. Med. Virol. 81:1627–1634, 2009. © 2009 Wiley‐Liss, Inc.     

Identification of a novel human papillomavirus type 16 E1 gene variant with potentially reduced oncogenicity

The human papillomavirus (HPV) 16 genome has been studied extensively, although no study has focused on the E1 gene that is implicated in viral DNA replication. After analyzing the E1 region of HPV 16 genomes in 429 cervical samples, 11.2% were found to contain a 63 nucleotides duplication in this region. Sequence analysis of the E6 and the E7 regions has shown that all samples containing this duplication were related to E6‐G350 variant of the HPV 16 (Chi square test, P = 0.0012). A comparison of cervical lesion severity of the examinees having regular or variant E1 genes has shown that the variant group had a significantly (Fischer's exact test, P = 0.0401) lower percentage of high grade disease cases, suggesting that this particular duplication might reduce the oncogenic potential of HPV 16, and also might clarify the differences of E6‐G350 variant oncogenicity observed in European populations. Albeit, a decreased incidence of high grade cervical lesions can be linked to the prevalence of multiple HPV infection, the additional decrease of those cases with the variant E1 gene versus those without (10.5% and 18.6%, respectively) can only be ascribed to the effect of this particular HPV variant. Further research is needed to clarify the biology of these HPV 16 E1 variants. J. Med. Virol. 80:2134–2140, 2008. © 2008 Wiley‐Liss, Inc.     

Patterns of cellular and HPV 16 methylation as biomarkers for cervical neoplasia

Aberrant promoter methylation of biologically relevant genes in cervical cancer and uneven CpG distribution within the human papillomavirus 16 (HPV 16) enhancer region have been reported. Cervical samples and questionnaires from 151 women screened for cervical cancer in Appalachian Ohio were analyzed. Methylation was measured by bisulfite sequencing in candidate gene sites in ESR1, DCC, p16, and LINE1 elements. Among 89 HPV 16-positive women, CpG sites in the E6 promoter and enhancer regions and the L1 region of the HPV 16 genome were measured. Methylation levels were compared by cervical cytology and HPV 16 status. HPV methylation was low regardless of cytology status, however E6 methylation was significantly higher in women with normal cytology. ESR1 and DCC methylation were significantly higher in HPV 16-positive women. Increased methylation at sites in the E6 promoter region was associated with lower odds of abnormal cytology. Increased methylation in candidate genes was associated with higher odds of abnormal cytology, particularly DCC region 2.4, DCC region 2.6, ESR1 region 3.2, and LINE1 site 1.2. HPV 16 genome CpG methylation was low except for the L1 region. In general, lower HPV 16 methylation and higher candidate gene methylation levels were associated with higher odds of abnormal cytology.     

南疆维吾尔族妇女宫颈癌与HPV感染及HLA-DRB1基因多态性的关系研究

目的 探讨人乳头状瘤病毒(human papilloma virus,HPV)感染及人类白细胞抗原(HLA)-DRB1基因多态性与南疆维吾尔族宫颈癌的关系.方法 采用导流杂交基因芯片技术及聚合酶链反应序列特异性寡核苷酸探针(polymerase chain reaction sequence-specific oligonucleotide,PCRSSO)法对200例南疆维吾尔族宫颈癌患者及200例正常妇女的宫颈组织检测HPV的21种型别(包括13种高危型:16,18,31,33,35,39,45,51,52,56,58,59,68;5种低危型:6,11,42,43,44;3种中国人群常见型:53,66,CP8304型)及HLA-DRB1的13个等位基因.结果 (1)200例官颈癌组织中HPV阳性者共177例(包括单一感染及多重感染),阳性率为88.5%;200例对照组中HPV阳性的标本为14例,阳性率为7.0%.HPV16在HPV阳性的宫颈癌中占的比例最高,其出现的频率为90.96%,其次为HPV18(5.08%)、HPV68(3.95%)、HPV45(3.39%)、HPV58(3.39%)、HPV39(1.69%)、HPV31(1.69%)、HPV56(1.13%)等.比较两组HPV总感染率及HPV16的阳性率,宫颈癌组明显高于对照组,两者差异有统计学意义(P＜0.0001).(2)官颈癌中HLA-DRB1*15阳性者HPV16的感染率高于阴性者,差异有统计学意义,说明携带HLA-DRB1*15等位基因的妇女更容易被HPV16感染.官颈癌中HLA-DRB1*12阳性者中HPV16的阳性率明显低于HLA-DRB1*12阴性者,说明HLA-DRB1*12对HPV16感染有保护作用.结论 南疆维吾尔族宫颈癌患者及正常人群中以HPV16感染为主,比例很高;其次为HPV18、HPV68,HPV68在第3位与文献报道不同,可能是南疆维吾尔族较易感染的类型.HLA-DRB1*15可能与维吾尔族妇女对官颈癌的遗传易感性及对HPV16感染易感性有关;HLA-DRB1*12为HPV16感染的保护基因.维吾尔族妇女官颈癌易感基因及保护基因的检测在宫颈癌高危人群的检测及群体遗传干预工作中有一定的指导意义.

Abstract：

Objective To investigate the relationships between the HPV infection and race susceptibility in the carcinogenesis of Uighur women with cervical cancer from the southern Xinjiang, one of the high risk region of cervical cancer in China. Methods To detect 21 subtypes of HPV and the 13 alleles of HLA from 200 cervical cancer cases and 200 normal tissues, by using flow-through hybridization and gene chip (HybriMax) method and polymerase chain reaction sequence-specific oligonucleotide method (PCRSSO). Results ( 1 )The proportion of HPV positive in cervical cancer and control group were 88.5% and 7.0% respecfively;HPV16 was the most common type in HPV positive cervical cancer patients with the rate of 90.96%, following were HPV18 (5.08%), HPV68(3.95% ),HPV45 (3.39%), HPV58 (3.39%),HPV39( 1.69% ), HPV31 ( 1.69% ), HPV56( 1.13% ). In cervical cancer and control group, the positive rate of HPV and HPV16 were significantly higher than that in control group. (2) In cervical cancer group the frequency of HLA-DRB1 * 15 in HPV positive cervical cancer cases was significantly higher than that among the HPV negative cases. While the frequency of HLA-DRB1 * 12 in HPV positive eervical caneer eases was significantly lower than that in the HPV negative e asea. Conclusion HPV16 was the most common type in both cervical cancer and control groups, the frequency of HPV16 in cervical carcinomas was very high, following HPV18 and HPV68, and HPV68 ranked third which was different from the results of other reports,this indicates that Uighur women are infected with this type more common. It appears that HLA-DRB1 * 15may be related to the susceptibility to cervical cancer and the HPV16 infection among the Uighur women,while the HLA-DRB1 * 12 the protective gene to HPV16 infection in Uighur women. The study of HLA alleles in the carcinogenesis of cervical carcinomas may play an important role in the gene intervention research of cervical cancer.