女性生殖道病毒感染现状

女性下生殖道病毒感染主要表现为宫颈、阴道与外阴的炎症,主要为直接接触感染,以单纯疱疹病毒,巨细胞病毒及人乳头瘤病毒感染较常见。     

安阳市宫颈病变患者人乳头瘤病毒感染现状及基因分型分析

目的:分析安阳市宫颈病变患者人乳头瘤病毒（human papillomavirus,HPV）感染现状,并分析其基因型。方法:选取2018年6月至2020年12月在本院门诊就诊或住院治疗的宫颈病变患者372例,参照宫颈组织病理活检结果分为宫颈炎、宫颈上皮内瘤变（cervical intraepithelial neopl...     

HPV疫苗有效性的真实世界研究

人乳头瘤病毒(human papillomavirus, HPV)是一种嗜上皮组织病毒, 高危型HPV感染可导致宫颈、阴道、外阴等部位癌前病变并最终进展为癌, 低危型HPV感染可导致尖锐湿疣、复发性呼吸道乳头瘤等良性病变。HPV感染是威胁人类健康的重要公共卫生问题之一。目前, 全球已有6种预防性HPV疫苗获批上市, 在一些较早开展疫苗接种的国家中, HPV疫苗在真实世界人群中的接种保护效果已逐渐显现, 对于HPV感染相关结局指标的保护效果良好, 人群中的疫苗型别HPV感染、宫颈高度病变、肛门-生殖器疣、复发性呼吸道乳头状瘤病等结局指标的发生率明显降低, 疫苗的群体保护效果突出, 同时双价HPV疫苗在真实世界的接种实践中表现出对非疫苗型别HPV(HPV31/33/45)的交叉保护性。     

不同型别人乳头瘤病毒感染不孕患者治疗方法的研究

目的 探讨不孕症患者感染不同型别高危型人乳头瘤病毒（HPV）的最佳治疗方法.方法 按宫颈病理学、宫颈状况和不孕患者生育欲望,将144例感染高危型人乳头瘤病毒的门诊不孕患者分为治疗组和不治疗组,以6个月为一复查周期,采用双色实时荧光定量PCR法,检测患者宫颈脱落细胞内的HPV-DNA,观察其阴转情况及受孕情况,并进行比较分析.结果 ①感染不同型别高危型HPV,治疗组的HPV阴转率（56.67%）较高;②次要高危型不治疗组的妊娠率（50.00%）较高,主要高危型治疗组的妊娠率（31.67%）较高,显著高于不治疗组（4.00%）;③主要高危型手术治疗后HPV阴转率和妊娠率（40.00%）均高于药物治疗（6.67%）,手术治疗二种方法中以Leep＋药物最佳.妊娠率为41.18%,高于药物治疗组的6.67%.结论 不孕患者应常规进行宫颈HPV筛查,主要高危型HPV感染是不孕的宫颈性病因,主要高危型HPV感染伴宫颈病变者以LEEP＋药物治疗为最佳.     

实时荧光定量PCR法与杂交捕获法在高危型HPV检测中的比较

大量研究已经证明,人乳头瘤病毒感染(HPV),特别是高危型人乳头瘤病毒感染,在妇女宫颈疾病的发生和发展中起着重要的作用。HPV感染是宫颈癌及宫颈上皮内瘤变(CIN)的主要病因,高危型HPV感染是宫颈癌及其癌前病变的必要条件。据报道[1],宫颈癌患者HPV阳性率可达到99.7%,HPV感染使宫颈癌的相对危险性增加200多倍,是可     

2018—2020年宁夏地区女性人乳头瘤病毒感染者病毒分型与宫颈病变的分析

目的:了解宁夏地区妇女人乳头瘤病毒(human papillomavirus, HPV)感染分布特征及与宫颈病变的关系。方法:选取2018—2020年接受宁夏宫颈癌筛查的140 498例妇女,采用荧光PCR法检测女性宫颈脱落细胞,分析HPV感染特征以及与宫颈病变的关系。结果:140 498例筛查女性,高危型HPV总阳性...     

妇科门诊患者HPV分型检测及结果分析

目的探讨人乳头瘤病毒（human papillomavirus,HPV）的感染在慢性宫颈炎、宫颈上皮内瘤样病变（CIN）及浸润性宫颈癌（ICC）中的表达,旨在提高宫颈上皮内瘤样病变及浸润性宫颈癌的诊断率。方法对就诊的有宫颈疾患的妇女794例,采用导流杂交HPV基因分型技术进行DNA检测。结果 HPV检测阳性113例,阳性率14.23%,其中单一型别HPV感染84例,占总数的74.33%,多型别感染的29例,占总数的25.67%,最常见的HPV基因型为52、16、58、18、53高危型感染率较低危型相比,上升趋势更为明显。结论在宫颈病变筛查中HPV检测可提高细胞学检测的有效性,是早期诊断CINⅢ及ICC的一个重要辅助方法。     

hTERC基因与高危型人乳头瘤病毒分型的相关性研究

目的：探讨宫颈上皮内瘤变石蜡标本中人染色体端粒酶基因( human telomerase gene, hTERC)表达情况及其与高危型人乳头瘤病毒测定的临床意义。方法收集2010年10月至2013年10月上海第八人民医院148例宫颈石蜡组织标本,其中对照组20例(正常宫颈),研究组128例( CINⅠ级30例, CINⅡ级53例, CINⅢ级45例)。应用荧光原位杂交( FISH)技术检测其hTERC基因的表达并采用凯普HPV-DNA分型测定上述受试者高危型人乳头瘤病毒感染情况。结果①随着宫颈病变级别增高, hTERC基因阳性表达率增加。不同级别宫颈上皮内瘤变hTERC基因扩增率与正常对照组比较,差异有显著统计学意义(χ2=63．707, P<0．05); CINⅡ级及以上病变的hTERC基因扩增率明显高于CINⅠ级,差异有显著统计学意义(χ2=36．973, P<0．05)。②受试者中高危型HPV感染阳性率为74．3%(110/148),高危型HPV感染阳性组hTERC基因扩增率和阴性组相比较,差异具有统计学意义(χ2=26．9, P<0．05)。结论宫颈上皮内瘤变组织中hTERC基因扩增与HPV感染具有一定相关性。     

干扰素对孕妇产道病毒的抑制作用

应用重组人ａ１ｂ型干扰素，对感染人乳头瘤病毒１６型和人巨细胞病毒的孕妇进行宫颈贴敷治疗，结果表明，疗前有孕妇ＨＰＶ－１６和ＨＣＭＶ的感染率分别为７０．６％和４１．０％，经干扰素治疗，ＨＰＶ－１６和ＨＣＭＶ的感染阳性率分别下降４１．０％和２３．５％。     

不同方法取材人乳头瘤病毒核酸检测结果对比

人乳头瘤病毒(human papillomavirus,HPV)感染是宫颈癌和癌前病变宫颈上皮内瘤变(cervicalintraepithelial neoplasia,CIN)的主要致病因子。国际宫颈癌生物学研究(the international biologicalstudy of cervical cancer,IBSCC)报道在98%以上宫颈癌组织中可以检出HPV DNA。目前     

Reduced acquisition and reactivation of human papillomavirus infections among older women treated with cryotherapy: results from a randomized trial in South Africa

Background  

Treatment of women for high-grade cervical cancer precursors frequently results in clearance of the associated high-risk human papillomavirus (hrHPV) infection but the role of treatment among women without hrHPV is unknown. We investigated whether cervical cryotherapy reduces newly detected hrHPV infections among HIV-positive and HIV-negative women who were hrHPV negative when treated.     

Toll样受体在人乳头瘤病毒感染致宫颈癌中的作用

高危型人乳头瘤病毒(high-risk human papillomavirus,HR-HPV)持续感染是宫颈癌发生的明确病因,但并非所有HR-HPV感染都会导致宫颈癌,说明多种因素参与调节HR-HPV的致病性。Toll样受体(Toll-like receptors,TLRs)是一类模式识别受体,能特异性识别病原体相关...     

Postmodern cancer: the role of human immunodeficiency virus in uterine cervical cancer.

The association between cervical cancer and human papillomavirus (HPV) is well known, but its association with human immunodeficiency virus (HIV) is controversial. Coinfection with HPV and HIV is to be expected and recent epidemiological data from Africa show that cervical cancer is the most common AIDS defining neoplasm in women. Unlike other AIDS defining neoplasms, the occurrence of cervical cancer is not dependent on immune compromise. HIV alters the natural history of HPV infection, with decreased regression rates and more rapid progression to high grade and invasive lesions, which are refractory to treatment, requiring more stringent intervention and monitoring. The more aggressive behaviour is mirrored by a different molecular pathway. HIV associated cervical cancers are thought to progress through the microsatellite instability pathway, whereas HIV negative ones progress through loss of heterozygosity. Interaction is probably via viral proteins, with HIV proteins enhancing effectiveness of HPV proteins, and perhaps contributing to cell cycle disruption. Dysregulation of the cellular and humoral arms of the local and systemic immune systems may ensure disease progression. Furthermore, HPV infection may predispose to HIV infection and facilitate its progression.     

Human papillomavirus: epidemiology and public health

Approximately 15 types of human papillomavirus (HPV) infection cause virtually all cases of cervical cancer. Human papillomavirus 16 is the major type, accounting for approximately 50% of cases. The major steps of cervical carcinogenesis include HPV infection, viral persistence and progression to precancer (as opposed to viral clearance), and invasion. Human papillomavirus is the most common sexually transmitted infection. However, most HPV infections become undetectable by even sensitive HPV DNA testing within 1 to 2 years. The prevalence of infection peaks at young ages and declines thereafter, perhaps as the result of HPV type-specific acquired immunity. Most HPV infections are neither microscopically evident nor visible, making HPV DNA detection the diagnostic reference standard. Poorly defined immunologic factors are the major determinants of viral outcome. Smoking, multiparity, and long-term oral contraceptive use increase the risk of persistence and progression. Other sexually transmitted infections (eg, Chlamydia trachomatis), chronic inflammation, and nutritional factors might also play a role. Overt, long-term viral persistence in the absence of precancer is uncommon. New prevention strategies can be derived from the evolving knowledge of HPV carcinogenesis. Human papillomavirus vaccination is the ultimate prevention strategy, and large-scale trials are already underway. In the meantime, HPV DNA diagnostics are more sensitive although less specific than cytology, permitting a consideration of lengthened screening intervals. In terms of public health education, clinicians and patients will need to shift discussions of the mildly abnormal Papanicolaou test to consideration of HPV infection as a common sexually transmitted infection that rarely causes cervical cancer.     

Detection of cervical infections in colposcopy clinic patients

The purpose of this study was to determine if Neisseria gonorrhoeae; Chlamydia trachomatis; herpes simplex virus; cytomegalovirus; Epstein-Barr virus; human herpesviruses 6, 7, and 8; or adeno-associated virus influenced the production of cervical intraepithelial neoplasia. Two hundred thirty-one cervical smear samples were tested for the presence of the organisms by PCR. In addition, human papillomavirus types in the samples were determined by PCR and classified into cancer risk types of high, moderate, and low. There was no link with cervical intraepithelial neoplasia status and detection of herpes simplex virus, cytomegalovirus, Epstein-Barr virus, human herpesviruses 6 and 8, gonorrhea, or chlamydia. However, high-grade cervical intraepithelial neoplasia was found more frequently with mixed infection by moderate-risk human papillomavirus types and human herpesvirus 7 than with these papillomavirus types alone. The presence of human herpesvirus 7 may increase the oncogenic potential of moderate-risk human papillomavirus types.     

Contemporary theories of cervical carcinogenesis: the virus, the host, and the stem cell.

Cervical cancer is a complex disease that, by its association with human papillomavirus (HPV), has elicited research in a broad range of areas pertaining to its basic diagnostic and clinical aspects. The complexity of this association lies not only in the fundamental relationship between virus and cancer but also in its translation to pathologic diagnosis and clinical management. Offshoots from the relationship of virus to pathology include studies targeting the link between papillomavirus infection and cervical epithelial abnormalities, the molecular epidemiology of papillomavirus infection, and the potential use of HPV testing as either a screening technique or a tool for managing women who have Pap smear abnormalities. A second variable that is critical to the pathogenesis of cervical neoplasia is the cervical transformation zone. The wide range of invasive and noninvasive lesion phenotypes associated with HPV infection in this region indicate that not only the virus but also specific host target epithelial cells in the transformation zone play an important part in the development of cervical neoplasia. Further understanding of this relationship between the virus and the host epithelium will hinge on determining the subtypes of epithelial cells in the transformation zone and their phenotypic response to infection. New technologies, such as expression arrays, promise to clarify, if not resolve, the complexity of molecular interactions leading to the multiplicity of tumor phenotypes associated with HPV infection of the uterine cervix.     

环氧化酶-2及血管内皮生长因子在宫颈癌及其癌前病变中的表达

目的探讨环氧化酶-2（cyclooxygenenase-2,COX-2）的表达与宫颈癌发生的关系以及COX-2与血管内皮生长因子vascular endothelial growth factor,VEGF）表达的关系。方法采用免疫组化（S-P）法检测20例正常宫颈、26例低度宫颈上皮内瘤变（cervical intraepithelial neoplasia,CIN;CIN Ⅰ）、28例高度CIN（CIN Ⅱ／Ⅲ）、25例宫颈癌组织中COX-2、血管内皮生长因子vascular endothelial growth faclor,VEGF）的表达,并分析COX-2与VEGF及高危HPV感染的关系。结果在正常宫颈、低度CIN、高度CIN、宫颈癌中COX-2的表达率分别为0、23．08％、57．14％、84％,VEGF的表达率分别为5％、30．77％、60．71％、88％,两者均随着病变的加重表达率明显增加,差异均有统计学意义（P〈0．001）。COX-2表达与VEGF呈显著正相关（P=0．001）。人乳头瘤病毒（HPV）在低度CIN、高度CIN及宫颈癌的感染率分别为30．77％、71．43％、100％,在宫颈癌及其癌前病变中,COX-2与高危HPV感染率呈正相关（P=0．021）。结论COX-2与宫颈癌的发生、发展有关,并可能与肿瘤的血管生成有密切的关系。COX-2可能成为宫颈癌早期防治的靶点。     

Epidemiological and clinical aspects of human papillomavirus detection in the prevention of cervical cancer

Cervical cancer is a major cause of death, and the second most frequent cancer in women worldwide. Many studies have indicated a causal relation between genital human papillomavirus (HPV) infections and cervical cancer. High-risk HPV genotypes have been detected in almost 100% of all cervical cancers, and the process of HPV mediated carcinogenesis has been partly clarified. The concept that HPV is a obligatory cause in cervical cancer development has lead to extensive research regarding the incorporation of HPV detection in (1) cervical cancer prevention programs, (2) triage of women with abnormal cervical scrapes in the screening program, and (3) follow-up of patients treated for cervical intraepithelial neoplasia (CIN). Epidemiological studies indicate that 50% of women becoming sexually active contract a genital HPV infection within 2 years. The lifetime risk of a genital HPV infection is estimated to be 80%, but very few of these women will develop cervical cancer. Several studies have shown that the persistence of genital HPV infections is especially related to the development of cervical cancer. As a result, HPV detection at a single moment was shown to be of limited clinical value in the triage of patients with abnormal cervical scrapes, or during follow-up after treatment for CIN. Furthermore, major variations in the sensitivity of different HPV detection methods, as well as differences in HPV detection related to the menstrual cycle, have shown that many facts regarding HPV transmission, replication, and detection need to be clarified, before HPV detection can be of clinical value.     

Human papillomavirus-related cervical and anal disease in HIV-infected individuals in the era of highly active antiretroviral therapy

HIV-infected men who have sex with men remain at high risk of developing anal cancer despite the widespread use of highly active antiretroviral therapy (HAART). In HIVinfected women, however, there is some evidence that HAART may be associated with regression of human papillomavirus (HPV)-related cervical disease. So far, epidemiologic data provided by cancer registries have shown no reduction in the incidence of cervical and anal cancer in patients with HIV infection since the initiation of HAART in 1996. Recent data suggest that HPV infection occurs in the anal canal of immunocompromised patients, as an opportunistic infection, in the absence of receptive anal intercourse. Taken together, these lines of evidence support the need for developing anal and cervical cancer screening programs for patients with HIV, whether untreated or on HAART.