Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 158 women who either HIV-infected or under iatrogenic immunosuppression were examined regularly during a 4-year period to evaluate if certain vulvar neoplasms and cervical neoplasia have similar associated risk factors. Patients with CIN were matched prospectively with immunocompetent controls with CIN. Forty-eight cervical lesions were detected among patients, including 2 invasive carcinoma and 15 CIN-3 lesions, compared to 11 vulvar lesions, including 2 invasive carcinoma and 7 VIN-3 lesions. Women who have more than five life-time partners were more likely to have HPV-DNA positive cervical swabs and vulvar scrapes as well as cervical and/or vulvar neoplasia. Compared to 2.7% of controls 15.2% of patients with CIN had coexisting high-grade lesions of the vulva. With 1 exception all patients with vulvar neoplasia either suffered from symptomatic immunodeficiency or received immunosuppressive drugs for more than 10 years. Except for 1 VIN-3 lesions, all vulvar neoplasms were associated with HPV-DNA types 16, 31, and/or 33. Six of nine patients as well as the 2 controls with coexisting vulvar and cervical neoplasia had the same HPV-type associated with both lesions. All vulvar lesions were classified as either "warty" or "basaloid". In conclusion cervical and bowenoid/basaloid vulvar neoplasia seem to have a similar HPV-related genesis. Malfunction of the cellular immune response appears to be a cofactor in the genesis of HPV-associated neoplasia at both sites.
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PMID:Human papillomavirus is associated with the frequent detection of warty and basaloid high-grade neoplasia of the vulva and cervical neoplasia among immunocompromised women. 855 24

It has been described that women infected with the human immunodeficiency virus (HIV) present more frequent cytological abnormalities in cervicovaginal smears, generally related to infection by human papillomavirus (HPV). The present work is a study of cervicovaginal smears of 147 HIV-seropositive women submitted to routine gynecological examinations. The smears were stained by the Papanicolaou method. Cytopathic effects of HPV were found in 38 (25.8%) cases. Nuclear atypias of cervical intraepithelial neoplasia (CIN) were evident in 36 (24.5%) of these cases: 27 (18.4%), CIN I; 6 (4.0%), CIN II and 3 (2.0%) CIN III. Also 2 (1.4%) invasive carcinomas and one (0.7%) endocervical dysplasia were found. Other agents observed were: Candida sp, 19 (12.9%) cases, Gardnerella vaginalis, 19 (12.9%), Trichomonas vaginalis, 13 (8.4%), Chlamydia trachomatis 5 (3.4%), Mobiluncus sp 2 (1.4%) and Herpes simplex virus 1 (0.7%). This study emphasizes the high frequency of HPV/CIN cervicovaginal abnormalities in HIV-seropositive in our population. It is possible that immunological factors and sexual promiscuity are involved in this phenomenon.
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PMID:Papillomavirus in cervicovaginal smears of women infected with human immunodeficiency virus. 873 Dec 85

The World Health Organization classification has clarified the typing of cervical tumours. The category of early stromal invasion has been eliminated from the International Federation of Gynecology and Obstetrics staging scheme of cervical carcinoma. Stage lal is defined now as depth of invasion less than or equal to 3 mm; stage la2 is defined as depth of invasion between 3 and 5 mm in depth. The width should not exceed 7 mm. Small cell carcinoma has been better delineated. An increased incidence of human papillomavirus infection and cervical intraepithelial neoplasia has been observed in patients suffering from the effects of human immunodeficiency virus, in whom invasive cervical cancers run a more aggressive course. The better understanding of pseudomalignant lesions, that is, deep cervical glands, various metaplasias and inflammatory pseudo tumours, as well as some rare tumours, enables the surgical pathologist to make a more accurate diagnosis, resulting in better patient care.
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PMID:The pathology of cervical neoplasia. 877 62

Cervical intraepithelial lesions associated with genital human papilloma virus (HPV) infection occur with increased frequency and severity among women with immunodeficiency. In this study, we considered 24 HIV-seropositive and 12 HIV-seronegative women. Each woman was interviewed and underwent a cytologic and colposcopic evaluation. Then colposcopic and cytologic findings were correlated with histologic and differences between HIV-seropositives and seronegatives were analyzed. Ten (41%) of 24 HIV-seropositive and one (9%) of 12 HIV-seronegative women had human papilloma virus infection. Among seropositives, eight (34%) had cervical intraepithelial (CIN): of those eight, 5 had CIN I, 2 CIN II and 1 CIN III. There (24%) of the 12 HIV-seronegative had CIN: two had CIN I and one CIN II. Six of the HIV-seropositive women were found to have multicentric disease (two or more sites). The objective of this study is to determine the relationship between human immunodeficiency virus (HIV) and human papilloma virus infection, sexual habits, reproducive history, and risk of cervical intraepithelial neoplasia (CIN). The results of this study suggest that cervical intraepithelial neoplasia is a common finding in HIV-infected women. Papanicolaou tests should be effective for detecting cervical disease in this population.
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PMID:[Incidence of HPV and CIN in HIV positive women]. 882 Mar 92

This article reviews the impact of infection with human immunodeficiency virus (HIV) on HPV infections and HPV-associated lesions of the female anogenital tract. Studies investigating HPV infections in HIV-seropositive women are presented as well as the possibility that HIV can influence HPV expression directly through molecular interactions between viral genes and indirectly through immunosuppression. Studies linking HIV infection to invasive cervical cancer and cervical intraepithelial neoplasia are reviewed; recommended protocols for cervical cancer screening in HIV-seropositive women for cervical disease also are presented.
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PMID:Anogenital papillomavirus infection and neoplasia in immunodeficient women. 898 79

The incidence of human papillomavirus (HPV)-related cervical intraepithelial neoplasia (CIN) and cervical cancer is increased with immunodeficiency, but the role of immune response, including cell-mediated immunity, in disease prevention is not well understood. In this study, T-cell proliferative responses to six synthetic peptides with predicted immunogenic determinants from the HPV-16 E4, E6, E7, and L1 open reading frames were analyzed in 22 sexually active women with new-onset CIN and 65 sexually active women without cervical disease, characterized by cytology, colposcopy, and HPV testing. T-cell proliferative responses were demonstrated to all six HPV-16 peptides. Although not statistically significant, rates of reactivity to E6 (24-45) were higher among sexually active women without disease (26%) than among women with current CIN (7%), as was the overall number of peptides stimulating a response. Women with CIN may not respond to selected HPV antigens as well as women without disease do.
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PMID:T-cell proliferative response to human papillomavirus type 16 peptides: relationship to cervical intraepithelial neoplasia. 899 37

The objectives of our study were to determine the prevalence of cervical intraepithelial neoplasia (CIN) in a southeastern human immunodeficiency virus (HIV)-positive population relative to an HIV-negative control group and to compare these findings with published reports from other geographic regions. Demographic, medical, and cytopathologic data were collected on 89 HIV-positive women receiving care at the Duke Adult Infectious Disease Clinic. Comparisons were made with 100 HIV-negative obstetric patients who delivered at Duke and with published reports from other regions of the United States and abroad. Cervical intraepithelial neoplasia was present in 43 (49%) of 87 HIV-positive women compared with 23% of the 100 HIV-negative patients. Two of the HIV-positive patients had invasive cancer. Comparison of these patients with patients from other geographic regions revealed similar odds ratios for the presence of CIN in HIV-positive patients compared with HIV-negative patients. These results suggest a significantly increased risk for cervical dysplasia in HIV-positive women in this southeastern population.
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PMID:Cervical intraepithelial neoplasia in HIV-infected women in a southeastern US population. 930 97

Infections of the genital and oral epithelia by human papillomaviruses cause condylomata, papillomas, and squamous intraepithelial neoplasms, some of which can progress to invasive cancers. We describe an induction of p21cip1/WAF1/sdi1 protein in a fraction of the spinous cells in benign lesions and in cervical intraepithelial neoplasia grades I and II. The induction appears to be post-transcriptional and independent of p53. p21cip1 antigen-positive cells were sporadic in cervical intraepithelial neoplasia III and rare and focal in carcinomas. In contrast, p21cip1 protein was below or at the threshold of detection in the differentiated cells of normal squamous epithelia from different body sites despite an up-regulation of p21cip1 RNA. In cervical intraepithelial neoplasias from patients who were also positive for the human immunodeficiency virus, there was an additional increase in p21cip1 RNA in the upper spinous cells without concomitant p21cip1 protein induction. A consistent inverse relationship was observed between the p21cip1 protein induction and abundant human papillomavirus DNA and RNAs. We propose that p21cip1 protein induction is a novel host response that inhibits viral DNA replication and thus prevents elevated viral transcription. This hypothesis can partly account for the heterogeneity and the differentiation-dependent viral activities commonly observed in benign human papillomavirus lesions.
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PMID:Post-transcriptional induction of p21cip1 protein in condylomata and dysplasias is inversely related to human papillomavirus activities. 954 62

Women who are infected with human immunodeficiency virus (HIV) are at greater risk for the development of lower genital tract neoplasia than are HIV-negative women. Among HIV-positive women, those who are more severely immunosuppressed appear to be at higher risk for cervical intraepithelial neoplasia (CIN), also known as squamous intraepithelial lesions (SILs). Women who are HIV-positive also are more likely than HIV-negative women to have multifocal lower genital tract neoplasia. Cervical cancer is one of the most important acquired immune deficiency syndrome (AIDS)--related malignancies in women. Cancer and intraepithelial neoplasia of the lower genital tract can be persistent, progressive, recurrent, and difficult to treat in HIV-positive women. The most effective method for treating SILs has not been determined. Regular performance of Pap smears in HIV-positive women is of critical importance, as is careful examination of the entire lower genital tract. Also, women with high-grade intraepithelial or cervical cancer should be tested for HIV.
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PMID:Lower genital tract neoplasia in women with HIV infection. 987 47

To evaluate the humoral immune response to human papillomavirus (HPV) in women infected with human immunodeficiency virus (HIV), serum samples of 83 HIV-positive individuals were analysed by ELISA for specific antibodies of the isotypes IgG, IgA and IgM recognizing HPV-6, -11, -16, -18 and -31 L1 virus-like particles (VLPs). Papillomavirus-related lesions were present in 30 of 83 HIV-positive women. Twenty-one women (25%) presented with high-/intermediate-grade anogenital squamous intraepithelial lesions. PCR analysis and sequencing for HPV typing was done from biopsy specimens of 18 women; PCR-positive results were obtained in 90% of cases. In addition, HPV DNA hybrid capture assays were performed from cervical swabs of 58 HIV-positive women, 53% of whom had a positive result for high-risk HPV. Overall, positive IgG reactivity to HPV-6/-11 and HPV-16/-18/-31 was seen in 19%/31% and 49%/30%/24% of HIV-positive women, respectively. HPV-seropositivity was even higher than in 48 HIV-negative cervical intraepithelial neoplasia/cancer patients with percentages as follows: 8%/2% and 31%/15%/15%. This difference was significant for HPV-16 (P=0.046). IgA responses were comparable to IgG. IgM responses were low. The extraordinarily high rate of antibodies to the capsid protein L1 of high-risk HPVs (HPV-16, -18 and/or -31) in 58% of HIV-positive women compared to 19% (P=0.00001) of 102 healthy HIV-negative control women suggests a high lifetime cumulative exposure to HPV and increased expression of capsid proteins due to cellular immunodeficiency in HIV-infected women.
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PMID:Specific serum IgG, IgM and IgA antibodies to human papillomavirus types 6, 11, 16, 18 and 31 virus-like particles in human immunodeficiency virus-seropositive women. 1067 7


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