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)

Human papillomavirus infection plays an important causal role in cervical intraepithelial neoplasia and carcinoma. The rate of infection with human papillomavirus as well as the incidence of cervical intraepithelial neoplasia and carcinoma are increased in immunosuppressed patients. We report a possible association between infection with human immunodeficiency virus and cervical intraepithelial neoplasia with human papillomavirus infection.
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PMID:Association of human immunodeficiency virus-induced immunosuppression with human papillomavirus infection and cervical intraepithelial neoplasia. 215 27

We have prepared EMBL3 libraries of DNA extracted from the cervix of a patient with cervical intraepithelial neoplasia (CIN) and isolated seven recombinant clones containing sequences that hybridize to human cytomegalovirus (HCMV) DNA. Restriction analysis of one clone with BamHI and SalI endonucleases revealed that the insert DNA showed a high degree of homology to the HCMV Ad169 genome over the region between the HindIII K/E site and the SalI site located within the BamHI P fragment. The HCMV insert in the CIN clone is integrated and flanked by cellular sequences. The major immediate early gene that encodes a polypeptide of approximately 69 kD was found to be conserved in the CIN clone. Transfection of clones encoding the immediate early region of HCMV resulted in cells that were positive in immunofluorescence studies with two monoclonal antibodies directed against the HCMV 69 kD immediate early polypeptide. Infection of human ectocervical cells with HCMV Ad169 revealed that they could express the 69 kD polypeptide encoded by the immediate early gene but could not replicate the virus, whereas HCMV was able to replicate productively in cultured endocervical cells. HCMV has been shown to activate endogenous retroviruses and also to transcriptionally activate the long terminal repeat of human immunodeficiency virus. Activation of virus and cellular genes by HCMV may be a means by which this virus is involved in the multistage process of oncogenesis and/or the activation of latent infections.
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PMID:Molecular cloning of DNA sequences from cervical intraepithelial neoplasia that hybridize to human cytomegalovirus DNA. 255 81

Multiple markers were used to count Langerhans' cells in the cervix. In the normal cervix, thymocyte antigen (T6) and adenosine triphosphatase (ATPase) demonstrated the largest population of Langerhans' cells. MHC Class II positive cells were equivalent to 60%, and S100 positive cells were equivalent to 35% of T6 or ATPase positive cells. Whereas Langerhans' cells demonstrated by T6, ATPase, and MHC Class II antigen were evenly distributed throughout the epithelium, the S100 positive cells were seen predominantly near lymphocytic aggregates and capillaries. In human papillomavirus infection and cervical intraepithelial neoplasia the numbers of T6, ATPase, or MHC Class II positive Langerhans' cells were reduced by 60% but the S100 positive cells were almost completely depleted. These findings suggested that there were different subpopulations of Langerhans' cells in the cervical epithelium. The depletion of Langerhans' cells, particularly the selective depletion of the S100 positive subpopulation, might cause a localized immunodeficiency that impairs immune surveillance and the cell-mediated immune response to human papillomavirus infection and cervical intraepithelial neoplasia.
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PMID:Subpopulations of Langerhans' cells in cervical neoplasia. 302 67

Lymphocyte phenotypes in cervical mucosa were studied using a panel of monoclonal antibodies. T lymphocytes were predominant both within the epithelium and in the subepithelial stroma. In the normal cervix, both the T4+ (helper/inducer) and T8+ (suppressor/cytotoxic) subsets were present in a ratio similar to that in the peripheral circulation. In human papillomavirus (HPV) infection and cervical intraepithelial neoplasia (CIN) there was depletion of intraepithelial lymphocytes, especially of T4+ subset, with reversal of the ratio of T4+ to T8+ subsets to less than one. In contrast, there was no significant reduction in the number of lymphocytes in the subepithelial stroma. Tac+ (antigen primed and clonal expanding) lymphocytes were absent both within the epithelium and in the subepithelial stroma. These findings support our suggestion that there is a localized immunodeficiency in HPV infection and CIN. The aetiological and therapeutic implications are discussed.
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PMID:Lymphocyte phenotypes in cervical intraepithelial neoplasia and human papillomavirus infection. 302 68

Gynecologic disease is commonly encountered in women infected with the human immunodeficiency virus (HIV). The clinical course of cervical intraepithelial neoplasia, invasive cervical cancer, pelvic inflammatory disease, syphilis, and vaginal candidiasis may be altered by HIV infection and may be refractory to standard treatment, especially with increasing degrees of immune suppression. Careful screening for gynecologic disease and vigilant surveillance for treatment failure are important in the care of women infected with HIV.
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PMID:Gynecologic disease in women infected with human immunodeficiency virus type 1. 760 Jan 2

Lower genital tract neoplasia appears to occur often and in multiple sites in women infected with the human immunodeficiency virus (HIV). To describe the prevalence of lower genital tract neoplasia in HIV-infected women in our clinic we performed a retrospective chart review of 38 HIV-infected women who had received screening colposcopy. Fourteen percent of the women had VIN on biopsy. In addition, 50% of the women had abnormal Pap smears and 24% had CIN on biopsy. In this study, lower genital tract neoplasia was multifocal in nature and included a relatively high prevalence of VIN not previously reported in the literature.
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PMID:Multifocal lower genital tract neoplasia in women with HIV disease. 761 25

The authors underline a synergism of HPV + HSV and HPV + CIN that, together with general immunodeficiency and local factors are responsible for the oncogenesis of cervico carcinoma. This thesis takes on importance after literature reports of an increase of 10% in viral infections from HSV and HPV with a middle incidence of the 1-2% in all the colpocytologic examination cases not in women between 18 and 65 years. To obtain a successful preventive treatment the authors recommend a colpocytologic examination each year, possibly in association with colposcopic, histologic and molecular studies in all HPV positive cases.
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PMID:[The Pap-test in the study of viral infections of the female genital tract]. 763 May 8

The Human Papilloma Virus is often involved in the pathogenesis of cervical lesions. A local or systemic immunodeficiency allows neoplasia outbreaks. We do not know if immunodepression only allows the virus to persist, or if the HPV induces a local immunodeficiency. Large warts are often associated with pregnancy, but cervical cancers are not increased in pregnant women. Induced immunodeficiency (among transplanted patients), or AIDS increase the rate of CIN and cervical cancers. The more serious the immunodeficiency is, the more multifocal and recurrent the lesions are. We have to look for an immunodepression and for AIDS when we observe multifocal or recurrent lesions of the cervix, specially when the lesions do not regress under correct treatment. Immunodeficient women would benefit from closer care of their cervix. We think that combine therapy (e.g. laser and local interferon) would be more efficient in case of immunodeficiency.
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PMID:[Cervical pathology and immunodepression]. 782 39

Most cases of low-grade cervical intraepithelial neoplasia (CIN) associated with oncogenic human papillomavirus (HPV) types regress spontaneously within years. Unknown co-factors seem to be necessary for a progression to malignancy. To determine the possible role of cellular immunodeficiency as such a co-factor in the genesis of genital neoplasia, 48 HIV-infected women and 52 allograft recipients were examined periodically during a 3-year period. Colposcopy, cytology and HPV-DNA typing (ViraType) were performed at each visit. Each cervical lesion was matched prospectively with 2 lesions from immunocompetent controls. In all, 29/100 patients suffered from cervical neoplasms, including 2 advanced cervical cancers and 9 CIN3 lesions. Correlation between grade of lesion and HPV DNA 16/18 was significant. Low-grade lesions among patients progressed more often than among controls and recurrent lesions after destructive treatment were seen more frequently among patients than among controls. All patients with CD4-lymphocyte counts of < 400/microliters or immunosuppression for more than 3 years suffered from progressive lesions. We conclude that malfunction of the cellular immune response following either HIV-induced depletion or iatrogenic inhibition of CD4-lymphocyte activation, enhances the progression of HPV-induced cervical lesions to malignancy.
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PMID:Cellular immunodeficiency enhances the progression of human papillomavirus-associated cervical lesions. 791 55

Papillomaviruses are the causative agents of benign and malignant epithelial tumors of the skin and mucosa. They encode a DNA-binding protein, E2, that regulates viral transcription and replication, making it an important therapeutic target. By deleting the amino-terminal trans-activation domain of human papillomavirus type 16 (HPV-16) E2 while retaining its carboxy-terminal DNA binding and dimerization domain, an E2 repressor (E2R) that efficiently inhibits transcriptional activation by full-length HPV E2 was generated. To deliver this repressor protein into animal cells, we have utilized the human immunodeficiency virus type 1 (HIV-1) Tat protein which itself is taken up efficiently into intact cells. Chimeras of E2R and the cellular uptake domain of Tat specifically inhibited E2-dependent reporter gene expression in COS-7 cells. Treatment of cervical intraepithelial neoplasia cells having episomally replicating HPV-31 DNA with this Tat-E2R protein led to a dose-dependent loss of HPV DNA copies and inhibition of cell growth. Tat-mediated delivery can be a valuable tool for assessing protein function and may allow the development of novel therapeutic proteins having intracellular targets.
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PMID:Specific inhibition of a human papillomavirus E2 trans-activator by intracellular delivery of its repressor. 794 33


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