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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unrecognized laryngeal tuberculosis (TB) poses a significant hazard to otolaryngologists. However, the changing manifestations of TB in patients with human immunodeficiency virus (HIV) infection can make its diagnosis difficult. In our population of 146 patients with TB involving the head and neck, HIV infection was present in 70 cases (48%). The prevalence of laryngeal TB in this population was 5.5% (8 patients). Concomitant HIV infection was present in 2 (25%) of 8 patients with laryngeal TB. A delay in the diagnosis of laryngeal TB occurred in 100% of patients with HIV infection, compared with 17% of non-HIV-infected patients (P = .055). The cause of the delayed diagnosis was multifactorial, mainly the presence of multiple confounding variables and the carcinoma-like appearance of the laryngeal TB lesions in HIV-infected patients. To reduce risk for transmission of TB to health care providers, a high level of suspicion must be present for all patients with laryngeal lesions, especially those with HIV infection.
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PMID:Laryngeal tuberculosis in HIV-infected patients: a difficult diagnosis. 884 93

Recent evidence suggests an association between cervical condyloma, dysplasia and HIV infection. However, the course of cervical cancer in immunodeficient patients has not yet been thoroughly researched. Cervical cancer presently amounts to 1% of the causes of death in AIDS patients. This percentage is bound to increase not only because an improved life expectancy has been obtained, but mainly because the virus is widely spreading among the female population. A 28 year-old AIDS patient, parity 1/0/1/1, underwent gynecological examination and colposcopy following an episode of vaginal bleeding. Biopsy revealed an invasive cervical carcinoma. The last gynecologic investigation, which included a Pap smear and colposcopy, was performed 14 months earlier and resulted negative. Cytologic reexamination of the specimen confirmed the previous Pap smear result. Proctoscopy and cystoscopy showed no mucose involvement. Urography was negative. The cat scan indicated minor spleen and liver enlargement but no signs of malignant abdominal spread were found. The neoplasia was classified as a stage IIB cervical carcinoma (according to the FIGO classification) due to the spread to the left cardinal ligament. In spite of radiation therapy, the disease rapidly progressed leading to a monolateral ureteral involvement which created a juxtavescical stenosis. The patient died three months later. Necroscopic examination revealed lung metastasis. Such a rapidly progressive form of cervical cancer could be related to the acquired immunodeficiency condition. Recurrent cytological and colposcopic examinations are to be considered mandatory in HIV patients.
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PMID:Rapidly progressive squamous cell carcinoma of the cervix in a patient with acquired immunodeficiency syndrome: case report. 885 13

Recent studies have demonstrated that the activation of HIV-1 provirus and of the Long Terminal Repeat of HIV-1 (HIV-1-LTR) may occur upon cell-to-cell contact between peripheral blood lymphocytes (PBLs) and infected or transfected (HT29) human colonic carcinoma cells. Using transient or stable transfections, we ascertained that the HIV-1 LTR was up-regulated by cell-to-cell contact in various cell lines. The degree of cell-to-cell contact responsiveness was cell type dependent. In contrast, in transient transfection, the HIV-1-LTR was strongly induced by Tat expression in all cell types tested. This indicates that there are differences in the induction mechanism for these two stimuli, even though Tat protein has been previously reported to induce cell adhesion. Except for the PBLs/transfected cells interactions, the results also demonstrate that the cell-to-cell contact-induced HIV-1-LTR activation was highest after contact between autologous as compared to heterologous cells. Previous experiments have shown that, in HT29 cells, cell-to-cell contact activation of the HIV-1-LTR involved the NF-kappa B tandem binding site and activates DNA binding of the nuclear factor NF-kappa B. In this work, we show that in a stably transfected cell line, the principal enhancer element was also involved in the HIV-1-LTR cell-to-cell contact activation. On the other hand, in the HT29 cell line, the NF-kappa B binding appeared to involve the RGD motif of the cell-binding domain, which indicates that a post-integrin receptor event could be implicated.
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PMID:Activation of the transcription from the human immunodeficiency virus type 1 (HIV-1) long terminal repeat by autologous and heterologous cell-to-cell contact. 889 48

The object of this study was to investigate the influence of reactive oxygen intermediates (ROI), such as H2O2, on HIV-1 infection of cell cultures. The CD4+ HeLa human epithelial carcinoma cell line clone pBKTRLac was infected with HIV-1MN that had been treated with 0.01-5mM H2O2. Virus infectivity was detected by 3 methods: (a) using transactivation of LTR-linked beta-Galactosidase, (b) viral core p24 antigen enzyme-linked immunoasorbent assay (ELISA), and (c) reverse transcriptase activity assay. Treatment of HIV-1MN cell free virus particles with 0.01 mM H2O2 resulted in a significant increase in virus infection. This effect declined with increasing H2O2 concentrations from 0.05 to 0.1 mM. Further increases in H2O2 concentration up to 5 mM resulted in significant suppression in virus infection. These observations indicate that H2O2 may play a role in affecting the course of HIV infection.
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PMID:Influence of hydrogen peroxide on the in vitro infectivity of human immunodeficiency virus. 890 98

As many as 40% of individuals infected with HIV will be diagnosed with a malignancy during the course of their illness. Although neoplasms of all organ systems have been reported in infected patients, Kaposi's sarcoma (KS), non-Hodgkin's lymphoma (NHL), primary central nervous system (CNS) lymphoma, and invasive squamous cell cervical carcinoma are considered to be diagnostic of AIDS in the presence of HIV infection. The rapidity with which these malignancies are diagnosed can affect the morbidity experienced by patients. The management of patients with AIDS-related malignancies poses several challenges for oncology nurses. First, most such patients are treated with either chemotherapy or radiotherapy, and use of these modalities is complicated by the underlying HIV infection. Second, patients with AIDS-related malignancies experience numerous symptoms, and again, management of these symptoms is compounded by the underlying disease. By applying their knowledge and experience, oncology nurses can greatly lessen morbidity in these patients.
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PMID:Nursing challenges of caring for patients with HIV-related malignancies. 890 43

Transcription of human immunodeficiency virus type 1 (HIV-1) is regulated by multiple cis-acting regulatory elements located in the viral long terminal repeats (LTRs). HIV-1 LTR enhancer is activated by a variety of heterologous viral, chemical, and physical agents. Studies have demonstrated that irradiation by X-rays induces transcription under the control of the HIV-1 LTR and that ionizing radiations activate DNA binding of the nuclear transcription factor NF-kappa B. Using various constructs expressing a reporter gene under the control of complete or deleted LTRs of HIV-1, we evidenced that a sequence located in the U3 region was involved in X-ray activation of the HIV-1 LTR in the human colonic carcinoma cell line HT29. The cis-acting element conferring X-ray responsiveness is indistinguishable from HIV NF-kappa B tandem repeat binding sites (HIV-1, kappa B). The present work has examined the effects of X-irradiation on the NF-kappa B transcription factor. Furthermore, we characterized the subunit composition of the two major nuclear NF-kappa B complexes that bind HIV-1 kappa B after X-ray irradiation.
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PMID:Activation of the HIV type 1 long terminal repeat by X-irradiation involves two main Re1/NF-kappa B DNA-binding complexes. 891 77

HIV-infected individuals are at an increased risk for development of cancers other than the three AIDS-defining malignancies. Two non-AIDS-defining cancers, germ cell tumors and Hodgkin's disease, have been reported in the setting of HIV infection with increased frequency compared with their incidence in the general population. Other non-AIDS-defining malignancies frequently reported in the setting of HIV infection include lung cancer, squamous and basal cell carcinomas of the skin, anal carcinoma, and pediatric leiomyosarcomas.
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PMID:Non-AIDS-defining malignancies in patients with HIV infection. 891 5

Patients affected by human immunodeficiency virus (HIV) infection present an elevated risk of developing cancer. In the last 10 years, the relationship between human papilloma virus (HPV) infection and female cervical intra-epithelial neoplasia (CIN) has been established. Several studies have described an increased prevalence of both cervical HPV infection and CIN among HIV-positive women compared to HIV-negative ones. A high recurrence rate of CIN after standard treatment has been noted in HIV-infected women and the severity of these lesions seems to be inversely correlated to immune function. Taking into account these data, the Centers for Disease Control (CDC) since 1993 have included invasive cervical carcinoma among the AIDS-defining conditions. Once cervical cancer develops in HIV-positive women, the disease may be aggressive and less responsive to treatment. A primary means by which HIV infection may influence the pathogenesis of HPV-associated cervical pathology is by molecular interaction between HIV and HPV genes. Although these have not been well defined, an upregulation of HPV E6 and E7 genes expression by HIV proteins (such as tat) has been postulated by some authors. Cervical cytology appears to be adequate as a screening tool for the cervical intra-epithelial neoplasia in HIV-positive women, but the high recurrence rate and multifocality of this disease reinforces the need for careful evaluation and follow-up of the entire anogenital tract in these women. Probably in the next few years, cervical tumours will represent one of the most frequent complications of HIV infection, a part of progression through AIDS. This points to a need for greater interdisciplinary co-operation for a best disease definition and for the development of effective prevention measures.
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PMID:Intra-epithelial and invasive cervical neoplasia during HIV infection. 903 2

Four new triterpene compounds, celasdin-A, celasdin-C, anti-AIDS celasdin-B and cytotoxic maytenfolone-A, were isolated from Celastrus hindsii. The structural determination of maytenfolone-A, celasdin-A, celasdin-B and celasdin-C, as well as the structure-activity relationships of these new compounds and derivatives, are discussed. Maytenfolone-A was further confirmed by X-ray studies. Biological evaluation showed that Maytenfolone-A demonstrated cytotoxicity against hepatoma (HEPA-2B, ED50 = 2.3 micrograms ml-1) and nasopharynx carcinoma (KB, ED50 = 3.8 micrograms ml-1). Celasdin-B was found to exhibit anti-HIV replication activity in H9 lymphocyte cells with an EC50 of 0.8 microgram ml-1).
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PMID:Antitumour and anti-AIDS triterpenes from Celastrus hindsii. 911 98

Cell-to-cell contact between peripheral blood lymphocytes and transfected human colonic carcinoma cell line HT29 activates transcription of the long terminal repeats (LTR) of human immunodeficiency virus. HIV-1 LTR transcription is controlled by a complex array of virus-encoded and cellular proteins. Using various constructs expressing a lacZ reporter gene under the control of the intact or three deleted forms of HIV-1 LTR, we obtained evidence that the kappaB regulatory elements located in the U3 region are involved in cell-to-cell activation of HIV-1 LTR. Cell-to-cell contact activates in vitro binding of the nuclear factor kappaB (NF-kappaB) p50/p65 heterodimer to an HIV-1 kappaB oligonucleotide. Cell-to-cell contact activation of NF-kappaB was only partially inhibited by 100 microM pyrrolidine dithiocarbamate and was not correlated with a significant decrease of cellular inhibitor kappaB alpha. NF-kappaB nuclear activation was not detectable before 1 h after cell contact and was dependent on protein synthesis.
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PMID:Cell-to-cell contact activates the long terminal repeat of human immunodeficiency virus 1 through its kappaB motif. 911 25


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