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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the recognition of Kaposi's sarcoma as a manifestation of the acquired immunodeficiency syndrome, subsequent malignancies such as non-Hodgkin's B-cell lymphoma and primary central nervous system lymphoma have been found to be associated with individuals infected with the human immunodeficiency virus (HIV). The epidemiology, clinical manifestations, and current concepts of pathogenesis are reviewed in this article. In addition, the relation between HIV and other malignancies, including Hodgkin's lymphoma, T-cell lymphomas, and anorectal carcinoma, is discussed. In general, HIV-related malignancies are more aggressive, respond poorly to treatment, and are associated with an extremely high rate of mortality.
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PMID:HIV-related malignancies. 187 28

Cytologic and histologic investigations of the uterine cervix and studies of the lymphocyte functions were performed in human immunodeficiency virus-infected and human immunodeficiency virus antibody-negative women to study possible linkages between human papillomavirus-induced dysplasia and degree of human immunodeficiency virus-induced immunosuppression. Cytologic smears of the uterine cervix of 111 human immunodeficiency virus-infected women were compared with findings in 76 female intravenous drug users negative for human immunodeficiency virus antibodies and in a group of 526 women of the outpatient population of the hospital. Cervical dysplasia-neoplasia (including five cases of invasive carcinoma) was seen in 41% of the human immunodeficiency virus-infected patients. In human immunodeficiency virus-negative intravenous drug users dysplasia-neoplasia was seen in 9%, and in the sample from outpatients in 4%, including two cases of invasive carcinoma (p less than 0.01). Cytologic features that were attributable to infection with human papillomavirus were observed in human immunodeficiency virus-infected women four times more often than in the sample from the outpatient population (p less than 0.01). Frequency and severity of dysplasia appear to increase with diminishing numbers of CD4+ helper/inducer T lymphocytes and correlated significantly (p less than 0.01) with a loss of blastogenic response to phytohemagglutinin, pokeweed mitogen, and tetanus toxoid. These results suggest an increased risk for the development of dysplasia of the uterine cervix in women with human immunodeficiency virus infection, which is related to the degree of immunosuppression.
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PMID:The increased frequency of cervical dysplasia-neoplasia in women infected with the human immunodeficiency virus is related to the degree of immunosuppression. 199 8

Two women with Stage II breast carcinoma treated with lumpectomy followed by breast irradiation and adjuvant chemotherapy developed Pneumocystis carinii pneumonia while receiving cytotoxic chemotherapy. Neither woman had evidence of immunosuppression before therapy. They both had profound lymphopenia, reversed CD4/CD8 ratios, and normal peripheral blood total leukocyte counts at the time of their infections. Both women were seronegative for human immunodeficiency virus type 1 and had no risk factors for such an infection. The patients' CD4 lymphocyte counts increased after chemotherapy for breast carcinoma was discontinued. Thus, it appears that the therapy they received may have caused severe T-lymphocyte mediated immunosuppression.
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PMID:Pneumocystis carinii pneumonia associated with profound lymphopenia and abnormal T-lymphocyte subset ratios during treatment for early-stage breast carcinoma. 201 44

As summarized here human papillomaviruses are associated with a wide spectrum of epithelial lesions, ranging from benign warts to invasive carcinomas. They have been difficult to study in part because they have not yet been propagated in tissue culture. Fortunately advances in molecular biology have allowed characterization of HPV genomes and identification of some HPV gene functions. In addition to their clinical importance HPVs represent an important tool for exploring virus-cell interactions, gene expression, cellular differentiation and cancer. HPV infections are not only common but also difficult to treat and prevent. Depending on the HPV type and location, the modes of HPV transmission may involve casual physical contact, sexual contact and perinatal vertical transmission. HPV DNA genomes replicate at a low copy number in basal cells and, as most clinicians know, are difficult to eradicate. There is often a long latent period and subclinical infections, and HPV DNA can be found in normal tissue adjacent to lesions. HPVs can cause widely disseminated lesions, especially in the immunocompromised host and in epidermodysplasia verruciformis. Aside from the rare carcinomas, the most serious life-threatening HPV-induced illness in children is recurrent respiratory papillomatosis. Somewhat surprisingly in malignant lesions HPV DNA is also found as fragments incorporated into the cellular genome. Unlike retroviruses such as human immunodeficiency virus which integrate into the cellular genome as part of their life cycle, HPV integration is a terminal event for viral replication. Such integration may be critical, however, for viral-induced abnormal cell growth. Perhaps the most important implication of the finding that some anogenital cancers are in part sexually transmitted infectious diseases is that they may be preventable. The data overwhelmingly suggest that avoidance of exposure to HPV via abstinence or monogamy in both partners markedly reduces the risk of cervical cancer. A more realistic goal, however is prevention of HPV transmission by the use of barrier method contraceptives, which may be protective against development of cervical carcinoma. The America Association of Pediatrics Committee on Adolescents has outlined the obligation of pediatricians to be actively involved in adolescent education on sexually transmitted diseases. Certainly a fundamental knowledge of HPV epidemiology, the risks of HPV-related sequelae and prevention of HPV infection are important considerations for adolescent sexuality. Although helpful, such awareness alone falls far short of making an impact on sexual behaviors. A significant reduction in HPV infection rates could be achieved only by inundating adolescents at an early age with a highly visible society-wide campaign directed at these issues.
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PMID:Human papillomaviruses: pediatric perspectives on a family of multifaceted tumorigenic pathogens. 164

Rectal dysplasia and carcinoma associated with human papillomavirus infection are increasing in prevalence among homosexual men, particularly those infected with the human immunodeficiency virus. We report a case involving a 39-year-old homosexual man with AIDS who developed a persistent rectal ulcer. A biopsy of the ulcer revealed severe squamous dysplasia, and human papillomavirus type 33 was detected in rectal tissue with use of in situ DNA hybridization. This genotype of virus has not been previously associated with anal or rectal dysplasia in homosexual men, including those infected with the human immunodeficiency virus. The rectal ulcer resolved after 2 months of oral therapy with 60 mg/d of isotretinoin, a retinoid.
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PMID:Persistent rectal ulcer associated with human papillomavirus type 33 in a patient with AIDS: successful treatment with isotretinoin. 217 42

Epstein-Barr virus (EBV) is a ubiquitous DNA virus that normally infects silently, establishing lifelong latency. Substantial empirical observations support the view that immunodeficiency is permissive in EBV-induced lymphoproliferative diseases (LPD). Primary immune deficient patients such as those with X-linked lymphoproliferative disease and individuals with acquired immune deficiency secondary to immunosuppressive drugs for organ transplantation or individuals infected with human immunodeficiency virus are also at very high risk for lethal LPD. The importance of immunodeficiency and EBV in the development of head and neck carcinomas and uterine cervical carcinoma is less clear. Methods are available for detecting immunodeficiency and EBV genome and thus preventive strategies are being developed to preclude LPD from occurring.
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PMID:Immune deficiency as a risk factor in Epstein-Barr virus-induced malignant diseases. 217 75

The immunodeficient state that evolves in persons infected with the human immunodeficiency virus (HIV) appears to increase their risk of certain types of cancer. Among these are primary lymphoma of the central nervous system, undifferentiated non-Hodgkin's lymphoma, squamous cell carcinoma, anorectal carcinoma, and cutaneous malignancies. These malignancies are similar in incidence to those seen in other immunodeficient patients. Lymphoma, in particular, is associated with a more aggressive disease state. In HIV-infected patients, the disease is usually diagnosed at a more advanced stage, frequently has extranodal involvement, and usually responds poorly to chemotherapy. Viruses, such as Epstein-Barr virus and papillomavirus, have been implicated in the pathogenesis of lymphoma and other malignancies in immunosuppressed patients, including those with HIV infection.
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PMID:Lymphoma and other HIV-associated malignancies. 219 54

To determine the relationship between human immunodeficiency virus (HIV) infection and cervical neoplasia, the characteristics of invasive and preinvasive cervical disease in 114 patients of known HIV status were assessed. Seven of thirty-seven patients (19%) under age 50 with invasive cervical carcinoma were HIV-positive, including a 16-year-old with stage IIIB disease. HIV-positive patients had more advanced invasive cancer than HIV-negative patients. Disease persisted or recurred in all HIV-positive patients compared to 37% of HIV-negative patients. In HIV-positive patients, the median times to recurrence and death were 1 and 10 months, respectively. No HIV-positive patient had HIV-related symptoms. The mean T4:T8 cell ratio in HIV-positive patients was 0.49, compared to 1.86 in HIV-negative patients. The mean T4 cell count was 362/mm3 in HIV-positive and 775/mm3 in HIV-negative patients. Colposcopic evaluations of the lower genital tract of 77 patients with abnormal smears revealed higher-grade cytology and histology in 25 HIV-positive than in 52 HIV-negative patients. HIV-positive patients had significantly more multifocal/extensive lesions, multisite involvement, perianal involvement, evidence of human papillomavirus (HPV) infection, and associated gynecologic infections than HIV-negative patients. In areas at high risk for HIV infection, we must anticipate a high prevalence of HIV seropositivity in women with invasive cervical cancer. In the HIV-infected, cervical cancer is of advanced stage and responds poorly to therapy. Intraepithelial neoplasia in HIV-positive patients may be of higher grade than in HIV-negative patients, with more extensive involvement of the lower genital tract.
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PMID:Human immunodeficiency virus infection and cervical neoplasia. 222 52

Patients with the acquired immunodeficiency syndrome are at increased risk for certain malignancies. Because acquired immunodeficiency syndrome and testicular cancer affect primarily young men, the potential complications that acquired immunodeficiency syndrome might impose raise significant concern. To address this question we performed a retrospective review of all cases of testicular cancer during an 11-year period. Of 140 patients 6 had human immunodeficiency virus infection and 7 were from human immunodeficiency virus risk groups. All cases were either stage I or II disease with seminoma in 8, teratocarcinoma in 3, embryonal cell carcinoma in 1 and teratoma in 1. The clinical presentations of these patients were comparable to those of patients without human immunodeficiency virus risk factors. The majority of the patients received standard therapy, including orchiectomy followed by lymphadenectomy, radiation therapy or chemotherapy depending on stage and pathological subtype. Patients tolerated therapy well with only 1 course of radiation therapy complicated by Pneumocystis carinii pneumonia. All patients achieved complete remission and none died of testicular cancer. Since treatment of these patients may worsen the immunosuppression, surveillance is recommended after orchiectomy for acquired immunodeficiency syndrome patients with stage I disease. However, the majority of patients with human immunodeficiency virus infection should receive standard therapy.
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PMID:Testicular carcinoma in patients positive and at risk for human immunodeficiency virus. 223 90

CD4 molecules on human cells function as a major receptor for human immunodeficiency virus (HIV); however, certain CD4-negative cell types may also be susceptible to infection. Therefore, we attempted to quantitate the relationship between HIV infection and CD4 expression on human cell lines before and after introduction of the CD4 gene by using a retrovirus vector. Prior to introduction of the CD4 expression vector, low levels of HIV infection were detected by a sensitive focal immunoassay on all three cell types studied. With several HIV strains in clones of human cervical carcinoma (HeLa) cells expressing different levels of CD4, HIV titer increased with increasing CD4 expression. In contrast, in squamous cell carcinoma cells (SCL1) and astroglial cells (U87MG), even high levels of CD4 expression failed to augment HIV infection. The CD4 protein expressed in these two cell lines had the expected molecular weight and was capable of binding HIV virions. However, in contrast to CD4-positive HeLa cells, CD4-positive U87MG and SCL1 cells were unable to form syncytia when cultured with cells expressing HIV envelope protein. Thus, the inability of HIV to infect these cells appeared to be due to lack of fusion between HIV virion envelope proteins and CD4-positive cell membranes. This block is infectivity was overcome when cells were infected with HIV which was pseudotyped with the envelope protein of amphotropic murine leukemia virus. Thus, in addition to CD4, other cell surface molecules appear to be required for successful HIV entry into and infection of these two human cell lines.
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PMID:Failure of human immunodeficiency virus entry and infection in CD4-positive human brain and skin cells. 229 63


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