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)

Bacillary angiomatosis (BA) is a recently described infection usually found in patients with human immunodeficiency virus disease. BA is caused by a Gram-negative coccobacillus. This organism is primarily responsible for skin lesions of the pseudo-botryomycoma type or inflammatory nodules, but it also produces fever, degradation of the general condition and visceral lesions involving the lymph nodes, the liver, the spleen and the bones. Histology shows vascular proliferation with turgid endothelial cells and mostly neutrophilic inflammatory infiltrates. BA is susceptible to many antibiotics. The authors describe the history of the disease and its clinical and histological features, discuss its differential diagnosis and principally deal with the relationship between BA and cat-scratch disease and between BA and verruca peruana. They also present the molecular biology technique which enables a genotypic diagnosis of the disease to be made, replacing a deficient phenotype.
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PMID:[Bacillary angiomatosis]. 147 Jun 25

Three males infected with the human immunodeficiency virus (HIV) were noted to have extensive flat warts of the face and/or body. In two there were also pityriasis versicolor-like lesions. Biopsies showed foamy, basophilic, distended cytoplasm in granular layer keratinocytes, characteristic of the human papillomavirus types seen in epidermodysplasia verruciformis. DNA hybridization techniques demonstrated the presence of HPV-type 8 in one patient and HPV 5 and 8 in another. Patients with immune suppression due to HIV infection may demonstrate the clinical features of epidermodysplasia verruciformis with the same potentially oncogenic HPV types.
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PMID:Epidermodysplasia verruciformis-associated papillomavirus infection complicating human immunodeficiency virus disease. 184 68

Oral lesions are frequently seen in association with all stages of infection with the human immunodeficiency virus (HIV). Many of these lesions occur as the first clinical sign of HIV infection. These lesions include candidiasis, hairy leukoplakia, warts, ulcers, and an aggressive form of periodontal disease. Careful oral examination may reveal lesions that alter Centers for Disease Control staging.
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PMID:Oral manifestations of HIV infection. 187 29

Viruses have recently become appreciated as nosocomial pathogens. There is insufficient data to characterize trends in rates of viral nosocomial infections, but there have been major trends in methodologies and concepts. New groups of patients, such as infants and the elderly, are becoming appreciated as being at risk for serious nosocomial viral infections, whereas other groups, such as immunodeficient patients are expanding because of the epidemic of human immunodeficiency virus (HIV) infection and expanded use of immunosuppressive treatment. The continued addition of new viruses, such as HIV, human parvovirus B19, and rabies virus, to the list of potential nosocomial pathogens suggest that most human viruses can probably be serious nosocomial pathogens under the right circumstances. Advances in medical treatments and procedures, such as cadaveric dura mater grafts and laser treatment of warts, have provided new avenues for nosocomial transmission of viruses. Improved and wider availability of diagnostics promises to be a major force in improving our understanding and ability to prevent viral nosocomial infections. With these advances, viral diagnostic laboratories should become an important member of the infection control team. In parallel with trends in methodologies and concepts, there have been major advances in our understanding of ways to prevent some nosocomial viral infections. Application of these prevention measures is an important challenge to the infection control practitioner.
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PMID:Major trends in nosocomial viral infections. 192 51

Homosexual men are at high risk of anorectal human papillomavirus (HPV) infection, HPV-related anal cancer, and precancer, conditions known to increase with immunosuppression. The relationship between anal HPV infection, human immunodeficiency virus (HIV) infection, and immunosuppression was studied in homosexual men seen at a sexually transmitted disease clinic. History or presence of warts on rectal examination, and detection of anorectal HPV DNA were each significantly associated with HIV seropositivity after adjusting for age, previous sexual behavior, and cultural or serologic evidence of other sexually transmitted diseases, including those previously identified as risk factors for acquisition of HIV infection. Decreased mean levels of T4 lymphocytes were significantly associated with the detection of anal HPV DNA. Prospective studies are needed to determine incidences of anal HPV infection and cancer among HIV-seropositive and -seronegative mean and to determine the temporal relationship of these infections to one another.
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PMID:Anal human papillomavirus infection among human immunodeficiency virus-seropositive and -seronegative men. 197 95

Human papillomavirus-induced infections may be associated with cellular immunodeficiency. However, very little is known about the dysfunctional interactions among T lymphocytes, B lymphocytes, and antigen-presenting cells. A 30-year-old heterosexual man with a 10-year history of persistent multiple refractory flat wart lesions containing human papillomavirus type 3-related DNA sequence was studied. The patient had a severe depletion of CD4+ T lymphocytes and a compensatory increase in the number of CD8+ T lymphocytes. Impaired T-lymphocyte response to various stimuli was found. Depletion of the increased number of CD8+ T lymphocytes, which suppressed immunoglobulin production in vitro, did not restore the impaired T-lymphocyte response. Immobilized anti-CD3 beads that stimulate the T lymphocyte antigen complex in the absence of antigen-presenting cells indicated a T-lymphocyte defect, rather than a decreased antigen-presenting cell function. Thus, the pronounced cellular immunodeficiency was due to abnormal function of the CD4+ helper/inducer T lymphocytes.
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PMID:Abnormal function of CD4+ helper/inducer T lymphocytes in a patient with widespread human papillomavirus type 3-related infection. 197 81

As condylomata acuminata often persist in individuals infected with the human immunodeficiency virus (HIV), an immunohistological study of warts from infected men was undertaken to further knowledge about human papillomavirus persistence in this group. Using an indirect immunoperoxidase method and a panel of monoclonal antibodies, the phenotypes of cells were studied in cryostat sections of perianal or anal warts removed from 14 HIV-infected men (10 homosexual and 4 heterosexual) and from 16 non-infected men (10 homosexual and 6 heterosexual). Although the median numbers of CD1+, CD3+ and CD4+ cells per unit area were similar in each group of individuals, the number of CD8+ cells was significantly higher in HIV-infected homosexual men when compared with non-infected individuals and HIV-infected heterosexual men. The median CD4+ cell count in the peripheral blood was significantly higher in HIV-infected heterosexual men than in HIV-infected homosexual men (P less than 0.05). These findings may reflect differences in duration of HIV infection between the two groups. There was no significant difference in the proportion of cells expressing interleukin-2 receptors between HIV-infected and non-infected individuals. Natural killer (CD16+) cells were not identified in any of the condylomata.
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PMID:Immunological study of condylomata acuminata in men infected with the human immunodeficiency virus. 198 71

Oral candidiasis, herpetic lesions, oral mucosal warts, human immunodeficiency virus-associated gingivitis and periodontitis, Kaposi's sarcoma, hairy leukoplakia, and non-Hodgkin's lymphoma are oral manifestations of infection by the human immunodeficiency virus. This paper will explain how to identify these lesions, their significance, and recommended treatments.
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PMID:Oral manifestations of human immunodeficiency virus infection. 199 2

Numerous flat and tinea versicolor-like warts developed on the face, trunk, and upper extremities of a 10-year-old boy with human immunodeficiency virus infection. Nucleic acid analysis of involved skin revealed human papillomavirus type 5, which has sometimes been associated with epidermodysplasia verruciformis. This human papillomavirus type has also been described in patients with common variable immunodeficiency and dyskeratosis congenita and in renal allograft recipients. Human immunodeficiency virus infection should be added to the list of immune-related disorders that predispose to widespread flat warts.
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PMID:Widespread flat warts associated with human papillomavirus type 5: a cutaneous manifestation of human immunodeficiency virus infection. 217 38

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


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