Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Forty-six patients with chronic hepatitis delta virus infection were followed between 6 and 116 mo (mean = 32.8 mo; median = 24 mo). Nineteen patients (41%) demonstrated clinical courses with episodes of biochemical reactivation (ALT levels greater than or equal to 10 times baseline values [group A]). Twenty-seven patients (59%) had stable clinical courses without biochemical reactivation (group B). Patients in group A were younger than those in group B (30.5 vs. 35.3 yr; p = 0.03), were less likely to be intravenous drug abusers (16% vs. 52%; p = 0.01) and were more likely to be homosexual (58% vs. 22%; p = 0.01). Serum hepatitis B virus DNA, hepatitis delta virus RNA, IgM antibody to HBc, HBeAg, antibody to HBe and IgG and IgM antibody to hepatitis delta virus were measured in all patients. In group A, these markers were studied before and during reactivation and during remission. In group B, these parameters were studied in a random fashion at 7- to 10-mo intervals. The presence of antibodies to human immunodeficiency virus and hepatitis C virus was assessed in all patients. A total of 38 biochemical reactivation episodes was noted among the 19 patients in group A. Eleven had sequential changes in hepatitis delta virus markers, suggesting that the exacerbations were due to hepatitis delta virus. In three, the sequential changes of viral markers were consistent with the exacerbations due to hepatitis B virus. In five other patients, no sequential changes in viral markers could be demonstrated to correlate with the biochemical exacerbations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneous exacerbation of disease activity in patients with chronic delta hepatitis infection: the role of hepatitis B, C or D? 138 Apr 78

Reported data on the isolation of the human immunodeficiency virus type 1 (HIV-1) from tears are controversial. The purpose of the study was to try to isolate HIV-1 from tears in a large sample of HIV-1-positive patients at different stages of infection. 53 tear samples were obtained from 50 patients. Additionally isolation of HIV-1 from peripheral blood lymphocytes (PBL) was attempted. HIV-1 was isolated from none (= 0%) of the 53 tear samples. Isolation from PBL was successful depending on absolute CD4+ lymphocyte count and Walter Reed staging (Walter Reed stage 6: 83%; stage 2 to 5: 11%; p less than 0.0001). Treatment with zidovudine was not related to the frequency of HIV-1 isolation. These results suggest that tears of patients infected with HIV-1 contain low or no quantities of tissue-culture-infectious units of HIV-1. Nosocomial infection with HIV-1 from tears appears to be unlikely. The known precautions for the prevention of spread of viral disease in ophthalmological practice are sufficient and should be strictly followed.
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PMID:[Differences in detectability of human immunodeficiency virus type 1 in tears and blood lymphocytes]. 138 1

Interferon-gamma (IFN-gamma) has been shown to inhibit human immunodeficiency virus (HIV) replication in macrophages. However, the site of its effect on the HIV infectious cycle is unknown. We show here that IFN-gamma inhibits the transactivation of HIV long terminal repeat (LTR) during viral infection and that it antagonizes tat effect in HT4LacZ-1 cells. HT4LacZ-1 is an indicator CD4+ HeLa cell line for HIV infectivity, because it harbors a HIV LTR-LacZ gene susceptible to transactivation by tat. It was used in combination with a computer-assisted image analyzer to quantify: (i) the number of transactivated foci following HIV infection, (ii) their individual level of transactivation, and (iii) the fusion potency of infected cells. IFN-gamma induced a 75% decrease of the number of transactivated foci following infection of HT4LacZ-1 cells by HIV. The remaining 25% foci still susceptible to transactivation were transactivated at a lower level than in control cultures, and the fusion potency of infected cells was strongly decreased. IFN-gamma acted after HIV entry into the cell and independently of reverse transcription. IFN-gamma antagonized tat-induced LTR transactivation: it inhibited transactivation of HT4LacZ-1 cells when tat was provided either from a SV40-based expression vector of tat or by polyethylene glycol-induced cell fusion with HeLa-tat-III cells. These results suggest that IFN-gamma affects the expression or the activity of cellular factors interacting with tat and that the high level of IFN-gamma production associated with HIV infection plays a role in the establishment of HIV latency.
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PMID:Antagonistic effect of interferon-gamma on tat-induced transactivation of HIV long terminal repeat. 140 Mar 76

To examine the actual and potential spread of human immunodeficiency virus (HIV) from an acquired immunodeficiency syndrome (AIDS) epicenter to surrounding neighborhoods, we studied the prevalence of the viral infection and AIDS risk behaviors from 1988 to 1989 in a representative sample of unmarried whites, African Americans, and Hispanics living in San Francisco. We surveyed 1,770 single men and women aged 20 to 44 years (a 64% response rate) in a random household sample drawn from 3 neighborhoods of varying geographic and cultural proximity to the Castro District where the San Francisco epidemic began. Of 1,369 with blood tests, 69 (5%) had HIV antibodies; all but 5 of these reported either homosexual activity (32% HIV-positive; 95% confidence interval [CI] = 23%, 41%), injection drug use (5% HIV-positive; CI = 1%, 14%), or both (59% HIV-positive; CI 42%, 74%). Homosexual activity was more common among white men than among African-American or Hispanic men, but the proportion of those infected was similar in the 3 races. Both the prevalence of homosexually active men and the proportion infected were much lower in the 2 more outlying neighborhoods. Risk behaviors in the past year for acquiring HIV heterosexually--sex with an HIV-infected person or homosexually active man or injection drug user, unprotected sexual intercourse with more than 4 partners, and (as a proxy) having a sexually transmitted disease--were assessed in 1,573 neighborhood residents who were themselves neither homosexually active men nor injection drug users. The prevalence of reporting at least 1 of these risk behaviors was 12% overall, and race-gender estimates ranged from 5% among Hispanic women to 21% among white women. We conclude that in San Francisco, infection with HIV is rare among people who are neither homosexually active nor injection drug users, but the potential for the use spread of infection is substantial, as 12% of this group reported important risk behaviors for acquiring the virus heterosexually.
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PMID:Risk for AIDS in multiethnic neighborhoods in San Francisco, California. The population-based AMEN Study. 141 40

Many details of the pathogenesis of the human immunodeficiency virus type 1 remain to be elucidated. Details of how the virus gains entry via the mucosal surface upon sexual contact or during breast feeding remain obscure. The means by which the infection travels throughout the body as well as the nature of the major reservoirs of virus infection remains, for the most part, unknown. Recent studies raise the possibility that cells of the Langerhans/dendritic lineage play a central role in human immunodeficiency virus (HIV-1) infection and pathogenesis. It has been known for several years that veiled dendritic cells in the circulation as well as skin Langerhans are infected in people with prolonged HIV-1 infections. More recently it has been found that a large burden of viral DNA sequences is found, not only in the circulating T-cell population, but also in a population that is defined as a non-T, non-B, non-monocyte/macrophage population rich in T-helper dendritic cells. Detailed analysis of infection of primary blood-derived T-helper dendritic cells by HIV-1 shows that such cells are the most susceptible cells in the blood to infection by this virus. The cells also produce much more virus per cell than do purified populations of other blood mononuclear cells. Moreover, primary blood-derived T-helper dendritic cells are not killed by infection by HIV-1. These cells are susceptible to lymphotropic, monocyte tropic, and primary isolates of HIV-1. The sensitivity of primary blood-derived T-helper dendritic cells to infection by HIV-1 has been shown to be attributable to rapid uptake of virus particles as well as rapid synthesis of viral DNA. Subsequent steps of virus replication also occur more rapidly and more efficiently in populations of primary blood-derived T-helper dendritic cells than they do in purified preparations of blood-derived T cells and monocyte/macrophages. Studies with primates using the simian immunodeficiency virus (SIV) show that dendritic cells at the surface of sexual mucosa are rapidly infected upon exposure to high concentrations of the virus. SIV is also produced in abundance in Langerhans cells located at the surface of the sexual mucosa in animals infected for prolonged periods of time.
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PMID:Infection of accessory dendritic cells by human immunodeficiency virus type 1. 143 Dec 41

Simian immunodeficiency virus (SIV) was used as a model to study the protective efficacy of an immunization regimen currently being evaluated as candidate vaccines against HIV in human subjects. Four Macaca fascicularis were first immunized with recombinant vaccinia virus expressing the envelope glycoprotein gp160 of SIVmne and then boosted with subunit gp160. Both cell-mediated and humoral immune responses against SIV, including neutralizing antibodies, were elicited. The macaques were shown to be protected from a homologous virus infection as determined by serology, lymphocyte cocultivation, polymerase chain reactions and in vivo transmission analyses. Four unimmunized control animals were readily infected. However, viremia in infected control animals could decrease substantially following the initial phase of infection so that persistent infection might not be readily detectable.
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PMID:Evaluation of protective efficacy of recombinant subunit vaccines against simian immunodeficiency virus infection of macaques. 143 62

In trauma surgery, bone transplantation was needed in nearly 15% of all operations for reconstruction of defects. A high risk of viral infection remains in transplantation, however, cocultivation procedures have shown that human immunodeficiency virus (HIV-1) resides in bone of HIV-infected persons. Safety guidelines for running bone banks were not always easy to follow, and physical or chemical procedures applied for disinfection failed to inactivate HIV-1. In the present study we show that the polymerase chain reaction technique is an appropriate and sensitive means of detecting the HIV-1 genome in bone material prior to transplantation and-used in this way-can help to diminish the risk of HIV-1 transmission via bone transplantation.
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PMID:[HIV detection in the bone transplant with polymerase chain reaction]. 143 59

Trends in mortality related to infection by human immunodeficiency virus type 1 (HIV-1) and to other causes were examined from 1978 to 1988 in a cohort of 8,906 homosexual men who participated in studies of hepatitis B virus infection in the late 1970s in New York City. HIV-related mortality rates increased from 1 per 10,000 person-years in 1980 to 181 per 10,000 person-years in 1986, followed by a plateau from 1986 to 1988. The standardized mortality ratio among white men in the cohort was 3.7 (95% confidence interval (Cl) 3.4-3.9) as compared with white men from across the United States. Higher HIV-related mortality rates were associated with a higher number of sexual partners, a history of gonorrhea and/or syphilis, and serologic markers of infection with hepatitis B virus. After adjustment for demographics and sexual behaviors, the relative risk of mortality for Hispanic men as compared with white men was 1.5 (95% Cl 1.1-1.9). This study illustrates the large excess in mortality among homosexual men over the last decade, with the excess accounted for by deaths from HIV-related diseases. The recent plateau in mortality may be due to the effect of new treatments and/or the decline in new HIV-1 infections among homosexual men. The excess in HIV-related mortality among Hispanic homosexual men was not explained by differences in demographics and factors associated with the sexual transmission of HIV-1.
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PMID:Mortality trends in a cohort of homosexual men in New York City, 1978-1988. 144 31

As of March 31, 1992, individuals 13 to 19 years of age had been diagnosed with acquired immunodeficiency syndrome; over one third were diagnosed in the past 2 years alone. Because of the long incubation period from initial infection to acquired immunodeficiency syndrome diagnosis, the majority of young adults with acquired immunodeficiency syndrome were probably initially infected as adolescents. In 1991, 34% of adolescents with acquired immunodeficiency syndrome were female, and their predominant mode of transmission was heterosexual contact. Human immunodeficiency virus seroprevalence studies of adolescents show a male-to-female ratio approaching 1:1, with many human immunodeficiency virus-infected adolescent women identifying none of the standard risk. Factors such as sexual and drug experimentation, risk taking, and sense of invulnerability so characteristic of adolescence put adolescents at special risk for human immunodeficiency virus. There is no published information on if or how clinical manifestations of human immunodeficiency virus disease in adolescents might differ from those seen in adults. Medical care should be broad-based and should include access to clinical trials for new drug treatments. General knowledge levels about acquired immunodeficiency syndrome are high among US adolescents, but behavioral changes have lagged behind. All adolescents should be targeted for intensive education about human immunodeficiency virus along with interventions designed to enhance their general coping, communication, and decision-making skills.
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PMID:Adolescents and human immunodeficiency virus infection. 145 Mar 49

The study of the clinical manifestations, progression, and outcome of human immunodeficiency virus (HIV) infection in women has begun in earnest. AIDS-defining diseases that are more common in women than in men include wasting syndrome, esophageal candidiasis, and herpes simplex virus disease, whereas Kaposi's sarcoma is rare. Non-AIDS-defining gynecological conditions such as vaginal candida infections and cervical pathology are prevalent among women at all stages of HIV infection. Associations have been documented between the presence of human papillomavirus, lower genital tract neoplasia, and HIV-related immunosuppression. Pregnancy has not been confirmed to have an effect on the clinical progression of HIV disease in women incremental to the effect of time. Differential access and utilization of therapeutic interventions appear to account for much of the reported gender discrepancy in survival. Well designed epidemiological and clinical studies will help further scientific knowledge leading to early diagnosis, appropriate treatment, and timely prevention of the manifestations of HIV disease in women.
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PMID:HIV disease and AIDS in women: current knowledge and a research agenda. 145 25


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