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

Human immunodeficiency virus type 1 (HIV-1) is the causative agent of the acquired immunodeficiency syndrome (AIDS). Currently, no satisfactory treatment for this viral disease is available. Somatic gene therapy has been proposed as an alternative to conventional therapies. Several antiviral gene therapy approaches including ribozymes, antisense inhibition, and RNA-decoy strategies, as well as dominant-negative mutants of HIV-1 proteins (Gag, Tat, and Rev) have been suggested. To prove the concept of trans-dominant inhibition of HIV-1 replication, we transduced CEM cells with a retroviral vector encoding a dominant-negative rev gene. Amplification of integrase-specific proviral sequences from high molecular weight DNA indicated successful HIV-1 human T-lymphotropic virus type IIIB (HTLV-IIIB) infection of all cells. In contrast to CEM cells and CEM cells expressing the rev wild-type (wt) gene, infection of two CEM-RevM10 clones with HIV-1 did not result in the release of significant levels of p24 Gag antigen as measured by antigen capture assay, indicating a block in HIV-1 replication due to the presence of the trans-dominant Rev protein. Furthermore, the parental CEM cells as well as CEM cells expressing the Rev wt protein were effectively killed in the course of the HIV-1 infection, whereas all CEM cells expressing the RevM10 protein were unaffected in their growth rate.
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PMID:Inhibition of human immunodeficiency virus type 1 replication in human T cells by retroviral-mediated gene transfer of a dominant-negative Rev trans-activator. 140 15

This multicenter retrospective study concerns 594 cases of HIV-1 positive patients. The majority were asymptomatic. Some had Aids-related complex and some had AIDS. They were all seen in seven hospitals of the western outskirts of Paris and in one Paris hospital between 1983 and 1988. There was a predominance of homosexuals and of cases of AIDS in the center of Paris. Intravenous (IV) drug users and asymptomatic cases were more numerous in the city outskirts, a reflection of the populations at risk around each hospital. The proportion of cases of AIDS was lower among IV drug users than among homosexuals or bisexuals probably due to the fact that the viral infection was discovered at an earlier stage in a population contaminated at a later date or to the tendency to ask for the test "systematically" in drug addicts. 22% of the cases were women with a sex ratio of 3.5. HIV infection was attributed to use of intravenous drugs in 51% and to heterosexual transmission in 18% of the women. But the incidence of heterosexual transmission increased significantly, essentially in women. Overall, the incidence of infection by the HIV 1 has decreased since 1986. A number of recent publications seem to indicate the same tendency. But this fundamental observation remains to be validated by further studies. The yearly incidence of AIDS increases. The 5 year calculated actuarial rate of probability of remaining asymptomatic decreased to 40% in 385 initially asymptomatic patients.
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PMID:[Retrospective study of 594 HIV-1 seropositive patients seen in 8 hospitals of western Paris]. 141 Aug 97

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

The diagnostic value of original immunoblot system depends on the availability of enveloped protein GP120 because it is the antibodies to this polypeptide that frequently indicate the running virus infection. This polypeptide is lost during purification of viral material but remains free in culture medium. The extraction of GP120 from culture fluid with immunosorbent based on sepharose 4B with ligated immunoglobulins from HIV-1-infected persons enriched the preparation for immunoblot with proteins increasing its diagnostic value.
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PMID:[The enhancement of the diagnostic reliability of immunoblot for HIV-1 antibodies by enriching the preparation for immunoblot with the HIV-1 gp120 protein]. 144 33

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

Conflicting data have been reported on ability of 3'-azido-3'-deoxythymidine (AZT) to protect mononuclear phagocytes from HIV-1 infection. We compared the antiviral potency of AZT in three types of primary human mononuclear phagocytes: peripheral blood monocytes, monocyte-derived macrophages (in vitro differentiated) and alveolar macrophages (in vivo differentiated). To establish highly-productive virus infection, purified cells (greater than 99%) from healthy donors were challenged with the macrophage-tropic HTLV-IIIBa-L strain at input multiplicities ranging from 0.05 to 20 TCID50 per cell. AZT (0.1 nM-10 microM) was added immediately after infection and either continued for the duration of the experiment or stopped 1-7 days after infection. The kinetics of HIV-1Ba-L replication were assessed by measuring p24 antigen production on days 4-28 post-infection. Continuous treatment with AZT reproducibly inhibited viral replication in a concentration-dependent manner in all three cell types. The IC90 of AZT was 0.04 microM in blood monocytes, 0.009 microM in monocyte-derived macrophages, and 0.0001 microM in alveolar macrophages (mean of 3-4 donors for each cell type). AZT was not cytotoxic at less than 10 microM as assessed by cell viability, cell protein, and interferon-gamma-activated H2O2-release. In experiments in which AZT treatment was stopped after infection, viral replication resumed after a lag of 7-14 days and increased exponentially toward control levels. This occurred despite initial inhibition of virus production to below the limit of p24 detection (approximately 50 pg/ml). These results indicate that AZT is a potent inhibitor of HIV-1 replication in primary mononuclear phagocytes regardless of the stage of cell differentiation, and that AZT is most active in tissue (alveolar) macrophages. AZT does not irreversibly block infection of mononuclear phagocytes, however, as viral replication resumes after removal of AZT.
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PMID:Anti-HIV-1 activity of 3'-azido-3'-deoxythymidine (AZT) in primary mononuclear phagocytes. 144 21

This review surveys the available published data on the impact of the type of factor VIII concentrate infused on T-helper lymphocyte count and factor VIII inhibitor induction in haemophiliacs. While concern has been expressed that certain products may have adverse effects on these parameters, only one trial published to date shows a significant benefit of a high purity product in reducing the rate of CD4 lymphocyte decline in HIV seropositive haemophiliacs. A number of other studies show no such significant benefit although the design of many of these might be criticized and few of them consider the potential impact of viral infection other than HIV, such as hepatitis C. More recent data on the incidence and prevalence of inhibitors in the haemophiliac population suggest that the reported high frequency of inhibitor formation for some products may lie within the expected normal range. This raises interest in why some products appear not to induce inhibitor formation, even in the group of patients at greater risk: multitransfused, severely deficient patients. The occasional reports of late onset high titre inhibitors in multitransfused haemophilia patients associated with the introduction of newer products are a matter of concern.
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PMID:The effects of type of factor VIII concentrate used in haemophilia on T-helper cell number and inhibitor incidence. 145 Mar 25

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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