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

Disseminated toxoplasmosis, one of the most severe acquired immune deficiency syndrome (AIDS)-associated infections in humans, is believed to develop from a latent infection after the cellular immune system is suppressed by human immunodeficiency virus type 1 (HIV-1). However, Toxoplasma gondii may serve as a cofactor in enhancing the immunodeficiency induced by HIV-1. This hypothesis is supported by the facts that: 1) co-infection with other pathogens in humans infected with HIV-1 may enhance the progression of the disease to AIDS; and 2) concomitant infection with T. gondii enhances feline immunodeficiency virus-induced immune dysfunction and is likely to cause a more rapid disease onset than an infection with HIV alone. It is possible that T. gondii infection induces tumor necrosis factor (TNF) production. TNF then stimulates the induction of T-cell proteins that bind to the long terminal repeat of HIV-1. This binding at the repeat site then leads to increased HIV-1 activation which causes the dysfunction of CD4 cells and a resulting immunodeficiency that allows even greater amounts of T. gondii replication.
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PMID:Toxoplasma gondii: an AIDS enhancing cofactor. 133 11

HIV infection is characterized by CD4+ lymphocyte depletion manifested through the loss of the immune response capacity. The resulting immunodeficit is expressed by the blocking of immune surveillance mechanisms and, thus, by the establishment of favourable conditions to the development of opportunistic infections and/or malignant processes. In tuberculosis, the immunodeficiency associated with HIV infection makes possible the evolution of a latent infection to a clinically manifest disease. Latent tuberculosis is characterized by the intracellular persistence of some metabolically inactive Tb bacillus forms which are incapable of multiplication. The conversion of these inactive into metabolically active forms capable of multiplication is usually neutralized by immunosurveillance mechanisms. The blocking of such mechanisms in case of CD4+ cell depletion will allow the multiplication of metabolically active Tb bacillus forms, and the development of a clinically manifest tuberculosis. CD4+ lymphocyte depletion is the result of facilitating antibodies and certain cytokines, and of some autoimmune processes which also affect the non-infected CD4+ cells. Therefore, it is necessary that Tb chemoprophylaxis in HIV infected subjects should also be addressed to the processes initiating the immune deficit, which include autoimmune mechanisms as well as those facilitating HIV infection.
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PMID:[AIDS and tuberculosis: the immunopathogenic processes]. 136 59

The effects of human immunodeficiency virus type 1 (HIV-1) and recombinant envelope glycoprotein gp120 on the in vitro growth of enriched human haematopoietic progenitors (CD34+ cells) have been investigated. A 2 h exposure to HIV-1 resulted in a progressive and significant reduction of viable CD34+ cell number in liquid cultures and of granulocyte-macrophage, erythroid and megakaryocytic progenitors in semisolid cultures. In virus-treated CD34+ cells, no signs of active virus replication were observed and the possibility of latent infection was excluded by quantitative polymerase chain reaction. Recombinant HIV-1 envelope glycoprotein gp120 added to CD34+ cell cultures displayed a dose-dependent inhibitory activity on CD34+ cell viability. Neutralizing antibody against gp120 was able to block completely the inhibitory activity on CD34+ cells of either HIV-1 or recombinant gp120. These results demonstrate that HIV-1 envelope glycoprotein gp120 has a direct cytotoxic effect on CD34+ cells.
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PMID:Human immunodeficiency virus type 1 envelope glycoprotein gp120-mediated killing of human haematopoietic progenitors (CD34+ cells). 137 43

In three subgroups of a clinically and socially well defined group of Dutch homosexual men, the prevalence of human immunodeficiency virus type 1 (HIV-1) sequences in seronegative blood samples was studied using the polymerase chain reaction (PCR). In 19 seronegative partners of seropositive persons, no HIV-1 sequences were found by PCR in either early (1984/1985) or more recent (1987) samples. In 42 seronegative persons selected by their high risk for HIV-1 infection, none harbored HIV-1 sequences in either early (1985/1986) or late (1989) samples. In 15 people who seroconverted for HIV-1, only 2 samples collected 3 months before seroconversion were PCR-positive. These persons were also HIV antigen-positive at this time. These data suggest that a latent infection greater than 6 months does not occur and that the combination of HIV antibody and HIV antigen tests is appropriate and conclusive in most cases of HIV-1 infection.
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PMID:Concordance of human immunodeficiency virus detection by polymerase chain reaction and by serologic assays in a Dutch cohort of seronegative homosexual men. 150 Jul 45

To detect latent infection with human immunodeficiency virus (HIV), specimens of peripheral blood leukocytes from HIV-seronegative hemophiliacs and from sexual partners of HIV-seropositive hemophiliacs were examined by polymerase chain reaction (PCR). The primer pair SK 38/39 derived from the gag region and/or the primer pair SK 68/69 corresponding to a conserved region of the env gene were used. Whereas HIV proviral DNA was detected by PCR in samples from 86 (97%) of 89 HIV-seropositive hemophiliacs, no HIV-DNA was found in blood samples of 198 HIV-seronegative hemophiliacs at risk. Of 40 HIV-seronegative sexual partners of HIV-infected hemophiliacs, none was PCR positive. Thus, PCR is proving to be a sensitive method by which to confirm infection in seropositive hemophiliacs, while the negative results in HIV-seronegative hemophiliacs and HIV-seronegative sexual partners of HIV-seropositive hemophiliacs suggest that a prolonged seronegative period of latent HIV infection is the exception.
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PMID:Absence of human immunodeficiency virus (HIV) proviral sequences in seronegative hemophilic men and sexual partners of HIV-seropositive hemophiliacs. 154 15

Infection of captive macaques with simian immunodeficiency virus (SIV) and domestic cats with feline immunodeficiency virus (FIV), both discovered in the last five years, represent excellent animal models for infection of humans with the human immunodeficiency virus (HIV). Protection against challenge infection and protection against development of simian and feline acquired immunodeficiency syndrome has been achieved in each model by use of inactivated whole virus or virus-cell vaccines. A recombinant SIV envelope peptide vaccine has also proved efficacious. These vaccines have protected against 10-100 animal infectious doses of the homologous cell-free virus given systemically, and, in the simian model, apparently show cross protection against a heterologous strain of SIV. Protected animals appear free of any latent infection although late breakthroughs of infection in a few animals imply that not all vaccinated animals are completely protected. The mechanism of protection in the simian model apparently involves envelope antibody but the role of neutralizing antibody remains unclear. Questions remaining to be answered in both SIV and FIV models are: (1) the duration of immunity, (2) the extent of protection against heterologous strains and mucosal infection, (3) protection against infection with cell-associated virus and (4) the role, if any, of cellular immunity in vaccine protection. Initial attempts at post-infection immunotherapy with SIV vaccines have not yet been successful. The inactivated whole SIV and FIV vaccines offer a promising start and provide hope that a prophylactic AIDS vaccine will be developed. Use of these animal models for antiviral therapy is just now getting underway. Both models should prove especially useful for studies of prophylaxis and therapy, especially during the early stages of infection and for investigations on drug pharmacokinetics or toxicity that can not be done as well in HIV-infected humans. The animals will also be ideal for testing the pathogenicity of drug-induced mutant forms of SIV and FIV. For these purposes it will be necessary to create self-sustaining specific pathogen-free macaque and cat breeding colonies and provide increased housing facilities for infected animals. The future of AIDS research is crucially dependent on the long term availability of these animal models.
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PMID:Simian and feline immunodeficiency viruses: animal lentivirus models for evaluation of AIDS vaccines and antiviral agents. 165 10

Cellular immunity is known to play a critical role in regulating Epstein-Barr virus (EBV) in the state of latent infection. Activity of EBV-specific cellular immunity decreases as the clinical stages of human immunodeficiency virus (HIV) infection progress, and many complications are induced by reactivated EBV in the late stages of HIV infection. However, in asymptomatic HIV carriers, some show the reduced activity of cellular immunity against EBV, while others still show normal range of the activity even in the presence of abnormality in other immunological parameters. In order to assess early immunological abnormality against EBV in these patients, asymptomatic HIV carriers with normal range of EBV-specific cellular immunity were studied in comparison with that in EBV seropositive healthy controls. 1. All of 4 asymptomatic HIV carriers showed normal range of EBV-specific cellular immunity as seen in healthy controls. 2. Asymptomatic HIV carriers had significantly elevated serum antibody titers to EBV-specific nuclear antigen (EBNA)2, viral capsid antigen(VCA), early antigen(EA), indicative of serological reactivation of EBV. 3. The number and percentage of peripheral CD4 positive lymphocytes, CD4/CD8 ratios were markedly decreased in asymptomatic HIV carriers. 4. In the presence of immunosuppressive agents, 4-deoxy phorbol ester(4-DPE), drastic decrease of EBV-specific cellular immunity was observed in asymptomatic HIV carriers at the concentration which did not affect that of healthy controls. 5. Reduced activity of EBV-specific cellular immunity induced by 4-DPE had no relation with surface marker expression on cytotoxic T cells which serve as cell-to-cell adhesion molecules. Based on these results, it is suggested that there is latent dysfunction of EBV-specific cellular immunity in asymptomatic HIV carriers, who seems to show normal range of immunity in usual assays.
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PMID:[The latent dysfunction of Epstein-Barr virus (EBV)-specific cellular immunity in asymptomatic human immunodeficiency virus (HIV) carriers]. 166 17

Hairy leukoplakia (HL) is an Epstein-Barr (EB) virus related lesion of oral mucosa that is principally associated with human immunodeficiency virus-induced immunosuppression. To understand the nature of EB virus involvement in these lesions, this study compares the distribution of EB virus DNA and EB viral gene products with the pattern of keratinocyte differentiation in 12 lateral tongue biopsies of HL. Evidence of replicating EB viral infection and abundant virus production was demonstrated in the superficial epithelium of most (92%) samples by means of in situ hybridization and immunocytochemical techniques. Epstein-Barr virus latent membrane protein also was identified in 45% of samples, suggesting that this viral gene product, which is usually associated with EB virus latent infection, may be transiently expressed during viral replication in HL epithelium. The absence of detectable EB virus involvement in basal keratinocytes, however, fails to support the theory that latent infection occurs in basal epithelium. From this study, EB viral gene expression in HL appears to be linked with epithelial maturation. Conversely, the normal patterns of keratinocyte differentiation in these lesions do not appear to be appreciably altered by association with EB virus.
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PMID:Epstein-Barr virus gene expression and epithelial cell differentiation in oral hairy leukoplakia. 166 Oct 74

The apparent detection of human immunodeficiency virus (HIV-1) DNA by the polymerase chain reaction (PCR) in seronegative individuals has been the subject of great concern. In this study, 324 seronegative participants in the San Francisco Men's Health Study were evaluated for evidence of infection using a PCR testing algorithm with multiple amplifications targeting different regions of the HIV-1 genome. While most PCR reactions were negative, 8.6% of the specimens showed weak reactivity with one or more primer sets. However, all were negative with at least one primer set and no definitively positive specimens were identified. This study addressed the possibility that some of these PCR reactions might represent latent infection or abortive exposure, leaving residual integrated DNA, rather than false-positive reactions. The frequency of such reactions was determined in homosexual men who have been at risk for HIV-1 infection and in exclusively heterosexual men who have little or no past exposure. The results demonstrate an identical frequency and distribution of equivocal PCR reactions in both populations. Assuming that there is minimal HIV-1 infection among seronegative heterosexual men in San Francisco, we conclude that PCR testing does not provide evidence for a reservoir of occult HIV-1 infection in seronegative homosexual men.
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PMID:An evaluation of the polymerase chain reaction in HIV-1 seronegative men. 185 94

The progression of the human immunodeficiency virus (HIV) infection from its early latent (asymptomatic) stage to active, late-stage acquired immunodeficiency syndrome (AIDS) apparently begins with the production of inflammatory cytokines that stimulate the expression and replication of the latent virus. We have shown that N-acetylcysteine, a cysteine precursor that is converted intracellularly into glutathione, blocks cytokine-stimulated HIV replication in an acutely infected T-cell line and in acutely infected peripheral blood mononuclear cells from normal individuals. In this report, we show that N-acetylcysteine also inhibits stimulated HIV expression in chronically infected monocyte and T-cell lines which are used as models for latent infection in AIDS. Furthermore, we show that N-acetylcysteine blocks viral production in monocyte cell lines more effectively than it blocks viral production in T cells. Since monocytes are a major reservoir for HIV in infected individuals, these results suggest that N-acetylcysteine may slow the change from latency to the later stages of AIDS in HIV-infected individuals.
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PMID:N-acetylcysteine inhibits latent HIV expression in chronically infected cells. 193 Dec 32


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