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)

Inguinal lymph nodes from 24 human immunodeficiency virus (HIV) type 1-infected subjects without Kaposi sarcoma-associated herpesvirus (KSHV)-associated diseases were examined for KSHV infection. KSHV-infected cells were detected at a very low frequency in the lymph nodes of 7 subjects (median frequency, 2 infected cells/10(7) lymph node cells). Latent, but not lytic, KSHV gene expression was detected and KSHV-infected cells were located in B cell-rich areas of lymph node follicles. These findings provide evidence that, in the absence of KSHV-associated diseases, latent infection of lymph node cells provides a mechanism for the persistence of KSHV in KSHV/HIV-1-coinfected persons.
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PMID:Persistence of Kaposi sarcoma-associated herpesvirus (KSHV)-infected cells in KSHV/HIV-1-coinfected subjects without KSHV-associated diseases. 1563 95

Previously, we have characterized feline CD4+ CD25+ T-regulatory (Treg) cells with regard to their immune regulatory properties and ability to support feline immunodeficiency virus (FIV) replication in vitro and in vivo. Our studies showed that while CD4+ CD25+ cells were capable of replicating FIV in the presence of interleukin-2 (IL-2) alone, CD4+ CD25- cells harbored a latent infection that required a strong mitogenic stimulus to activate virus replication. In the present study, we investigated the mechanisms governing the preferential replication of FIV in highly purified CD4+ CD25+ Treg cells compared to their CD4+ CD25+ counterparts. Studies aimed at elucidating mechanisms regulating infection of these cells revealed that CD4+ CD25- cells were less susceptible to FIV binding and entry than CD4+ CD25+ cells, which correlated with increased surface expression of FIV coreceptor CXCR4. In addition, the number of CD4+ CD25+ cells that expressed the primary receptor CD134 was greater than for CD4+ CD25- cells. Although increased permissiveness to FIV infection of CD4+ CD25- cells following mitogenic stimulation correlated strongly with upregulation of surface CXCR4, it did not correlate with CD134 expression. Further, study of intracellular factors regulating FIV replication revealed that CD4+ CD25+ but not CD4+ CD25- T cells showed constitutive and IL-2-responsive transactivation of activating transcription factor, CAAT enhancer binding protein, and activating protein 1 transcription factors that are important for FIV replication. These factors were upregulated in CD4+ CD25- T cells following ConA stimulation, which correlated with FIV replication. This is the first report elucidating the mechanisms that allow for productive lentiviral infection of CD4+ CD25+ Treg cells.
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PMID:Preferential feline immunodeficiency virus (FIV) infection of CD4+ CD25+ T-regulatory cells correlates both with surface expression of CXCR4 and activation of FIV long terminal repeat binding cellular transcriptional factors. 1579 82

Human immunodeficiency virus (HIV) infection is the most powerful known risk factor for progression from latent infection with Mycobacterium tuberculosis to active tuberculosis (TB) disease. The worldwide HIV epidemic has affected TB in every aspect: immunopathology, epidemiology, diagnosis, treatment, and prevention. Of the 42 million people infected with HIV worldwide, more than a quarter of them are also infected with TB, and most live in countries with limited resources for health care in Africa and Asia. This chapter emphasizes HIV-associated TB in resource-limited settings. TB-infected persons with HIV-associated immunosuppression progress to TB disease at a rate of up to 10% per year. Standard TB diagnostic tools have diminished sensitivity in HIV co-infected cases. Standard TB treatment regimens may be less effective, particularly those that do not use a rifamycin throughout. Treatment is further complicated by toxicity, malabsorption, drug-drug interactions and immune reconstitution paradoxical reactions. TB control in the United States was destabilized in part by the HIV epidemic in the early 1990s; massive political will and resources were required to rebuild the public health infrastructure. Africa, Asia, and potentially the former Soviet Union are facing even greater destabilization of TB control due to the dual burden of disease and limited resources. An international response has been initiated but will require even greater political will and resources.
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PMID:Tuberculosis and HIV/AIDS: epidemiological and clinical aspects (world perspective). 1608 74

This article reports on key presentations at the 5th International Conference on Human Herpesvirus (HHV)-6 and -7, organized by the HHV-6 Foundation. New assays for HHV-6 and -7 promise to be more accurate and better able to distinguish between HHV-6A and B or differentiate active from latent infection. Nevertheless, more research is needed to enhance the sensitivity and specificity of these assays. Cellular receptors for both HHV-6 and -7 have been identified. Both viruses have in vitro tropism for neurons and dendritic cells of the central nervous system (CNS), and their role in producing CNS disease in the immunocompromised (particularly transplant recipients and the HIV-infected) is well established. HHV-6 may enhance the progression of simian immunodeficiency virus in monkeys, as suggested by in vivo data. In immunocompetent children and adults, HHV-6 and/or -7 may play a role in triggering and perpetuating several diseases of the nervous system, namely encephalitis, multiple sclerosis, chronic fatigue syndrome and epilepsy.
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PMID:Highlights from 5th International Conference on HHV-6 and -7. 1714 13

Human immunodeficiency virus type 1 can occasionally be detected as a cryptic or latent infection in seronegative, asymptomatic patients. To develop an animal model of host latency, cats were mucosally challenged with 10(2)-10(6) feline immunodeficiency virus (FIV)-infected T cells. Although high-dose exposure (10(4)-10(6) T cells) resulted in progressive infection, no evidence of infection was seen in 5 of 6 cats exposed to 10(2) or 10(3) T cells. However, after ex vivo CD8(+) T cell depletion and phorbol myristate acetate treatment, FIV could be reactivated in tissues from 4 cats. Thus, latent tissue viral reservoirs can be induced by low-dose cell-associated mucosal challenge, providing a model to dissect the mechanisms that control reservoir establishment.
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PMID:Mucosal administration of low-dose cell-associated feline immunodeficiency virus promotes viral latency. 1735 56

The varicella-zoster virus (VZV) Oka vaccine offers potential as a recombinant vaccine against other pathogens. In this study, recombinant simian varicella viruses (rSVV) expressing simian immunodeficiency virus (SIV) envelope (env, gp130) and gag antigens were constructed. Expression of the SIV env and gag transcripts and antigens in rSVV-infected Vero cells was confirmed. The rSVV-SIVenv and rSVV-SIVgag viruses replicated as efficiently as wild-type SVV in cell culture. The immunogenicity of rSVV-SIVenv and rSVV-SIVgag was investigated in immunized vervet monkeys. Humoral immune responses to the SIV gp130 and gag antigens were detected as early as 4 weeks after the initial immunization with higher antibody titers following a booster immunization. Cellular immune responses against the SIV gp130 antigen were detected by ELISPOT assay. The rSVV established latent infection in neural ganglia. A subsequent study will evaluate the ability of rSVV vaccines expressing SIV antigens to protect nonhuman primates against simian AIDS.
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PMID:Recombinant simian varicella viruses induce immune responses to simian immunodeficiency virus (SIV) antigens in immunized vervet monkeys. 1743 52

Quiescent T lymphocytes containing latent human immunodeficiency virus (HIV) provide a long-lived viral reservoir. This reservoir may be the source of active infection that is reinitiated following the cessation of antiretroviral therapy. Therefore, it is important to understand the mechanisms involved in latent infection to develop new strategies to eliminate the latent HIV reservoir. We have previously demonstrated that latently infected quiescent lymphocytes can be generated during thymopoiesis in vivo in the SCID-hu mouse system. However, there is still a pressing need for an in vitro model of HIV latency in primary human cells. Here, we present a novel in vitro model that recapitulates key aspects of dormant HIV infection. Using an enhanced green fluorescent protein-luciferase fusion protein-containing reporter virus, we have generated a stable infection in primary human CD4(+) CD8(+) thymocytes in the absence of viral gene expression. T-cell activation induces a >200-fold induction of reporter activity. The induced reporter activity originates from a fully reverse-transcribed and integrated genome. We further demonstrate that this model can be useful to study long terminal repeat regulation, as previously characterized NF-kappaB response element mutations decrease the activation of viral gene expression. This model can therefore be used to study intricate molecular aspects of activation-inducible HIV infection in primary cells.
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PMID:Primary cell model for activation-inducible human immunodeficiency virus. 1747 39

The ability of human immunodeficiency virus type 1 (HIV-1) to persist in a latent stage in memory T cells in the presence of antiretroviral therapy poses a major obstacle to the development of an HIV-1 therapy with curative intent. As latently infected cells are phenotypically not distinguishable from uninfected cells, therapeutic reactivation of the latent infection, followed by the death of the host cell induced by viral cytopathicity, is considered the only means to eliminate this viral reservoir. To identify compounds with the potential to reactivate latent HIV-1, we have developed a series of latently HIV-1-infected reporter cell lines that allow for high throughput drug screening (HTS) in a 384-well plate-based format. The latent reporter cell lines use enhanced green fluorescence protein (eGFP) as a direct and quantitative marker of HIV-1 expression. To aid identification of specific compounds, the cells are engineered to constitutively express a second, red fluorescent protein that has no spectral overlap with eGFP, which allows for the simultaneous quantification of cell viability (inversely correlated to compound toxicity). Thus, these reporters enable prioritization of compounds most likely to have a favorable therapeutic window. The high dynamic signal range and the excellent reproducibility of the primary screening assay result in a Z' -factor of 0.89, which characterizes the HTS system as very robust. The assay has been implemented for automated drug screening, and we here discuss the advantages and limitations of the HTS system based on the data obtained for 1,600 compounds during a limited proof-of-concept drug screen.
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PMID:High throughput drug screening for human immunodeficiency virus type 1 reactivating compounds. 1747 27

Bovine leukemia virus (BLV) induces a persistent but latent infection in cattle. Viral latency is invoked by a protein known as plasma blocking factor (PBF) that is found in both bovine and human plasma. We report here on pathways that mediate latency in the presence of PBF. Reporter-gene constructs driven by the promoters of 6 retroviruses were used to measure the production of chloramphenicol acetyl transferase (CAT) in cell lines cultured with or without defibrinated bovine plasma. Plasma inhibited CAT production only in constructs containing an NFkappaB-binding element proximal to the initiation site (BLV, human immunodeficiency virus, and human T-cell leukemia virus). The promoters of Bovine immunodeficiency virus, Feline immunodeficiency virus, or Feline leukemia virus were not inhibited in the presence of bovine plasma. Using gel mobility shift assays, we demonstrated that activation of viral transcription upon stimulation with phorbol esters and ionomycin was mediated through the NFkappaB element and that this was abrogated in the presence of plasma. Furthermore, analysis of individual NFkappaB proteins in nuclear extracts of mononuclear cells or Jurkat cells showed that all 5 members of the NFkappaB family were upregulated in response to stimulation, but only p52 was significantly downregulated in the presence of bovine plasma. Thus, we infer that plasma effects are mediated through interference with either p52 translocation to the nucleus or p52 synthesis.
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PMID:Defibrinated bovine plasma inhibits retroviral transcription by blocking p52 activation of the NFkappaB element in the long terminal repeat. 1747 75

Rheumatoid arthritis (RA) is associated with an increased risk of developing lymphoma. Although the pathogenesis is still unclear, the increased risk appears to be related to the high inflammatory activity of RA, immunosuppressive agents, or Epstein-Barr virus (EBV) infection. We investigated the relationship between EBV latent infection and methotrexate (MTX)-associated lymphoma in RA patients. Nine patients were diagnosed with non-Hodgkin's lymphoma (NHL) during MTX treatment for RA in a multicenter study. The pathologic findings were consistent with diffuse large B-cell lymphoma in 8 patients and peripheral T-cell lymphoma, unspecified in 1. EBV infection was detected in 3 patients by in situ hybridization. Among all 9 patients who were initially treated by MTX withdrawal alone, 2 obtained spontaneous complete response (CR), 1 had partial response, 2 had stable disease (SD), and 4 had progressive disease. Both patients who had a CR and 1 who had SD were positive for EBV. Further examination of the latent EBV infection patterns revealed that 2 patients who obtained a CR had latency Type III, and the other with SD had latency Type II. These results demonstrate that immunodeficiency caused by MTX treatment is associated with the development of EBV-related NHL in RA patients. In patients who were treated by MTX for RA and developed NHL, remission can be observed following MTX withdrawal especially in NHL with latency Type III EBV infection. The analysis of EBV infection, including the latency types, is useful to decide the optimum therapeutic strategy.
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PMID:Remission of lymphoma after withdrawal of methotrexate in rheumatoid arthritis: relationship with type of latent Epstein-Barr virus infection. 1765 84


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