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: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The C-type particles observed by electron microscopy in PK-15 cells were demonstrated to have biochemical and biophysical properties associated with the oncornavirus group: density of 1:16 in a sucrose gradient, 70S RNA, and the RNA-dependent DNA polymerase. The group-specific interspecies antigen, gs-3, was not present. Evidence of a latent infection with a porcine parvovirus was also obtained.
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PMID:Antigenic and biochemical characterization of the C-type particle of the stable porcine kidney cell line PK-15. 412 28

We have examined for synergy between the IIIB strain of HIV-1 and Epstein-Barr virus (EBV) during infection of a homogeneous cell type. In order to obtain a cell population consisting of a homogeneous cell type, CD19-positive B lymphocytes were purified from human tonsils by flow cytometry. CD19-positive lymphocytes did not express detectable surface CD4 antigen. However, CD4 mRNA could be detected in CD19-positive lymphocytes by reverse transcription coupled to polymerase chain reaction and by dot blot hybridization using an antisense riboprobe. Transcription of CD4 mRNA in CD19-positive lymphocytes was suppressed by infection with the B95-8 strain of EBV and lost in B95-8-transformed lymphoblastoid cell lines. In contrast, the P3HR-1K strain of EBV had no effect on the level of CD4 mRNA. HIV-1 could infect CD19-sorted B cells as measured by accumulation of reverse transcriptase and syncytia induction after coculture with SupT1 cells. HIV-1 infection of CD19-bearing lymphocytes was blocked by OKT4a antibodies. The ability of HIV-1 to replicate in CD19-positive B lymphocytes declined following preinfection with B95-8 but not with P3HR-1K. These results as well as results with an EBNA-2 expression vector suggest that down-regulation of both CD4 mRNA and HIV-1 infection in human B cells is a function of EBV nuclear antigen EBNA-2. The fact that native CD19-positive B lymphocytes express sufficient CD4 receptor mRNA to allow HIV-1 infection strengthens the possibility that HIV-1 replication in B cells directly participates in AIDS pathogenesis. In addition, infection with EBV may modulate the ability of HIV-1 to infect and establish a latent infection in B lymphocytes in co-infected individuals.
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PMID:CD4 mRNA expression in CD19-positive B cells and its suppression by the Epstein-Barr virus. 750 84

Various cobalamins act as important enzyme cofactors and modulate cellular function. We investigated cobalamins for their abilities to modify productive human immunodeficiency virus-1 (HIV-1) infection of hematopoietic cells in vitro. We show that hydroxocobalamin (OH-Cbl), methylcobalamin (Me-Cbl), and adenosylcobalamin Ado-Cbl (Ado-Cbl) inhibit HIV-1 infection of normal human blood monocytes and lymphocytes. The inhibitory effects were noted when analyzing the monocytotropic strains HIV-1-BaL and HIV-1-ADA as well as the lymphocytotropic strain HIV-1-LAI. Cobalamins did not modify binding of gp120 to CD4 or block early steps in viral life cycle, inhibit reverse transcriptase, inhibit induction of HIV-1 expression from cells with established or latent infection, or modify monocyte interferon-alpha production. Because of the ability to achieve high blood and tissue levels of cobalamins in vivo and the general lack of toxicity, cobalamins should be considered as potentially useful agents for the treatment of HIV-1 infection.
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PMID:Inhibition of productive human immunodeficiency virus-1 infection by cobalamins. 763 33

Acute HIV-1 infection of H9 and C8166 cultures has been shown to be suppressed by certain flavonoids, and evidence for inhibition of HIV-1 protease, integrase, and reverse transcriptase by flavonoids also exists. The present aim was to determine whether flavonoids inhibit HIV-1 activation in models of latent infection. By screening flavonoids from six different classes, three structurally related compounds (chrysin, acacetin, and apigenin) were identified that inhibited HIV expression in TNF-alpha-treated OM-10.1 cultures. The three compounds had favorable potencies against HIV activation in relation to their growth inhibitory effects (therapeutic index 5-10). Chrysin also inhibited HIV expression in response to PMA in OM-10.1 cells, in ACH-2 cells stimulated with either TNF-alpha or PMA, and in 8E5 cultures. Furthermore, return to viral latency in OM-10.1 cells previously exposed to TNF-alpha occurred over a shorter time interval when chrysin was added. The inhibition of HIV activation was not dependent on preincubation with flavonoids relative to TNF, and was characterized by a lack of HIV RNA accumulation by Northern analysis. Gel-shift experiments revealed that NF-kappa B activation after TNF-alpha treatment was not inhibited by these agents, suggesting that some other critical factor(s) needed for viral transcription was being affected. These findings indicate that flavonoids inhibit HIV-1 activation via a novel mechanism, and that these agents are potential candidates for therapeutic strategies aimed at maintaining a cellular state of HIV-1 latency.
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PMID:Inhibition of HIV activation in latently infected cells by flavonoid compounds. 882 17

Human immunodeficiency virus infection of a human bone derived cell line was initiated by either cell free virus or with a cell to cell transmission method. The human bone derived cells were examined for 8 weeks, and virus infection was not detected when assessed by microscopy, immunofluorescence, reverse transcriptase activity, or infection of cocultivated human T lymphoid cells susceptible to human immunodeficiency virus. Polymerase chain reaction analysis of human bone derived cells inoculated with the cell to cell infection format showed less than 0.1% infected cells. It is possible that the infected cells detected by polymerase chain reaction were lymphocytes used in the cell to cell infection format. Alternatively, latent infection may have been established in the bone derived cells with no apparent expression of the proviral genome. A large proportion of bone is represented by human bone derived cells, and it is unlikely that bone will contribute to a significant human immunodeficiency virus reservoir in vivo. The blood of bone allograft donors is likely to have a greater virus bioburden than is bone. Methods to sterilize bone should be assessed by their efficacy to inactivate the virus in blood contaminating the graft, and methods to detect human immunodeficiency virus deoxyribonucleic acid in a bone graft may be less sensitive than examining the donor's blood.
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PMID:Human immunodeficiency virus infection of human bone derived cells. 889 52

These guidelines update previous CDC recommendations for the diagnosis, treatment, and prevention of tuberculosis (TB) among adults and children coinfected with human immunodeficiency virus (HIV) in the United States. The most notable changes in these guidelines reflect both the findings of clinical trials that evaluated new drug regimens for treating and preventing TB among HIV-infected persons and recent advances in the use of antiretroviral therapy. In September 1997, when CDC convened a meeting of expert consultants to discuss current information about HIV-related TB, special emphasis was given to issues related to coadministration of TB therapy and antiretroviral therapy and how to translate this information into management guidelines. Thus, these guidelines are based on the following scientific principles: * Early diagnosis and effective treatment of TB among HIV-infected patients are critical for curing TB, minimizing the negative effects of TB on the course of HIV, and interrupting the transmission of Mycobacterium tuberculosis to other persons in the community. * All HIV-infected persons at risk for infection with M. tubercu losis must be carefully evaluated and, if indicated, administered therapy to prevent the progression of latent infection to active TB disease and avoid the complications associated with HIV-related TB. * All HIV-infected patients undergoing treatment for TB should be evaluated for antiretroviral therapy, because most patients with HIV-related TB are candidates for concurrent administration of antituberculosis and antiretroviral drug therapies. However, the use of rifampin with protease inhibitors or nonnucleoside reverse transcriptase inhibitors is contraindicated. Ideally, the management of TB among HIV-infected patients taking antiretroviral drugs requires a) directly observed therapy, b) availability of experienced and coordinated TB/HIV care givers, and in most situations, c) use of a TB treatment regimen that includes rifabutin instead of rifampin. Because alternatives to the use of rifampin for antituberculosis treatment are now available, the previously recommended practice of stopping protease inhibitor therapy to allow the use of rifampin for TB treatment is no longer recommended for patients with HIV-related TB. The use of rifabutin-containing antituberculosis regimens should always include an assessment of the patient's response to treatment to decide the appropriate duration of therapy (i.e., 6 months or 9 months). Physicians and patients also should be aware that paradoxical reactions might occur during the course of TB treatment when antiretroviral therapy restores immune function. Adding to CDC's current recommendations for administering isoniazid preventive therapy to HIV-infected persons with positive tuberculin skin tests and to HIV-infected persons who were exposed to patients with infectious TB, this report also describes in detail the use of new shortcourse (i.e., 2 months) multidrug regimens (e.g., a rifamycin, such as rifampin or rifabutin, combined with pyrazinamide) to prevent TB in persons with HIV infection. A continuing education component for U.S. physicians and nurses is included.
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PMID:Prevention and treatment of tuberculosis among patients infected with human immunodeficiency virus: principles of therapy and revised recommendations. Centers for Disease Control and Prevention. 980 43

Although the pathogenic effects of a primary cytomegalovirus (CMV) infection on hematopoiesis has been largely investigated so far, the effects of a persistent or latent infection have yet to be elucidated. The effects of persistent CMV infection on hematopoiesis thus were examined using BALB/c mice at 4 weeks postinfection with 0. 2 LD50 of murine CMV (MCMV) infection as a persistent infection model. The parameters of constitutive hematopoiesis of MCMV persistently infected mice were completely identical to those of the control. However, the inductive hematopoiesis, examined by the autologous marrow reconstitution after 5-fluorouracil administration, was significantly impaired in the MCMV persistently infected mice (P < 0.05). In a colony-forming unit-spleen assay and a long-term bone marrow culture system, a decreased capacity of bone marrow stromal cells to support hematopoiesis was observed in the MCMV-infected mice in comparison with the controls. The existence of MCMV DNA in the adherent cells of long-term bone marrow culture from the MCMV-infected mice were confirmed by a polymerase chain reaction but not in the nonadherent cells. Furthermore, the increased expression level of tumor necrosis factor-alpha by stromal cells was also observed by semiquantitative reverse transcriptase-polymerase chain reaction. These results therefore strongly suggest that MCMV remains to infect the stromal cells while also inhibiting inductive hematopoiesis through the impairment of the stromal cell functions in the MCMV persistently infected mice.
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PMID:In vivo disturbance of hematopoiesis in mice persistently infected with murine cytomegalovirus: impairment of stromal cell function. 991 73

The program(s) of gene expression operating during murine gammaherpesvirus 68 (gammaHV68) latency is undefined, as is the relationship between gammaHV68 latency and latency of primate gammaherpesviruses. We used a nested reverse transcriptase PCR strategy (sensitive to approximately one copy of gammaHV68 genome for each genomic region tested) to screen for the presence of viral transcripts in latently infected mice. Based on the positions of known latency-associated genes in other gammaherpesviruses, we screened for the presence of transcripts corresponding to 11 open reading frames (ORFs) in the gammaHV68 genome in RNA from spleens and peritoneal cells of latently infected B-cell-deficient (MuMT) mice which have been shown contain high levels of reactivable latent gammaHV68 (K. E. Weck, M. L. Barkon, L. I. Yoo, S. H. Speck, and H. W. Virgin, J. Virol. 70:6775-6780, 1996). To control for the possible presence of viral lytic activity, we determined that RNA from latently infected peritoneal and spleen cells contained few or no detectable transcripts corresponding to seven ORFs known to encode viral gene products associated with lytic replication. However, we did detect low-level expression of transcripts arising from the region of gene 50 (encoding the putative homolog of the Epstein-Barr virus BRLF1 transactivator) in peritoneal but not spleen cells. Latently infected peritoneal cells consistently scored for expression of RNA derived from 4 of the 11 candidate latency-associated ORFs examined, including the regions of ORF M2, ORF M11 (encoding v-bcl-2), gene 73 (a homolog of the Kaposi's sarcoma-associated herpesvirus [human herpesvirus 8] gene encoding latency-associated nuclear antigen), and gene 74 (encoding a G-protein coupled receptor homolog, v-GCR). Latently infected spleen cells consistently scored positive for RNA derived from 3 of the 11 candidate latency-associated ORFs examined, including ORF M2, ORF M3, and ORF M9. To further characterize transcription of these candidate latency-associated ORFs, we examined their transcription in lytically infected fibroblasts by Northern analysis. We detected abundant transcription from regions of the genome containing ORF M3 and ORF M9, as well as the known lytic-cycle genes. However, transcription of ORF M2, ORF M11, gene 73, and gene 74 was barely detectable in lytically infected fibroblasts, consistent with a role of these viral genes during latent infection. We conclude that (i) we have identified several candidate latency genes of murine gammaHV68, (ii) expression of genes during latency may be different in different organs, consistent with multiple latency programs and/or multiple cellular sites of latency, and (iii) regions of the viral genome (v-bcl-2 gene, v-GCR gene, and gene 73) are transcribed during latency with both gammaHV68 and primate gammaherpesviruses. The implications of these findings for replacing previous operational definitions of gammaHV68 latency with a molecular definition are discussed.
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PMID:Three distinct regions of the murine gammaherpesvirus 68 genome are transcriptionally active in latently infected mice. 997 15

The immunobiology of human immunodeficiency virus (HIV) and the role of laboratory testing in the diagnosis and management of HIV infection are reviewed. HIV is one of a family of RNA viruses called retroviruses. HIV has three structural genes (one of which codes for reverse transcriptase) and six regulatory and maturation genes. Upon infection in humans, HIV commandeers the immune system by infecting and lysing T-helper lymphocytes. Since these cells are key to directing the body's immune defenses, the person becomes susceptible to a variety of opportunistic infections, neoplasias, and neurologic disorders. Laboratory tests for HIV are used for three purposes: screening of large populations (such blood donors), diagnosis of current or latent infection, and monitoring of disease progression. Diagnosis of HIV infection relies on HIV antibody detection, viral cultures, antigen detection, or polymerase chain reaction viral genome detection. Disease progression can be estimated using immunophenotyping with flow cytometry or using other immunologic markers. The immunologic variables associated with HIV infection disclose a growing spectrum of immune deficits. New tests for diagnosing and monitoring patients infected with HIV have been quickly incorporated into clinical practice.
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PMID:HIV infection: immunobiology and laboratory diagnosis. 1017 56

The clinical evidence of a relationship between severe hypersensitivity to mosquito bite (HMB) and clonal expansion of EBV-infected NK cells has been accumulated. In order to clarify the mechanism of EBV-induced NK cell proliferation and its relationship with high incidence of leukaemias or lymphomas in HMB patients, we studied clonally expanded NK cells from three HMB patients and succeeded in establishing an EBV-infected NK-like cell line designated KAI3. Immunoblotting and reverse transcriptase-polymerase chain reaction (RT-PCR) analyses revealed that KAI3 cells as well as infected NK cells exhibited an EBV latent infection type II, where EBV gene expression was limited to EBNA 1 and LMP1. As KAI3 was established by culture with IL-2, IL-2 responsiveness of peripheral blood NK cells from patients was examined. The results represented markedly augmented IL-2-induced IL-2R alpha expression in NK cells. This characteristic property may contribute to the persistent expansion of infected NK cells. However, KAI3 cells as well as the NK cells from patients were not protected from apoptosis induced by either an anti-Fas antibody or NK-sensitive K562 cells. Preserved sensitivity to apoptosis might explain the relatively regulated NK cell numbers in the peripheral blood of the patients. To our knowledge, KAI3 is the first reported NK-like cell line established from patients of severe chronic active EBV infection (SCAEBV) before the onset of leukaemias or lymphomas. KAI3 cells will contribute to the study of EBV persistency in the NK cell environment and its relationship with high incidence of leukaemias or lymphomas in HMB patients.
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PMID:Characterization of Epstein-Barr virus (EBV)-infected natural killer (NK) cell proliferation in patients with severe mosquito allergy; establishment of an IL-2-dependent NK-like cell line. 1019 7


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