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)

A distinct subset of patients with peripheral T-cell lymphoma (PTCL) is described which reacts with Leu-19 (CD56), an antibody that has been shown to identify the neural cell adhesion molecule (NCAM). These NCAM-positive PTCL patients (11 of a series of 46 PTCL; 24%) exhibited a striking predilection for unusual anatomic sites of involvement: central nervous system (36%), muscle (18%), gastrointestinal tract, and nasopharynx (27% each). Additional extranodal sites of involvement included the pituitary, thyroid, parathyroids, adrenals, and pancreas. The NCAM-positive subset also exhibited a characteristic phenotypic profile, with significantly lower expression of CD3 and CD5 compared with the NCAM-negative group. RNA transcripts consistent with the NCAM gene were detected in tissue samples from five Leu-19-positive cases using a reverse transcriptase-polymerase chain reaction assay, supporting the idea that Leu-19 recognizes NCAM in these patient samples. This suggests that the expression of the NCAM plays a role in the behavior and localization of lymphomas. Because of the unique clinical and phenotypic characteristics of this group it may be designated as "NCAM-positive peripheral T-cell lymphoma."
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PMID:Neural cell adhesion molecule-positive peripheral T-cell lymphoma: a rare variant with a propensity for unusual sites of involvement. 138 3

The evidence that schizophrenia may involve infection by a virus (or viruses) has been indirect. The recent discovery, however, of the human retroviruses--human T-cell lymphoma-leukemia virus-I, and II (HTLV-I, -II) and human immunodeficiency virus (HIV)--now also known to affect the central nervous system (CNS), together with the development of new techniques in retrovirology, have made it possible to investigate more directly the role of this class of viruses as an etiology of schizophrenia. In our first effort to screen for the presence of a T-cell lymphotropic virus in schizophrenia, short-term tissue cultures of peripheral lymphocytes from 17 chronic schizophrenic patients and 10 normal controls were established. The cells were cultured in the presence of T-cell growth factor (TCGF, IL-2), and the culture supernatants were tested for the presence of the retroviral enzyme reverse transcriptase. No T-cell-associated reverse transcriptase activity was detected in cultures from patients or normal controls. Therefore, the data do not provide evidence for a role for T-cell lymphotropic retroviruses as an etiology of schizophrenia.
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PMID:Lack of evidence for a role of T-cell-associated retroviruses as an etiology of schizophrenia. 246 91

Moloney murine leukemia virus (M-MuLV) is a replication-competent retrovirus which induces T-cell lymphoma in mice. The enhancer sequences present within the M-MuLV long terminal repeat (LTR) region of the proviral genome have been shown to influence the disease specificity of the virus strongly. We examined the contribution of the M-MuLV enhancers to the transcriptional activity and pathogenesis of M-MuLV by constructing LTRs containing heterologous enhancer elements. The simian virus 40 enhancer region (72- and 21-base-pair repeats) was inserted into the U3 region (at -150 base pairs) of the M-MuLV LTR (Mo + SV) and also into a deleted form of the LTR which lacks the M-MuLV enhancer sequences (delta Mo + SV). These chimeric LTRs were used to generate infectious M-MuLVs by transfection of corresponding proviral plasmids into mouse fibroblasts. The relative infectivities of Mo + SV and delta Mo + SV recombinant viruses as determined by rat XC cell plaque assay and reverse transcriptase assay were 60 to 70% of wild-type M-MuLV levels. To study the pathogenicity of these two recombinant viruses, we inoculated newborn NIH Swiss mice with either Mo + SV or delta Mo + SV M-MuLV. Both viruses induced disease more slowly than M-MuLV, which induces disease 2 to 4 months postinoculation. Mo + SV M-MuLV-inoculated animals became moribund at 3 to 13 months postinoculation, whereas delta Mo + SV M-MuLV-inoculated animals became moribund at 6 to 24 months postinoculation. The tumors induced by the two viruses were characterized histologically and molecularly. Mo + SV M-MuLV-induced tumors were primarily T-cell-derived lymphoblastic lymphomas containing extensive rearrangements of the T-cell receptor beta gene. In contrast, delta Mo + SV M-MuLV induced pre-B- and B-cell lymphoblastic lymphomas, B-cell-derived follicular-center cell lymphomas, and acute myeloid leukemia. The delta Mo + SV tumor DNAs from B-lineage tumors were typically rearranged at the immunoglobulin gene loci and contained germ line configurations of the T-cell receptor beta gene. Southern blot hybridization confirmed that the tumor DNAs contained the predicted Mo + SV M-MuLV or delta Mo + SV M-MuLV provirus.
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PMID:Addition of substitution of simian virus 40 enhancer sequences into the Moloney murine leukemia virus (M-MuLV) long terminal repeat yields infectious M-MuLV with altered biological properties. 283 23

HTLV strain CR (HTLVCR) is a retrovirus which was isolated from a human T-cell lymphoma cell line. A protein of molecular weight 24,000 p24, was purified from this virus. Several results indicate that this p24 is an internal core protein of HTLVCR. (i) The p24 copurified with viral cores. (ii) It was labeled with 125I after disruption of the virus, but not when undisrupted virus was iodinated. (iii) The amount of p24 was directly proportional to the amount of HTLVCR. (iv) In chromatographic properties, the HTLVCR p24 behaved similarly to the major structural protein (24,000- to 30,000-molecular-weight protein) of other retroviruses. A rabbit antiserum raised against disrupted HTLVCR precipitated the labeled p24, and the precipitation was competed for by unlabeled HTLVCR and by cytoplasmic proteins from cells producing HTLVCR, but not by proteins from normal human cells, including normal growing human T-cells, and several cultured human cutaneous T-cell lymphoma lines. Proteins from several mammalian type B, type C, and type D viruses also failed to compete in this precipitation. Moreover, HTLVCR did not react in homologous and interspecies assays for p30 antigens of several mammalian type C and type D viruses. These observations agree with immunological comparisons between reverse transcriptase of HTLVCR and other retroviruses and nucleic acid sequence homology studies which indicate that the various HTLVCR isolates represent new retroviruses found in some human T-cell neoplasias.
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PMID:Immunological properties of a type C retrovirus isolated from cultured human T-lymphoma cells and comparison to other mammalian retroviruses. 626 63

Retroviruses received widespread attention in the past not only because they caused tumors in animals and, perhaps, in man, but also because they served as useful tools to elucidate molecular mechanisms involved in the control of eukaryotic gene expression. In this brief overview, evidences are presented that retrovirus-like particles can regularly be demonstrated in human teratocarcinomas cultured in vitro. These viruses are morphologically reminiscent of animal retrovirus strains but show also unique structural features. The viruses possess endogenous reverse transcriptase activity and can be banded at 1.16 g/ml in sucrose gradients, a density characteristic of retroviruses. They can clearly be distinguished from animal retrovirus strains on immunological grounds. We will also briefly summarize the data accumulating for the human T-cell lymphoma viruses (HTLV) which were recently discovered first by Gallo et al. and independently by Hinuma and Miyoshi. HTLV seem to play an etiological role in the establishment of human adult T-cell leukemia/lymphoma and thus represent the first pathogenic human retroviruses.
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PMID:Retroviruses in human tumors. 631 18

In order to better understand the genomic diversity and molecular phylogeny of the human retroviruses, the plasmas from 250 Zairean patients collected in 1969 were tested for antibodies to human T-cell lymphoma and human immunodeficiency viruses (HTLV or HIV) using ELISA and confirmatory Western blots and for viral nucleic acids by reverse transcriptase-directed PCR (RT-PCR). Interestingly, none of the patients was confirmed positive for HIV, even though this region is now endemic for HIV-1. However, 74 (30%) and 3 (1%) of the samples were positive for antibodies to HTLV-I and II, respectively. Forty-four of 74 (59%) Western blot-positive Zairean samples were RT-PCR positive for HTLV-I, while 1 of 3 (33%) of HTLV-II-seropositive samples was RT-PCR positive. On the contrary, none of the Western blot-negative or indeterminate samples were RT-PCR positive for either HTLV-I or HTLV-II. We have cloned and sequenced 140 bp of the pol gene flanked by SK110/SK111 from 8 HTLV-I- and 1 HTLV-II-positive archival samples from Zaire. The HTLV-I isolates from Zaire cluster together as a phylogenetic group, diverging from the prototype Japanese HTLV-I (ATK) by a range of 1.4 to 3.6%. Their close homology to some African STLV-I isolates suggests relatively recent interspecies transmission. The Zairean HTLV-II isolate is closely grouped with the HTLV-II substrain of isolates found in Paleo-Amerindians of the New World, making it unlikely that it represents an endemic African strain.
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PMID:Serological and nucleic acid analyses for HIV and HTLV infection on archival human plasma samples from Zaire. 791 21

CD44 is a cell surface glycoprotein involved in cell migration and cell docking in target organs via interactions with various ligands, including hyaluronic acid (HA), which is the principal ligand of this receptor. Alternative splicing generates many isoforms of CD44, including standard CD44 (CD44s) and CD44 variants (CD44v). LB T-cell lymphoma, which predominantly expresses CD44s, acquires additional CD44v and HA binding capacity after activation with phorbol ester. The HA9 cell line, isolated from parental LB cells, expresses CD44v and constitutively binds HA. Downregulation of CD44v isoforms of HA9 cells, by CD44v specific antisense inhibited their ability to bind HA, indicating that CD44v, rather than CD44s, is associated with the activation status of this molecule. Using the reverse transcriptase polymerase chain reaction, we found that LB cells after infiltrating spleen and lymph nodes of BALB/c mice, contain an enriched repertoire of CD44v, implying that the metastatic cells acquired the activated form of this receptor.
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PMID:The CD44 receptor of the mouse LB T-cell lymphoma: analysis of the isoform repertoire and ligand binding properties by reverse-transcriptase polymerase chain reaction and antisense oligonucleotides. 1075 21

Genes of the MAGE-A family are expressed in several types of solid tumors but are silent in normal tissues with the exception of male germline cells, which do not carry HLA molecules.Therefore, peptides encoded by MAGE-A genes are strictly tumor-specific antigens that can be recognized by CTL and constitute promising targets for immunotherapy. The expression of 6 genes of the MAGE-A family was tested with reverse transcriptase-polymerase chain reaction in lymphoma samples. Among 38 samples of non-Hodgkin lymphoma, 1 anaplastic large cell lymphoma expressed genes MAGE-A1, -A2, -A3, -A4, and -A12, and 1 lymphoepithelioid T-cell lymphoma expressed gene MAGE-A4. Five of 18 samples (28%) from patients with Hodgkin disease expressed gene MAGE-A4. In tissue sections, staining by a monoclonal antibody that recognizes the MAGE-A4 protein was observed in 11 of 53 samples (21%) from patients with Hodgkin disease. In the positive samples, the Reed-Sternberg cells were strongly stained whereas the surrounding cells were not. These results indicate that Hodgkin disease may be a target for specific immunotherapy involving MAGE-A4 antigens.
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PMID:Expression of gene MAGE-A4 in Reed-Sternberg cells. 1082 39

A definitive diagnosis of T-cell lymphoma may be contingent on the rearrangement profile of the T-cell receptor. This is most accurately done by molecular analysis of the beta-chain of the T-cell receptor (TCR beta) by Southern blotting hybridization that requires unfixed tissue. We describe a reverse transcriptase in situ PCR (RT in situ PCR) method that permits the target-specific direct incorporation of the reporter nucleotide into the different transcripts that comprise the TCR beta, using paraffin-embedded, formalin-fixed tissue. Each of the 25 possible V beta segment rearrangements was documented in three lymph nodes with nonspecific lymphadenitis, with clonal expansion evident in a case of metastatic melanoma. Monoclonal expression was documented in seven tissues diagnostic of a T-cell lymphoma. We analyzed five additional tissues for which a definitive diagnosis of T-cell vs B-cell lymphoma could not be rendered on the basis of histological, immunohistological, and flow cytometric analysis. RT in situ PCR for TCR beta expression with CD3 co-labeling demonstrated which of these lesions was a B-cell-rich T-cell lymphoma. We conclude that the RT in situ PCR methodology will allow the routine determination of monoclonal vs multiclonal expression patterns of the TCR beta using archival paraffin-embedded tissues.(J Histochem Cytochem 49:139-145, 2001)
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PMID:In situ determination of T-cell receptor beta expression patterns. 1115 82

We evaluated the anti-HIV-1 activity of the T-cell-specific protein inhibitor PEG-asparaginase (PEG-ASNase) in human HIV-1-infected T-cells. We further examined the drug synergism between PEG-ASNase and the protease inhibitor Saquinavir (SAQ), both alone and in combination with nucleoside analog reverse transcriptase inhibitors (NRTI). Our drug synergism studies served as a model for an HIV-induced T-cell lymphoma. Phytohemagglutinin [PHA(+)] stimulated T-cells were infected with HIV-1 and then treated with one or more drugs 90 minutes from the viral exposure. To measure inhibition of viral replication, we examined HIV-1 RT and HIV-1 RNA in the supernatant and intracellularly on day 7 post-infection and drug treatment. Last, we examined the effect of administering drugs immediately after HIV-1 infection of T-cells to simulate treatment after an accidental exposure to the virus. PEG-ASNase, even when used alone, has anti-HIV-1 activity in PHA(+)-stimulated T-cells due to inhibition of protein synthesis. When the drug was used with SAQ, the combination was synergistic in inhibiting HIV-1 RT and RNA in the supernatant and intracellularly by 2.5 log10 in comparison with controls. PEG-ASNase and SAQ were even more effective in inhibiting HIV-1 replication when combined with the NRTI inhibitors azidothymidine (AZT) and (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC, lamivudine). The addition of ribonucleotide reductase inhibitor, 2-methyl-1H-isoindole-1,3-dione (MISID), further potentiated the antiviral effect of the regimen. HIV-1 RT and RNA analyses showed that the administration of the PEG-ASNase + SAQ drug combination immediately following exposure to HIV-1 completely inhibited the infection of T-cells in our in vitro T-cell model. From these results we conclude that PEG-ASNase is a valuable T-cell-specific protein inhibitor against HIV-1 infection, when used singly or in combination with a protease inhibitor, an RT inhibitor and an RR inhibitor. Since PEG-ASNase is a drug of choice for the treatment of T-cell lymphomas, a combination regimen containing PEG-ASNase could be very effective in the treatment of HIV-1-induced T-cell lymphoma and possibly AIDS. Future studies are needed in HIV-infected and/or HIV-induced T-cell lymphoma patients to investigate these findings.
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PMID:Synergistic antiviral effect of PEG-asparaginase (ONCASPAR), with protease inhibitor alone and in combination with RT inhibitors against HIV-1 infected T-cells: a model of HIV-1-induced T-cell lymphoma. 1128 17


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