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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An N-ecotropic murine leukemia virus (OA MuLV), originally isolated from spontaneous osteomas of strain 101 mice, was molecularly cloned. The virus induces osteomas, osteopetrosis, and malignant lymphomas in NMRI mice. The cloned virus was analyzed by heteroduplex analysis, restriction enzyme mapping, and oligonucleotide mapping. The data show a very close relationship to the endogenous Akv prototype virus with some differences in the gag and the env region. The nucleotide sequence of the U3 region of OA MuLV LTR revealed a structure within the presumable enhancer region very similar to the U3 sequences of the FBJ murine sarcoma virus and its associated helper virus. The significance of these specific structures for the oncogenicity of the virus and the development of the typical disease pattern is discussed.
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PMID:Oncogenic retrovirus from spontaneous murine osteomas. II. Molecular cloning and genomic characterization. 300 46

The nucleotide sequence of the 3'-terminal region of the cloned bovine leukaemia virus cDNA (1474 bp) was elucidated using both Sanger and Maxam-Gilbert techniques. This DNA region contains U3 and R parts of the BLV LTR and an upstream sequence with four open reading frames (ORF) of unknown function. The comparison of the nucleotide substitutions in these ORF with the two variants of proviral BLV DNA suggests that the only pX1 ORF possesses a coding function. The role of the pX1 protein is discussed.
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PMID:[Primary structure of the 3'-terminal region of the cloned DNA of the bovine leukemia virus]. 300 63

Human T-cell leukemia virus type I has a unique sequence, pX, between the env gene and the 3'LTR (long terminal repeat). This sequence codes for p40x, which was proposed to trans-activate transcription from the LTR. Recently, we identified novel pX proteins coded by frame III, which mostly overlaps frame IV (x-lor, coding for p40x), in a region also overlapped by frame II. To determine which product is responsible for the trans-acting function, we constructed an active provirus clone, pMTPX, that contained a genomic fragment of the env, pX and 3'LTR, and introduced site-directed mutations into the active site. The effects of various deletions and point mutations that distinguished each of the overlapping open reading frames (ORFs), II, III and IV, on trans-activation of pLTR-CAT were treated by co-transfection assays. The results showed that only mutations which affected p40x expression resulted in loss of activity for transcriptional activation. These findings clearly indicate that p40x coded by frame IV is responsible for the transcriptional activation of the LTR. This conclusion was confirmed by studies on expression of cDNA of pX mRNA.
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PMID:Direct evidence that p40x of human T-cell leukemia virus type I is a trans-acting transcriptional activator. 301 13

Provirus from a component of Rauscher leukaemia virus (RLV) has been cloned. The provirus (the size of 5000 b. p.) contains two LTR sequences and shares expressed sequence homology with Mo-MuLV. Restriction analysis and determination of the LTR nucleotide sequence and of the site from 3'-end of proviral genome have shown the cloned provirus to be the SFEV component of RLV. LTR from this cloned provirus contains all sites necessary for transcription: CAAT and TATA sequences, "cap" site and polyadenylation signal. The LTR of the cloned provirus from SFEV component of RLV has been shown to function as a promoter in E. coli cells.
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PMID:[Molecular cloning of provirus sequences of Rauscher leukemia virus from mouse erythroleukemia cell genome]. 302

Human T-cell leukemia virus (HTLV) types I and II are unusual among replication-competent retroviruses in that they contain a fourth gene (chi) necessary for replication. The chi gene product, p chi, transcriptionally transactivates the viral long repeat (LTR), and is thus a positive regulator. To investigate p chi transactivation, sequences from the U3 regions of the LTRs of HTLV-I and -II were inserted into the Moloney murine leukemia virus (M-MuLV) LTR by recombinant DNA techniques. Transient expression assays of the chimeric LTRs indicated that the HTLV sequences conferred to the M-MuLV LTR responsiveness to HTLV p chi protein. M-MuLV enhancers were not required for function of the chimeric LTRs. Infectious recombinant M-MuLVs containing chimeric LTRs were also generated. These viruses showed higher infectivity when assayed in mouse cells expressing HTLV-II p chi protein compared to normal mouse cells. Thus the HTLV sequences were able to confer p chi responsiveness to infectious M-MuLV. The generation of a virus dependent on a transactivating protein for its replication has implications for the evolution of the human T-cell leukemia viruses.
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PMID:U3 sequences from HTLV-I and -II LTRs confer pX protein response to a murine leukemia virus LTR. 302 96

Gibbon ape leukemia viruses (GALV) are a group of retroviruses which have been associated with hematopoietic neoplasms in primates. Two of the viruses, GALV-SEATO and GALV-San Francisco (GALV-SF), are associated with myeloid and lymphocytic leukemias, respectively, in apes. Using an assay based on the transient expression of the bacterial gene chloramphenicol acetyltransferase (CAT), we examined the transcriptional activity of GALV-SEATO and GALV-SF. The results suggest that high level expression of GALV is due primarily to cis-acting enhancer sequences. Sequence delineation analysis of GALV-SEATO showed the GALV-SEATO enhancer sequences to be located within a 45-bp tandem repeat in GALV-SEATO. GALV-SF, which has two- to fivefold lower transcriptional activity, contains only a single copy of the 45-bp element with 6-bp differences from those in the GALV-SEATO enhancer element. This 45-bp element is highly homologous to sequences within the LTRs of several murine leukemia viruses but has not been examined for enhancer function in these retroviruses. Expression of GALV was not restricted to hematopoietic cells but was extraordinarily high in MLA 144 cells, a gibbon ape T-cell line known to be infected with GALV-SF. However, expression of constructs containing the CAT gene directed by GALV-SEATO LTR sequences was similar in uninfected and GALV-infected fibroblasts, indicating the lack of virally encoded or virally induced trans-activating factors capable of increasing expression in these cells.
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PMID:Cis-acting transcriptional regulatory sequences in the gibbon ape leukemia virus (GALV) long terminal repeat. 302 59

Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia (ATL) and a trans-acting viral function was proposed to be involved in ATL development because of the non-specific provirus integration in leukemic cells and the frequent immortalization of helper T-cells by in vitro infection. An extra sequence "pX" in the HTLV-1 genome codes for three proteins, p40x-, p27x- and p21x-, and the p40x- is trans-activator of transcription from the viral LTR. A sequence of 21 bp repeats in the LTR was found to be an enhancer and respond to the trans-activation by p40x-. The transient expression of p40x- also activates a cellular gene for interleukin 2 receptor (IL-2R) in helper T-cell lines. This induction of IL-2R may explain the mechanism of preferential growth of HTLV-1 infected cells and may be an early event of ATL development. For practical purposes, the env gene fragments was expressed in E. coli as fusion proteins with beta-galactosidase. Using these fusion proteins, a diagnostic system detecting anti-env antibodies was developed. Immunization of monkeys with these envelope-fusion proteins protected the monkeys from the viral infection, suggesting possible usage of envelope proteins as vaccine.
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PMID:Mechanism of the gene expression of HTLV-I and its association with ATL. 303 Mar 50

Integration of retroviral DNA is a site-specific reaction involving an endonuclease encoded by the viral pol gene (pol-endo). In vitro the pol-endo from avian sarcoma and leukosis viruses (ASLVs) cleaves both DNA strands near the U5-U3 junction of tandem long terminal repeats (LTR-LTR junction) in single-stranded and replicative form (RF)-I substrates. We have reported previously that the sequences that are required for cleavage of single-stranded substrates by the alpha beta form of the pol-endo differ for the plus and minus strands (G. Duyk, M. Longiaru, D. Cobrinik, R. Kowal, P. deHaseth, A. M. Skalka, and J. Leis, J. Virol. 56:589-599, 1985). This is not the case with RF-I substrates, in which a maximum of 22 base pairs of U5 and 8 base pairs of U3 were required for alpha beta pol-endo cleavage in each strand. Insertion of a palindromic octanucleotide (CATCGATG) at the LTR-LTR junction abolished cleavage in RF-I but not in single-stranded DNA substrates. Deletion of the four nucleotides (TTAA) at the junction prevented cleavage in the plus strand of RF-I DNA, but did not affect cleavage of single-stranded DNA. Furthermore, the alpha beta form of ASLV pol-endo did not recognize heterologous LTR-LTR junction sequences from the reticuloendotheliosis virus or Moloney murine leukemia virus in either substrate form, despite their sequence and structural similarities to the ASLV junction. These results support a role for a sequence-specific interaction between the ASLV pol-endo and the LTR-LTR junction domains that are required for cleavage. By using the infectious Rous sarcoma virus clone pATV8-K, we introduced a set of deletions into the U5 region that would be incorporated into the LTR-LTR junction on viral replication. In the unintegrated provirus, the deletions started 43 base pairs from the LTR-LTR junction and extended various lengths toward the junction. Results of transfection studies with these clones indicated that the U5 sequences that are required for virus production in vivo correspond to those that are required for cleavage of RF-I DNA in vitro.
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PMID:Avian sarcoma and leukosis virus pol-endonuclease recognition of the tandem long terminal repeat junction: minimum site required for cleavage is also required for viral growth. 303 27

The complete nucleotide sequence of an infectious molecular clone of a radiation murine leukemia proviral DNA RadLV/VL3(T+L+) has been determined. The sequence of the RNA genome is 8318 nucleotides long and contains three large open reading frames encoding the gag, pol, and env gene products. With the exception of a xenotropiclike R peptide and the LTR which bears structural similarities to a xenotropic LTR, displaying typical enhancerlike sequences, the remaining sequences are strikingly similar to the endogenous, ecotropic Akv murine leukemia virus. Therefore, it could be postulated that the leukemogenic properties of RadLV/VL3(T+L+) were generated by a recombination event between a xenotropic virus and an Akv-like ecotropic virus.
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PMID:Nucleotide sequence of a radiation leukemia virus genome. 303 97

The gibbon ape leukemia virus (GALV)-infected T-cell line, MLA 144, constitutively makes the lymphokine, interleukin 2 (IL 2), without stimulation by antigen or mitogen. This line contains two GALV insertions in the IL-2 gene: one in the 3' untranslated region of the gene and one 1200 bp 5' to the gene. It is likely that one or both of these viral insertions is(are) involved in activation of IL-2 expression. We investigated the ability of sequences within the LTR of MLA 144 cells (GALV-MLA) to act as transcriptional elements and have demonstrated here the presence of cis-acting sequences in the GALV LTR capable of enhancing transcription of the GALV promoter as well as two heterologous promoters, SV40 early and IL-2. The results indicate that insertion of the enhancer element(s) alone is not sufficient to activate IL-2 expression but can enhance levels of IL-2 expressed from the activated gene.
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PMID:Transcriptional activity of the gibbon ape leukemia virus in the interleukin 2 gene of MLA 144 cells. 303 78


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