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At least 19 recordsLinked to original sources
PubMed1985

Characterization of long terminal repeat sequences of HTLV-III.

The nucleotide sequence of the long terminal repeat sequence (LTR) of the human T-cell leukemia (lymphotropic) virus type III (HTLV-III) was determined. This virus is associated etiologically with the acquired immune deficiency syndrome. The LTR was found to be 634 base pairs in length with U3, R, and U5 regions of 453, 98, and 83 bp, respectively. The proviral DNA is flanked by a 7-base-pair direct repeat. The promoter and polyadenylation signals are situated 27 and 24 base pairs upstream from the respective transcriptional initiation and polyadenylation sites. The primer binding site is complementary to transfer RNA-lysine. The LTR of HTLV-III, like that of HTLV-I, showed a limited homology to enhancer-like sequences within two genes expressed specifically in T lymphocytes, T-cell growth factor, and gamma-interferon. Structural comparisons revealed that the LTR of HTLV-III is distantly related to those of HTLV-I, HTLV-II, and bovine leukemia virus.

Biological Evolution↗
PubMed2000

The binding site of transcription factor YY1 is required for intramolecular recombination between terminally repeated sequences of linear replicative hepatitis B virus DNA.

In the replication cycle of hepadnavirus DNA, the double-stranded linear form of viral DNA is generated as a minor replicative intermediate, which is efficiently converted to covalently closed circular DNA (cccDNA) by intramolecular recombination (W. Yang and J. Summers, J. Virol. 69:4029-4036, 1995). We previously found a binding site of transcription factor Yin and Yang 1 (YY1) in one terminal region of the double-stranded linear replicative hepatitis B virus (HBV) DNA (M. Nakanishi-Matsui, Y. Hayashi, Y. Kitamura, and K. Koike, J. Virol. 74:5562-5568, 2000). However, it is not known whether the YY1-binding site is required for the intramolecular recombination of HBV DNA. In this study, we established an HBV-producing system in which the cccDNA appeared to be generated from the transfected linear DNA or the linear replicative DNA by nonhomologous end joining (NHEJ) or by both NHEJ and homologous recombination between terminally repeated sequences, respectively. When the YY1-binding site in the terminal region of transfected linear viral DNA was mutated, the cccDNA was generated merely by NHEJ. Results suggest that the YY1-binding site in the terminal region of linear replicative HBV DNA is required for intramolecular recombination between terminally repeated sequences.

Base Sequence↗
PubMed1983

Long terminal repeat sequences of intracisternal A particle genes in the Syrian hamster genome: identification of tRNAPhe as a putative primer tRNA.

We have determined the nucleotide sequences of long terminal repeat (LTR) regions of Syrian hamster intracisternal A particle (IAP) genes. The size of the LTRs was 350 base-pairs (bp) and 376 bp in two clones, H10 and H18, respectively. Two LTRs at both ends of the IAP gene were linked to directly repeating 6 bp hamster sequences. Many structural features common to the integrated retroviral LTRs such as "CAT" box, "TATAA" box, polyadenylation signal, and terminal inverted repeat (3 bp), were present on each LTR. The estimated length of R region (about 60 bp) was similar to that of the murine leukemia-sarcoma virus. In contrast, the calculated U5 region of 54 bp was the shortest among those of the retroviruses so far studied. Furthermore, from the analysis of primer binding sites, phenylalanine tRNA was for the first time identified as a presumed primer tRNA for reverse transcription. These results clearly distinguish Syrian hamster IAP LTRs from other retroviral ones. Based on the comparison of the sequences between Syrian hamster and laboratory mouse LTRs, the structural features peculiar to the IAP LTRs and the origin of the IAP genes are discussed.

Animals↗
PubMed2003

Inhibition of Moloney murine leukemia virus integration using polyamides targeting the long-terminal repeat sequences.

The retroviral integrase (IN) carries out the integration of the viral DNA into the host genome. Both IN and the DNA sequences at the viral long-terminal repeat (LTR) are required for the integration function. In this report, a series of minor groove binding hairpin polyamides targeting sequences within terminal inverted repeats of the Moloney murine leukemia virus (M-MuLV) LTR were synthesized, and their effects on integration were analyzed. Using cell-free in vitro integration assays, polyamides targeting the conserved CA dinucleotide with cognate sites closest to the terminal base pairs were effective at blocking 3' processing but not strand transfer. Polyamides which efficiently inhibited 3' processing and strand transfer targeted the LTR sequences through position 9. Polyamides that inhibited integration were effective at nanomolar concentrations and showed subnanomolar affinity for their cognate LTR sites. These studies highlight the role of minor groove interactions within the LTR termini for retroviral integration.

Animals↗
PubMedDate not supplied

Hexamethylene bisacetamide and cis-platin stimulate the expression from the HIV-1 long terminal repeat sequence in human MCF-7 cells.

We have employed a recombinant plasmid pBHIV-1 carrying the Long Terminal Repeat sequences (LTR) of the Human Immunodeficiency Virus (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phosphotransferase (aph) gene as a selectable marker. We have introduced pBHIV-1 DNA in human breast cancer MCF-7 cells and obtained the MCF-7HIV-1 cell line, resistant to geneticin. We have studied the effect of hexamethylene-bisacetamide (HMBA), cis-platin, interferon-aB, dexamethasone and tamoxifen on the LTR regulated CAT activity in MCF-7HIV-1 cells. It was found that HMBA and cis-platin stimulated CAT activity, whereas interferon-aB, dexamethasone and tamoxifen had no significant effect.

Acetamides↗
PubMed1991

Doxorubicin stimulates transcription from the human immunodeficiency virus long terminal repeat sequences.

A recombinant plasmid carrying the long terminal repeat (LTR) of the human immunodeficiency virus 1 (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene was stably introduced into rat liver cells. The transfectant cells expressed CAT activity from the HIV LTR. The response to doxorubicin was studied and it was found that at the optimum concentration of 20 micrograms/ml doxorubicin, the expression of CAT from the HIV LTR was stimulated by 65-fold. Our results suggest caution against therapy including doxorubicin in the treatment of AIDS patients.

Animals↗
PubMed2003

HIV type 1 C and C' subclusters based on long terminal repeat sequences in the Ethiopian type 1 subtype C epidemic.

While the Ethiopian HIV-1 epidemic is dominated by subtype C, two distinguishable cocirculating C genotypes have been identified based on sequences of the C2V3 envelope region. In this study we sequenced and analyzed the long terminal repeat (LTR) sequence from 22 Ethiopian HIV-1-positive individuals. The two phylogenetically distinguishable genotypes C (n = 13) and C' (n = 4) are separated by significant bootstrap values. Nucleotide differences between the two groups were identified in the NF-AT, TCF-1alpha, and SP1 transcription factor binding sites, whereas the NF-kappaB and NRE-core sequences were identical between the two groups. Five isolates that could not be classified C or C' were found to be recombinants within the LTR sequence upon boots can analysis. Comparison of all the LTR sequences with their corresponding C2V3 envelope sequence revealed four intersubtype C/C' recombinant isolates. Thus, the prevalence of C/C' recombinant viruses is well over 40%. Interestingly, the C2V3 envelope sequences of all recombinant viruses belonged to the genotype C', whereas every LTR sequence belonged to the genotype C. This result indicates that recombination between the two genotypes is unidirectional, possibly as the result of evolutionary pressure on the respective biological functions of the LTR promoter and the envelope protein.

Base Sequence↗
PubMed1982

Carcinogen- and radiation-transformed C3H 10T1/2 cells contain RNAs homologous to the long terminal repeat sequence of a murine leukemia virus.

Carcinogen- or radiation-transformed C3H 10T1/2 murine fibroblasts transcribe a set of poly(A)+RNAs that contain sequences homologous to the long terminal repeat (LTR) sequence of Moloney murine sarcoma virus. These LTR-containing RNAs consist of a series of discrete bands ranging in size from about 38 to 18 S. The higher molecular weight molecules (30-38 S) in this set of RNAs also contain sequences homologous to the gag, pol, and env genes of a murine leukemia virus. A 24S RNA contains sequences homologous to the env gene of murine leukemia virus. A 20S and an 18S RNA also share homology with the LTR probe but fail to hybridize to the gag, pol, or env probes or to a probe for the U3 region of the LTR sequence. Thus, the latter transcripts do not appear to arise from a known endogenous murine leukemia virus genome. Although this entire set of RNAs is absent from normal C3H 10T1/2 cells (or is present at an extremely low level), these RNAs are induced by BrdUrd or 5-azacytidine. The presence of these RNAs may provide highly sensitive molecular markers of transformation of murine cells.

Animals↗
PubMed1992

Carboplatin as opposed to cisplatin does not stimulate the expression of the human immunodeficiency virus long terminal repeat sequences.

The recombinant plasmid pBHIV1 carrying the long terminal repeat (LTR) of the human immunodeficiency virus 1 (HIV-1), linked to the chloramphenicol acetyl transferase (CAT) gene, was introduced into human and rat fibroblasts. Stable transfectants resistant to geneticin expressed CAT activity from the HIV-1 LTR. It was found that the cytotoxic drug cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II) (carboplatin) at concentrations from 1 x 10(-6) to 1 x 10(-4) M does not stimulate the expression of CAT from the HIV-1 LTR. These results differ from previous studies with the related drug cis-diamminedichloroplatinum(II) which showed stimulation of gene expression from the HIV-1 LTR and suggest that carboplatin could be used in the treatment of cancer patients with Acquired Immune Deficiency Syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Murine leukemia virus long terminal repeat sequences can enhance gene activity in a cell-type-specific manner.

We tested the ability of sequences in the long terminal repeat (LTR) of a mink cell focus-forming (MCF) murine leukemia virus to function as an enhancer in a cell-type-specific manner. In a stable transformation assay, the MCF or Akv LTR and the simian virus 40 enhancer had similar activities in murine fibroblasts. In contrast, the MCF LTR had a significantly greater activity in murine T lymphoid cells than did either the simian virus 40 enhancer or the Akv LTR.

Animals↗
PubMed1993

Mitomycin C stimulates the expression of human immunodeficiency virus long terminal repeat sequences in rat and human fibroblasts.

We have employed a recombinant plasmid, pBHIV1, carrying the long terminal repeat (LTR) sequences of the human immunodeficiency virus-1 (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phosphotransferase (aph) gene as a selectable marker. We have introduced pBHIV1 into rat 208F and human MRCSV40TGR fibroblasts and obtained stable geneticin resistant RFBHIV1-1 and SVTGHIV1-1 cells, respectively. Both transfectant cells express CAT activity from the HIV LTR promoter. The response to the antineoplastic drug mitomycin C was studied on the LTR regulated CAT activity in both cell lines. It was found that mitomycin C at 10 micrograms/mL concentration stimulates the expression of CAT from the HIV LTR 77-fold in rat RFBHIV1-1 and 3.1-fold in human SVTGHIV1-1 cells.

Animals↗
PubMed1992

Hexamethylene bisacetamide stimulates the expression of human immunodeficiency virus long terminal repeat sequences in rat and human fibroblasts.

We have employed a recombinant plasmid, pBHIV1, carrying the long terminal repeat (LTR) sequence of the human immunodeficiency virus-1 (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phosphotransferase (aph) gene as a selectable marker. We have introduced pBHIV1 in rat 208F and human MRCSV40TGR fibroblasts and obtained stable geneticin resistant RFBHIV1-1 and SVTGHIV1-1 cells, respectively. Both transfectant cells express CAT activity from the HIV LTR promoter. The response to anti-neoplastic drug hexamethylene bisacetamide (HMBA) was studied on the LTR regulated CAT activity in both cell lines. It was found that HMBA at 5mM concentration stimulates the expression of CAT from the HIV LTR in rat and human cells by 28- and 1.9-fold, respectively.

Acetamides↗
PubMed1980

Inverted terminal repeat sequence in the macronuclear DNA of Stylonychia pustulata.

The structure of macronuclear DNA of a hypotrichous ciliate, Stylonychia pustulata, was examined by both electron microscopy and nucleotide sequence analysis. The DNA in the macronucleus consists of small linear molecules with average length of about 3400 base pairs (bp). Most, if not all, of these DNA molecules have identical inverted terminal repeat sequence of 20 nucleotide residues. This sequence is 5'-CCCCAAAACCCC-AAAACCCC.

Animals↗
PubMed1990

Cisplatin stimulates the expression from the human immunodeficiency virus long terminal repeat sequences in human fibroblasts.

A recombinant plasmid carrying the long terminal repeat (LTR) of the human immunodeficiency virus 1 (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene was stably introduced into human fibroblasts. The transfectant cells expressed CAT activity from the HIV LTR. The response to anti-neoplastic drugs, i.e. cisplatin, a platin derivative, and hexadecylphosphocholine, was studied. It was found that at 5 x 10(-6) M concentrations cisplatin stimulates by 2.2-fold the expression of CAT from the HIV LTR. Our results extend our observations on the effect of cisplatin on HIV LTR in rodent fibroblast cells and suggest caution against therapy including cisplatin in the treatment of AIDS patients.

Antineoplastic Agents↗
PubMed2001

Four new inverted terminal repeat sequences from bovine adenoviruses reveal striking differences in the length and content of the ITRs.

The inverted terminal repeat (ITR) of the genome of four bovine adenovirus (BAdV) types have been sequenced, analysed and compared to the ITRs of other adenoviruses. The length of ITRs of the examined BAdVs ranged between 59 and 368 base pairs, thus the presently known longest adenovirus ITR sequence is from BAdV-10. The conserved motifs and characteristic sequence elements of the ITRs providing different binding sites for replicative proteins of viral and cellular origin seemed to be distributed according to the proposed genus classification of BAdVs. The ITRs of BAdV-10 share similarity with the members of the genus Mastadenovirus, while the ITRs of the other three sequenced serotypes (BAdV-4, 5 and strain Rus) which are candidate members of the genus Atadenovirus are very short and contain NFI and Sp1 binding sites only. The analysis of the new ITRs implied that the nucleotide sequence of the so-called core origin is highly preserved within the mastadenovirus genus only.

Adenovirus E2 Proteins↗
PubMed1999

Effects of long terminal repeat sequence variation on equine infectious anemia virus replication in vitro and in vivo.

The long terminal repeat (LTR) is reported to be one of the most variable portions of the equine infectious anemia virus (EIAV) genome. To date, however, no information is available on the effects of observed sequence variations on viral replication properties, despite a widespread assumption of the biological importance of EIAV LTR variation. EIAV LTR sequence variability is confined mostly to a small portion of the enhancer within the U3 segment of the LTR. Analysis of published EIAV LTR sequences revealed six different types of LTR based on the pattern of putative transcription factor motifs within the variable region of the enhancer. To test directly the significance of LTR variation, the in vitro and in vivo replication properties of two variant LTR species were investigated using two isogenic viruses, EIAV(19-2) and EIAV(19-2-6A), differing only within the enhancer region. The results of these studies demonstrated that the two variants replicated with similar kinetics and to equal levels in cultured equine fibroblasts or in equine macrophage, the natural target cell of EIAV, even after prolonged serial passage in the latter cell type. Furthermore, EIAV(19-2) and EIAV(19-2-6A) variants demonstrated similar replication levels in experimentally infected ponies. However, ponies infected with EIAV(19-2-6A) exhibited a rapid switch in the prevalent LTR type, such that by 112 days postinfection, no original-LTR-type viruses were evident. This specific and rapid shift in LTR quasispecies indicates an in vivo selection that is not reflected in simple in vitro replication rates, suggesting undefined selection pressures in vivo that drive LTR variation during persistent EIAV infection.

Animals↗
PubMed1988

Trans-activation of the human immunodeficiency virus long terminal repeat sequences, expressed in an adenovirus vector, by the adenovirus E1A 13S protein.

The human immunodeficiency virus 1 (HIV-1) long terminal repeat (LTR) sequences were inserted into adenovirus in place of the E1 region. The HIV-1 LTR contained in this recombinant adenovirus responds to trans-activation by tatIII in a HeLa cell line constitutively expressing that HIV-1 gene product. In addition, the HIV-1 LTR is activated by the adenovirus E1A 13S, but not 12S or 9S, gene product when it is supplied in trans by a coinfecting wild-type adenovirus. The Rous sarcoma virus LTR, in a similar recombinant adenovirus, is insensitive to tatIII but is also trans-activated by the E1A 13S protein. The action of the 13S E1A and tatIII proteins are additive for the HIV-1 LTR in the context of adenovirus and they appear to act at the transcriptional level. As in HeLa cells, the adenovirus-borne HIV-1 LTR is inactive in the absence of a trans-activator in H9 and Jurkat cells, two human leukemic T-cell lines. This suggests that recombinant adenoviruses have diagnostic potential for the detection of trans-activators of the HIV-1 LTR that are present in circulating human lymphocytes.

Adenovirus Early Proteins↗
PubMedDate not supplied

Transcriptional activation of the human immunodeficiency virus long terminal repeat sequences by retinoic acid in human epithelial and fibroblast tumor cell lines.

We employed a recombinant plasmid, pBHIV1, carrying the long terminal repeat (LTR) sequences of HIV-1 linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phosphotransferase (aph) gene as a selectable marker. We introduced pBHIV1 into human epithelial and fibroblast tumor cell lines (HeLa and MRCSV40TGR), and obtained stable geneticin-resistant HLHIV1-A and SVTGHIV1-A cells, respectively. The response to the retinoic acid was studied on the LTR regulated CAT activity in both cell lines. It was found that retinoic acid at a concentration of 1x10(-5) effects a 3.2 -fold increase in CAT expression compared to HIV LTR in HLHIV1-A, but requires a concentration of 5x10(-5) M to enhance this expression 4.6-fold in SVTGHIV1-A cells. These data show that retinoic acid may play a critical role in HIV-1 expression in human epithelial and fibroblast cell lines.

Cell Division↗