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Four Classes of HERV-K Long Terminal Repeats and Their Relative Promoter Strengths for Transcription.

The human genome contains abundant copies of HERV-K endogenous retrovirus sequences. These remnants of ancient infection have the potential to reshape the genome by retrotransposition or infection since they are highly expressed in cells of germ line origin. When conserved nucleotide sequence variations in the U3 region of the HERV-K 3' LTR were used to distinguish between individual HERV-K proviruses, 4 major classes of HERV-K LTRs were identified. HERV-K U3 regions from the different classes were compared in an in vitro transcription assay and were found to vary significantly in their promoter activities. Copyright 1997 S. Karger AG, Basel

Journal Article↗
PubMed1996

Subtyping of human T-lymphotropic virus type I by amplification of long terminal repeat sequences and restriction fragment length polymorphism analysis in carriers with multiple transfusions.

Five major subtypes of human T-lymphotropic virus type I (HTLV-I) have been proposed: cosmopolitan, Japanese, West African, Central African, and Melanesian. Based on nucleotide variations specific to particular subtypes, it was possible to genotype HTLV-I rapidly by restriction fragment length polymorphism (RFLP) studies following polymerase chain reaction (PCR). In this study, the restriction patterns of two LTR fragments were analyzed using eight restriction endonucleases (AvaI, Eco57I, BsoFI, NdeI, SacI, DraI, MaeII, and MaeIII). Genotyping of HTLV-I was done in nine patients with adult T-cell leukemia or HTLV-I-associated myelopathy/tropical spastic paraparesis, in three prostitutes, and in 19 carriers with multiple transfusion in Taiwan. The subtyping results of RFLP studies using these eight restriction endonucleases were in accordance with those of phylogenetic analysis. A substitution of G by A at nucleotide position 503, which creates the DraI site but suppresses the SacI site, was found not only in the Japanese subtype but also in a minority of the cosmopolitan subtype. A mutation near the position of subtype-specific nucleotide variations might suppress the restriction site and lead to unexpected restriction patterns. Amplification of more than one proviral fragment and RFLP studies with a group of appropriate restriction endonucleases may provide rapid and accurate genotyping of HTLV-I. More carriers are required to evaluate the possibility of mixed infection with different HTLV-I subtypes.

Base Sequence↗
PubMed1989

Detection of enhancer binding proteins recognizing the human immunodeficiency virus long terminal repeat by in situ gel retardation.

We have examined the formation of a DNA "enhancer" - protein complex occurring in situ. Oligonucleotides corresponding to the human immunodeficiency virus (HIV) core enhancer sequence were synthesized, annealed and radiolabeled. The DNA was electroporated either into Jurkat cells or into fresh human peripheral blood T lymphocytes. After the appropriate incubation time and stimulation with various mitogenic agents, cells were lysed and the lysates were electrophoresed on a native polyacrylamide gel. The specific protein-nucleic acid complexes which we obtained were apparently identical to those observed with the "classical" in vitro gel mobility shift assay: one complex seems to be constitutive and the other is induced by mitogens. Additionally competition experiments using "cold" oligonucleotides demonstrated binding specificity in situ. We recommend this novel method for studying DNA-binding proteins and their activation since it requires as few as 10(6) cells, may use primary tissue isolates, and furthermore, allows the rapid assessment of cellular activation signals involved in the post-transcriptional modification of trans-acting factors.

Base Sequence↗
PubMed1987

Methylation of the enhancer region of avian sarcoma virus long terminal repeat suppresses transcription.

The effect of methylation of an enhancer on transcription was studied. A 245 bp enhancer-containing a fragment of the LTR of the avian sarcoma virus was methylated in vitro and ligated back into a vector which lacked the upstream enhancer sequence. The transient expression in QT6 cells indicated that methylation of the enhancer-containing sequence severely reduced the extent of transcription.

Avian Sarcoma Viruses↗
PubMed1985

Long terminal repeat of Friend-MCF virus contains the sequence responsible for erythroid leukemia.

Friend-MCF virus induces erythroid leukemia when injected into newborn NFS mice whereas Moloney virus induces T-cell lymphoma. To identify the portion of Friend-MCF virus responsible for erythroid leukemia induction four in vitro recombinant viruses were constructed in which env regions or U3 regions of LTR were reciprocally exchanged between Friend-MCF and Moloney viruses. A FrMCF-Mol (LTR) virus whose genome was derived primarily from Friend-MCF virus together with 621 nucleotides of Moloney virus at its 3' end including the U3 region of LTR was a thymic lymphoma-inducing virus. A Mol-FrMCF (LTR) virus with the genome derived primarily from Moloney virus but 596 nucleotides of Friend-MCF virus information at the same region as FrMCF-Mol (LTR) was an erythroid leukemia-inducing virus. A Mol-FrMCF (env) virus whose genome was derived primarily from Moloney virus but which had 2.3 kbp of Friend MCF at the 3' end of the pol gene including most of the env gene with all of gp70 and the N terminal of p15E was a lymphoid leukemia-inducing mink cell focus-inducing virus. FrMCF-Mol (env) virus whose genome was derived primarily from Friend-MCF virus but had 2.7 kbp of Moloney virus at the same region as Mol-FrMCF (env) virus was an erythroid leukemia-inducing ecotropic virus. The Mol-FrMCF (LTR) and Mol-FrMCF (env) viruses induced mixed leukemia of erythroid and lymphoid cells in some mice.

Animals↗
PubMed1987

Cis-acting transcriptional regulatory sequences in the gibbon ape leukemia virus (GALV) long terminal repeat.

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.

Acetyltransferases↗
PubMed1988

Identification of sequences in the long terminal repeat of avian sarcoma virus required for efficient transcription.

Two different vectors, LTR-NEO-LTR and LTR-CAT-LTR, were constructed and deletions were introduced in the upstream LTR at -299 and at -140. These deletion mutants were introduced into QT6 cells under transient expression conditions, and the levels of transcription were monitored by dot blot hybridization or by CAT assays. The results indicate that the nucleotides between -208 and -201 and between -141 and -119 in the U3 region of RSV LTR are required for efficient transcription.

Avian Sarcoma Viruses↗
PubMed1989

Molecular cloning of a feline leukemia provirus integrated adjacent to the c-myc gene in a feline T-cell leukemia cell line and the unique structure of its long terminal repeat.

This paper reports the molecular cloning of a rearranged c-myc region from the FT-1 cell line, which was derived from a spontaneous feline T-cell leukemia carrying the feline leukemia virus (FeLV). An abnormal c-myc EcoRI fragment of about 18 kilobases, detected by Southern blotting, was molecularly cloned from the DNA of the FT-1 cell line. The c-myc rearrangement in FT-1 was due to direct integration of the FeLV provirus genome immediately upstream of the c-myc gene in the opposite transcriptional orientation. Nucleotide sequencing showed that the LTR of this provirus had three copies of an enhancer-like sequence, unlike the sequences of FeLVs reported previously, which have only a single copy of this enhancer-like sequence.

Base Sequence↗
PubMed1992

Myb protein binds to multiple sites in the human T cell lymphotropic virus type 1 long terminal repeat and transactivates LTR-mediated expression.

The members of the c-myb proto-oncogene family encode sequence-specific transcriptional activators. In T cells, expression of c-myb and the related B-myb gene is induced following mitogenic stimulation. Using a purified recombinant protein, we report here that the human T cell lymphotropic virus type 1 (HTLV-1) LTR contains six specific binding sites for Myb. We also show that HTLV-1 LTR chloramphenicol acetyl transferase reporter plasmids are specifically transactivated by c-Myb. These data suggest a role for members of the Myb family as a link between transcriptional activation of the HTLV-1 LTR and T cell activation events.

Base Sequence↗
PubMed2005

In vitro selective suppression of feline myeloid colony formation is attributable to molecularly cloned strain of feline leukemia virus with unique long terminal repeat.

Molecularly cloned feline leukemia virus (FeLV)-clone 33 (C-33), derived from a cat with acute myelocytic leukemia (AML), was examined to assess its relation to the pathogenesis of AML and myelodysplastic syndrome (MDS). To evaluate in vitro pathogenicity of FeLV C-33, bone marrow colony-forming assay was performed on marrow cells infected with FeLV C-33 or an FeLV subgroup A strain (61E, a molecularly cloned strain with minimal pathogenicity). The myeloid colony-forming activity of feline bone marrow mononuclear cells infected with FeLV C-33 was significantly lower than that of cells infected with 61E. This suggests that FeLV C-33 has myeloid lineage-specific pathogenicity for cats, and that FeLV C-33 infection is useful as an experimental model for investigating pathogenesis of MDS and AML.

Animals↗
PubMed1999

The X gene of hepatitis B virus shows a high level stimulation of the Rous sarcoma virus long terminal repeat in the methylotropic yeast, Pichia pastoris.

In order to study the transactivational property of the X gene in the methylotropic yeast Pichia pastoris, a Rous sarcoma virus-chloramphenicol acetyltransferase (RSV-CAT) cassette was co-transformed and integrated into the host yeast strain as a reporter which showed an overwhelming CAT activity. Immunoprecipitation of the yeast cell extracts with an X-specific monoclonal antibody, however, showed a low level expression of the X gene. Therefore besides a trans-effect of the X protein, the enhanced reporter activity could be a manifestation of a cis-effect of the X gene sequences also. Therefore, unlike the transactivation studies with X gene in animal cells where limited functional activity is observed, P. pastoris appears to be an excellent system to study cis- and trans-aspects of gene regulation by the X gene.

Avian Sarcoma Viruses↗
PubMed2003

Mutations that abrogate transactivational activity of the feline leukemia virus long terminal repeat do not affect virus replication.

The U3 region of the LTR of oncogenic Moloney murine leukemia virus (Mo-MuLV) and feline leukemia viruses (FeLV) have been previously reported to activate expression of specific cellular genes in trans, such as MHC class I, collagenase IV, and MCP-1, in an integration-independent manner. It has been suggested that transactivation of these specific cellular genes by leukemia virus U3-LTR may contribute to the multistage process of leukemogenesis. The U3-LTR region, necessary for gene transactivational activity, also contains multiple transcription factor-binding sites that are essential for normal virus replication. To dissect the promoter activity and the gene transactivational activity of the U3-LTR, we conducted mutational analysis of the U3-LTR region of FeLV-A molecular clone 61E. We identified minimal nucleotide substitution mutants on the U3 LTR that did not disturb transcription factor-binding sites but abrogated its ability to transactivate the collagenase gene promoter. To determine if these mutations actually have altered any uncharacterized important transcription factor-binding site, we introduced these U3-LTR mutations into the full-length infectious molecular clone 61E. We demonstrate that the mutant virus was replication competent but could not transactivate cellular gene expression. These results thus suggest that the gene transactivational activity is a distinct property of the LTR and possibly not related to its promoter activity. The cellular gene transactivational activity-deficient mutant FeLV generated in this study may also serve as a valuable reagent for testing the biological significance of LTR-mediated cellular gene activation in the tumorigenesis caused by leukemia viruses.

3T3 Cells↗