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PubMed1992

The open reading frames in the 3' long terminal repeats of several mouse mammary tumor virus integrants encode V beta 3-specific superantigens.

Mice expressing the minor lymphocyte stimulation antigens, Mls-1a, -2a, or -3a, singly on the B10.BR background have been generated. Mls phenotypes correlate with the integration of mouse mammary tumor viruses (MTV) in the mouse genome. The open reading frames within the 3' long terminal repeats of the integrated MTVs 1, 3, 6, and 13 encode V beta 3-specific superantigens. Sequence data for these viral superantigens is presented, indicating that it is the COOH-terminal portion of the viral superantigen that interacts with the T cell receptor V beta element.

Amino Acid Sequence↗
PubMed1987

Structure of the long terminal repeat of simian lymphotropic virus type III (African green monkey) and its relatedness to that of HIV.

The simian T-lymphotropic virus type III (STLV-III[AGM]) is a retrovirus in wild African green monkeys which is serologically related to the human T-lymphotropic virus type III (HTLV-III/LAV-1/HIV) and other related human retroviruses. The long terminal repeats (LTR) contained in clones of viral DNA of (STLV-III[AGM]) were subcloned in M13 and their DNA sequence was determined and compared with that of HIV (HTLV-III[BH10]). The STLV-III(AGM) LTR is considerably larger than that of HTLV-III(BH10) (800 bp vs 634 bp) and contains a 498 bp U3 region, a 176 bp R region, and a 126 bp U5 region. These two LTR sequences share regions of significant homology. Regions of greatest homology include the 5' portion of U3, a core enhancer sequence in U3, sequences including and surrounding the TATAA promoter box in U3 and the AATAAA polyadenylation/termination signal in R, and the 3'-most region of U5. The relatively larger size of the STLV-III LTR is due to the presence in all three parts of the LTR of sequences which have no apparent homolog in the HIV LTR. Overall, the two LTRs are 47% homologous. Even greater homology (75%) is evident with a 300 bp segment including R and some of U3 from the LTR of another human retrovirus, HIV-2/LAV-2. The STLV-III LTR contains an imperfect 28 bp direct repeat in the R region which is not present in HIV. There are no obvious direct repeats in U3 homologous to the 10 bp repeat in the U3 of HTLV-III.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

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.

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.

Alpharetrovirus↗
PubMed1989

Binding of androgen-receptor complexes to alpha 2u-globulin genes and to the long terminal repeat of mouse mammary tumor virus.

The binding of androgen-receptor complexes to fragments derived from two alpha 2u-globulin genes (RAP 01 and RAO 01) was studied using a DNA-cellulose competition assay. Rat prostate cytosol labelled with [3H]mibolerone was used as a source of the androgen receptor. Two controls were included in these studies: the long terminal repeat (LTR) of mouse mammary tumor virus which has previously been shown to act as an androgen response element and a fragment of the C3 gene of prostatic binding protein which has been demonstrated to bind androgen-receptor complexes. Our experiments indicate that androgen-receptor complexes bind specifically and with comparable affinity to the C3 gene fragment, the LTR and a fragment of RAP 01 located in the 5'-upstream region (bp -642 up to -584). No specific interaction was observed with fragments derived from RAO 01. The region of RAP 01 which binds androgen-receptor complexes has previously been shown to interact with glucocorticoid receptors and contains a 17 bp sequence homologous with the consensus sequence for glucocorticoid-receptor binding. A mutation in this sequence in RAO 01 may be responsible for the loss of glucocorticoid and androgen-receptor binding. It is concluded that at least one member of the alpha 2u-globulin gene family interacts directly with androgen-receptor complexes with an affinity comparable to that observed for other androgen-dependent genes. The binding is observed in a region displaying also affinity for the glucocorticoid receptor.

Alpha-Globulins↗
PubMed1988

A transcriptionally defective long terminal repeat within an endogenous copy of mouse mammary tumor virus proviral DNA.

Mouse mammary tumor virus proviral DNA is endogenous to most inbred strains of mice but in many strains is not transcriptionally active. This inactivity may be due to defects in the proviruses themselves or to position effects mediated by DNA sequences flanking the proviral units. The transcriptional competence of long terminal repeats (LTRs) derived from endogenous proviral DNA at genetic loci Mtv-8, Mtv-9, and Mtv-17 of the C57BL/6 mouse strain was examined with a transient transfection assay in which gene expression was monitored by expression of chloramphenicol acetyltransferase. LTRs from Mtv-8 and Mtv-9 were able to direct glucocorticoid-induced chloramphenicol acetyltransferase expression in this assay, while the LTR from Mtv-17 was only about 5% as effective. Analysis of chimeric LTRs indicated that the glucocorticoid-inducible transcriptional enhancer element within the Mtv-17 LTR is active when linked to a functional promoter from Mtv-8, whereas the promoter from Mtv-17 is defective in directing hormone-induced gene expression, even when linked to the Mtv-8 glucocorticoid-responsive enhancer. The DNA sequence of transcriptional control regions of the LTRs of all three endogenous proviral units was determined; this analysis revealed that the source of the defect in Mtv-17 is a single G-to-A transition at position-75 with respect to the site of transcription initiation that resides within the previously defined binding site for the transcription factor nuclear factor 1. Competition experiments with a gel electrophoresis mobility shift assay indicated that the affinity of nuclear factor 1 for DNA derived from Mtv-17 is significantly less than for comparable sequences derived from Mtv-8.

Animals↗
PubMed1986

Evidence of sequences resembling avian retrovirus long terminal repeats flanking the trout protamine gene.

Additional TATA boxes are present in the flanking regions of trout protamine genes. Their activity as promoters was assayed using an in vitro transcription system. These additional TATA boxes, together with polyadenylation signals that include the consensus AATAAA and CACTG sequences very close to the promoters, suggest that these sequences may be closely related to retroviral long terminal repeat (LTR) sequences. Other features of retroviral LTRs that are also present are short inverted repeats. The LTR-like sequences flanking the trout protamine gene show significant homology to the avian sarcoma virus LTR over a 40-bp region. The trout protamine gene falls into the relatively rare intronless class of eukaryotic genes. This suggests that the gene could have been derived from a processed gene introduced into the genome by reverse transcription of a mature mRNA. The protamine-mRNA-coding region is flanked by AACA... TGTT sequences, which might represent vestigial traces of past recombination events and whose presence supports the notion that the protamine gene sequence was of foreign origin. Recent attempts in this laboratory to transfer the protamine gene into mouse cells have resulted in a high frequency of deletions similar to those observed with constructs in which a retrovirus was used as a vector to transfect foreign DNA with promoters. The distribution of protamine genes in the animal kingdom is very sporadic, which suggests that protamine genes appeared relatively late in evolution. The nonuniform occurrence of the gene among lower vertebrates may have been the result of its horizontal transmission only to certain species, possibly by infection with retroviruses that acquired it from a different species.

Animals↗
PubMed1985

Mapping of DNase I-hypersensitive sites in the 5' and 3' long terminal repeats of integrated moloney murine leukemia virus proviral DNA.

The chromatin state of integrated Moloney murine leukemia virus (M-MuLV) proviral DNA was investigated. Nuclei from M-MuLV-infected mouse NIH 3T3 cells were digested with limited amounts of DNase I, and hypersensitive (HS) sites were mapped by the indirect end labeling technique. Particular emphasis was placed on the 5' long terminal repeat (LTR), since viral transcription initiates there. M-MuLV proviral DNA showed two strong DNase I-HS sites in the 5' LTR, one coincident with the transcription initiation (cap) site and the other with the transcriptional enhancers. Two weaker DNase I-HS sites were also detected in internal proviral DNA. The 3' LTR also showed a strong HS site in the region of the enhancers, but an HS site at the cap site of the 3' LTR was not detected. Thus, the chromatin configurations of the 5' and 3' LTRs of integrated M-MuLV proviruses appear to be different. The chromatin configuration of M-MuLV proviruses which contain LTR insertions of polyomavirus enhancer sequences was also studied. The 5' LTR of M-MuLV proviruses containing polyoma enhancer sequences substituted for the M-MuLV enhancers showed two strong HS sites, one in the polyoma sequences and one at the cap site. The 5' LTR of M-MuLV proviruses containing polyoma enhancer sequences inserted into the wild-type M-MuLV LTR between the cap site and the M-MuLV enhancers showed three HS sites. Two HS sites corresponded to those of the wild-type M-MuLV LTR, whereas the third mapped to the inserted polyoma sequences. The HS site associated with the inserted polyoma sequences was considerably stronger than the M-MuLV-associated HS sites.

Animals↗
PubMed2002

The abundant polyadenylated transcript 2 DNA sequence of the pathogenic protozoan parasite Entamoeba histolytica represents a nonautonomous non-long-terminal-repeat retrotransposon-like element which is absent in the closely related nonpathogenic species Entamoeba dispar.

While comparing gene expression in the pathogenic organism Entamoeba histolytica and the closely related but nonpathogenic species Entamoeba dispar, we discovered that the E. histolytica abundant polyadenylated transcript 2 (ehapt2) and corresponding genomic copies are absent in E. dispar. Although polyadenylated, ehapt2 does not contain any overt open reading frame. Southern blot and sequence analyses revealed that about 500 copies of ehapt2 genomic elements were present in each cell and that the copies were distributed throughout the ameba genome. The various ehapt2 elements are regularly located in the vicinity of protein-encoding genes, downstream of pyrimidine-rich sequence stretches (40 to 125 bp; CT content, 79.2 to 85.5%), and are flanked by duplicated target sites of variable length. Target site duplications were obviously generated during integration of ehapt2 into the E. histolytica genome as one copy of the flanking repeat and the complete ehapt2 element are specifically absent in orthologous E. dispar genomic sequences. ehapt2 shares 3' sequences with EhRLE, a recently identified non-long-terminal-repeat (non-LTR) retrotransposon-like element of E. histolytica, which contains a conceptual open reading frame for reverse transcriptase. Thus, ehapt2 has all of the properties of nonautonomous non-LTR retrotransposons. A comparison of various E. histolytica isolates suggested that transposition of ehapt2 takes place at a very low frequency as the genomic localization of ehapt2 elements was found to be well conserved. A mobile element such as ehapt2 could be a suitable mechanism to explain the infrequent and late transition of E. histolytica from a harmless gut commensal to an invasive pathogen.

Animals↗
PubMed2004

A non-long terminal repeat retrotransposon family is restricted to the germ line micronucleus of the ciliated protozoan Tetrahymena thermophila.

The ciliated protozoan Tetrahymena thermophila undergoes extensive programmed DNA rearrangements during the development of a somatic macronucleus from the germ line micronucleus in its sexual cycle. To investigate the relationship between programmed DNA rearrangements and transposable elements, we identified several members of a family of non-long terminal repeat (LTR) retrotransposons (retroposons) in T. thermophila, the first characterized in the ciliated protozoa. This multiple-copy retrotransposon family is restricted to the micronucleus of T. thermophila. The REP (Tetrahymena non-LTR retroposon) elements encode an ORF2 typical of non-LTR elements that contains apurinic/apyrimidinic endonuclease (APE) and reverse transcriptase (RT) domains. Phylogenetic analysis of the RT and APE domains indicates that the element forms a deep-branching clade within the non-LTR retrotransposon family. Northern analysis with a probe to the conserved RT domain indicates that transcripts from the element are small and heterogeneous in length during early macronuclear development. The presence of a repeated transposable element in the genome is consistent with the model that programmed DNA deletion in T. thermophila evolved as a method of eliminating deleterious transposons from the somatic macronucleus.

3' Untranslated Regions↗
PubMedDate not supplied

In vivo events of retroviral long terminal repeat integration into Marek's disease virus in commercial poultry: detection of chimeric molecules as a marker.

The present study demonstrated, for the first time, that not only in vitro, but also in vivo, coinfections with Marek's disease virus (MDV) and each of the three avian retroviruses (reticuloendotheliosis virus [REV], avian lymphoid leukosis virus [ALV], and ALV-J) lead to retroviral long terminal repeat (LTR) integration into MDV. A total of 306 chicken and 59 turkey commercial flocks, submitted for differential avian oncogenic virus diagnosis, served to evaluate the flock mixed virus infection rate, the rate of birds with a multiple virus infection, and the issue of retroviral LTR integration into MDV in vivo. About a quarter of the tumor-bearing commercial flocks carried a mixed MDV and retrovirus infection. A total of 2926 DNA samples were analyzed, including 2428 chicken and 498 turkey DNA samples. Of these, 991 DNAs originated from flocks with a multiple virus infection. In 103 DNA preparations from that group (103/991, 10.4%), including 38 and 56 from chicken blood and tumor tissues, respectively, and nine samples from turkey blood, multiple virus sequences were detected by polymerase chain reaction (PCR). Fifty-six of the 103 samples were further analyzed by the previously developed hot spot-combined (HS-cPCR assay, of which 48% (27/56) contained chimeric MDV and retroviral LTR molecules. When extrapolated to the total samples derived from the flocks with multiple virus infection, that rate implies that about 5% of the DNA samples would carry MDV-retrovirus integration events. Several birds held a variety of chimeric molecules, indicating that several recombination events occurred simultaneously. The validation of the MDV and retroviral LTR chimeric constitution of these molecules was derived by the MDV and retroviral heterologous primers used for their creation by the HS-cPCR assay, Southern blotting and their detection by retroviral LTR probes, and LTR amplification from the gel-purified chimeric molecules. From several molecules, the LTR was sequenced, and a 161-bp retroviral LTR sequence was demonstrated. Our biochemical data imply that a recent integration occurred in the birds. The viability of recombinant viruses represented by the chimeric molecules will be further approached.

Animals↗
PubMed1989

cDNA sequence of the long terminal repeat of a PrB strain of the Rous sarcoma virus.

The cDNA library of the polyA+ RNA from Prague B strain of RSV infected cells was constructed by the use of oligo(dT) primer and the reverse transcription method. The clones containing the LTR sequences were studied. The DNA sequences of several clones were studied and compared with the cDNA sequence of the long terminal repeat (LTR) region of a PrB strain of Rous sarcoma virus (RSV) which had previously been determined. By the analyses of several different cDNA clones, mutations were detected in the R region as well as in the U3 region of the LTR in two different cDNA clones. By comparing the DNA sequences of these cDNA clones with the original viral LTR, the error-prone hypothesis of the RSV reverse transcriptase was confirmed.

Avian Sarcoma Viruses↗
PubMed1996

[Nucleotide sequence and restriction fragment length polymorphism (RFLP) analysis of the long terminal repeat of human T-cell lymphotropic virus type II (HTLV-II)].

Molecular studies have demonstrated the existence of two major subtypes of human T-cell lymphotropic virus type II, HTLV-IIa and HTLV-IIb. In attempts to further classify this family of viruses we have carried out nucleotide sequence and restriction fragment length polymorphism (RFLP) analysis of the long terminal repeat (LTR), a region which has been shown in previous studies to have the greatest intra-and inter-subtype genomic divergence. Analysis of the nucleotide sequences suggested the existence of distinct phylogenetic groups in each subtype, and based on predicted differences in restriction endonuclease sites, RFLP analysis allowed the identification of four groups within the IIa subtype (a1-a4), and six within the IIb subtype (b1-b6). Nucleotide sequence analysis also suggested the possible existence of HTLV-II quasispecies. However this appeared not to be significant, and preliminary studies suggest that these would not be expected to appreciably influence the results of RFLP analysis. The validity of the RFLP method was demonstrated in an analysis of thirty-six randomly chosen samples from the blood donors from the New York City Blood Center where it could be shown that all could be successfully classified. Moreover, the RFLP analysis correctly matched the viruses in donors and recipients of contaminated blood in four situations where HTLV-II was inadvertently transmitted by transfusion. RFLP analysis of the LTR appears to be a rapid and reliable method to identify HTLV-II infection. This should prove useful in studies of the epidemiology and the characterization of viruses present both in non-indigenous in indigenous populations.

Base Sequence↗
PubMed1993

The use of a DNA-binding domain replacement method for the detection of a potential TR3 orphan receptor response element in the mouse mammary tumor virus long terminal repeat.

TR3 orphan receptor is a human homologue of the mouse nur77, N10 and rat NGFI-B, TIS1 genes which may represent an early response gene involved in the control of cell proliferation. We have studied potential target genes for TR3 orphan receptor using the DNA-binding domain replacement method. We found that mouse mammary tumor virus long terminal repeat-linked chloramphenicol acetyltransferase expression can be activated in transfected cells by a chimeric androgen receptor/TR3 orphan receptor/androgen receptor construct (AR/TR3/AR) in the presence of androgen. By deletion analysis, a region with 20 nucleotides in length between positions -1178 and -1159 of the mouse mammary tumor virus long terminal repeat was confirmed as a potential TR3 orphan receptor response element. These results suggest that feasibility of using the DNA-binding domain replacement method to detect target sequences of orphan receptors.

Androgens↗
PubMed1984

Repetitive structure in the long-terminal-repeat element of a type II human T-cell leukemia virus.

The majority of human T-cell leukemia virus isolates (HTLV-I) are associated with clinically aggressive adult T-cell leukemia/lymphomas. By contrast, HTLV-II has been isolated from a patient with a relatively benign hairy T-cell leukemia. To characterize differences in the viral genomes that might contribute to these different pathologies, we determined the nucleotide sequence of the long terminal repeat (LTR) of a HTLV-II provirus. Comparison with the type I HTLV LTR reveals that, whereas the overall structural features are similar, the two sequences differ markedly throughout most of the length of the LTR. Despite the overall differences, the sequences of several functional regions of the two LTRs are conserved. These include the 5' boundary of U3, the RNA cap site, and the tRNAPro-binding site immediately 3' to the LTR. Another point of similarity is a 21-base sequence that is repeated four times in the U3 region of HTLV-II and three times in the U3 region of HTLV-I. This sequence has a formal analogy to, but no common sequence with, viral transcriptional enhancers. The U3 region of HTLV-II possesses a series of imperfect tandem direct repeats, 42 bases long, 21 bases long, 19 bases long, and 7 bases long. These structures differ from those of HTLV-I except for the 21-base repeat sequence. Thus, the structure of HTLV-II differs substantially from that of HTLV-I in the region that governs transcriptional initiation and tissue specificity. Such differences may account for some of the differences in clinical presentation of HTLV-associated adult T-cell leukemia/lymphomas and hairy T-cell leukemia.

Base Sequence↗
PubMed1996

The promoter activity of long terminal repeats of the HERV-H family of human retrovirus-like elements is critically dependent on Sp1 family proteins interacting with a GC/GT box located immediately 3' to the TATA box.

The HERV-H family of endogenous retrovirus-like elements is widely distributed in the human genome, with about 1,000 full-length elements and a similar number of solitary long terminal repeats (LTRs). HERV-H LTRs have been shown to direct the transcription of both HERV-H-encoded and adjacent cellular genes. Transcripts of HERV-H elements are especially abundant in placenta, teratocarcinoma cell lines, and cell lines derived from testicular and lung tumors. Here we report that only a subset of HERV-H LTRs display promoter activity in human cell lines and that these LTRs are characterized by the presence of a GC/GT box immediately downstream of the TATA box. This GC/GT box is required for promoter activity, while, surprisingly, the TATA box is dispensable. The ubiquitously expressed transcription factors Sp1 and Sp3 bound to this GC/GT box and stimulated transcription from the promoter-active LTRs in the teratocarcinoma cell line NTera2-D1. However, in HeLa and Drosophila SL-2 cells, Sp1 acted as a transcriptional activator of the LTRs, while Sp3 acted as a repressor of Sp1-mediated transcriptional activation. Cotransfection studies also revealed that the tissue-specific Sp1-related protein BTEB bound to this GC/GT box and stimulated transcription from the LTR promoters in NTera2-D1 cells. These results show that members of the Sp1 protein family are crucial determinants for transcriptional activation of HERV-H LTR promoters and suggest that these proteins may also be involved in determining the tissue-specific expression pattern of HERV-H elements.

Animals↗
PubMed1997

The cellular stress response enhances human T-cell lymphotropic virus type 1 basal gene expression through the core promoter region of the long terminal repeat.

Viral protein expression is postulated to play a critical role in the pathogenesis of human T-cell lymphotropic virus type 1 (HTLV-1)-associated diseases. Therefore, knowledge of the cellular events which initiate or enhance viral gene expression is important in understanding the mechanism of HTLV-1-induced disease. In this report, we examined the modulation of transcription of the HTLV-1 long terminal repeat (LTR) following induction of the cellular stress response. We demonstrate by both in vitro transcription assays and transient transfections that induction of the stress response increases basal transcription from the LTR. Transient cotransfection assays indicate that stress induction of viral transcription is Tax independent. In addition, we provide evidence that the sequences responsible for the enhanced transcription are -52 through +157 of the U3/R region of the HTLV-1 LTR. Finally, our data suggest that the increase in transcription is mediated through an intermediate polymerase II/polymerase III transcriptional complex, demonstrated by the inability to abolish the effect with low concentrations of alpha-amanitin.

Amanitins↗
PubMed1999

SR2 elements, non-long terminal repeat retrotransposons of the RTE-1 lineage from the human blood fluke Schistosoma mansoni.

As in other eukaryotes, a substantial portion of the genome of the human blood flukes belonging to the genus Schistosoma appears to be composed of mobile genetic elements and other repetitive sequences. The constitutent elements and their relative organization are not well understood, although retroposons (the SM alpha elements) and a family of non-long terminal repeat (LTR) retrotransposons (the SR1 elements) have been reported from the genome of Schistosoma mansoni. Here, we report the presence of a second family of non-LTR retrotransposons from S. mansoni which we have termed the SR2 elements. SR2 elements are members of a recently described lineage of non-LTR retrotransposons typified by the RTE-1 non-LTR retrotransposon of Caenorhabditis elegans. We determined the sequence for approximately 3.9 kb of a consensus full-length SR2 element, which included a long 5' untranslated region (UTR), potential first and second open reading frames (ORFs) of 78 and 1,018 amino acid residues, respectively, a short 3' UTR, and an A-rich 3' terminus. SR2 elements were bound by target site duplications. The putative first and second ORFs did not overlap. The second ORF was homologous to retroviral pol and encoded an apurinic/apyrimidinic endonuclease and a reverse transcriptase. A number of extremely short SR2 elements of less than 0.5 kb, reminiscent of SINEs, were also characterized. These consisted solely of the 5' and 3' UTRs of full-length SR2 elements, having both ORFs deleted. Analysis indicated that these SINE-like SR2 elements were produced by replication of a SINE-like SR2 element, rather than by repeated deletions within larger SR2 elements.

Amino Acid Sequence↗
PubMed1990

Analysis of long terminal repeat circle junctions of human immunodeficiency virus type 1.

Circle junctions of unintegrated human immunodeficiency virus type 1 strain IIIB were analyzed after polymerase chain reaction amplification. Among the 28 colonies sequenced, eight unique circle junction species were detected. Five of the eight species resulted in circle junctions with larger inserts than predicted. A majority of these could result from heterogeneity in generating the U5' long terminal repeat terminus.

Base Sequence↗