Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Proviruses”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1989

Structural analysis of proviruses in additional hamster tumour cell lines transformed by provirus II rescued from XC cells and definition of a new cell line harbouring amplified proviruses.

Additional 18 Syrian hamster tumour cell lines induced independently with the virus rescued from XC cells (provirus type II) have been analysed by restriction mapping. Taking into account the already published results of an analysis of other six tumour cell lines, altogether 24 tumour cell lines were characterized. In 62.5% of these lines a complete proviral unit has been integrated; 20.8% of the lines harbour altered proviral structures where the 3' end of the gag gene and the entire pol gene had been deleted; 8.3% of the lines carry both such a deleted provirus and a complete provirus. Apart from the already published cryptic provirus found in H-19 cells, no such provirus has been found in another cell line. Therefore the appearance of the cryptic provirus represents an infrequent event (4.16%). Similarly, the significant amplification of proviruses accompanied with a rearrangement in the env gene was found only in one tumour cell line. H-42, in the genome of which five proviral units are accommodated. The probable arrangement of amplified proviruses and the mechanism of their genesis are discussed.

Animals↗
PubMed1999

Defective and wild-type human T-cell leukemia virus type I proviruses: characterization of gene products and trans-interactions between proviruses.

Defective provirus genomes of human T-cell leukemia virus type I are frequently detected in lymphocytes from infected individuals and in infected cell lines. One type of defective provirus contains internal deletions spanning gag, pol, and env genes but retains portions of open reading frames for trans-regulatory proteins. The deleted proviruses could potentially contribute to viral pathology by producing novel gene products that directly affect cell metabolism or that modulate expression of resident, wild-type proviruses. Virus gene products and the control of their expression were examined in cells transfected with defined molecular clones of wild-type and defective proviruses. Internally deleted provirus clones, which are unable to produce functional Tax and Rex proteins, were transcriptionally inactive in transfected cells. Ectopic expression of p40Tax activated transcription of the deleted provirus, resulting in the accumulation of a two-exon mRNA that yields a truncated form of Rex (p21Rex). Although this two-exon mRNA also has a potential initiation codon in the tax frame, a truncated form of Tax was not detected by immunoblotting or in transactivation assays. When complemented with p40Tax and p27Rex, cells transfected with deleted proviruses accumulated an unspliced mRNA that could potentially encode gag-pX fusion proteins. Although expression of deleted proviruses was dependent on trans-acting factors produced from intact proviruses, gene products from defective proviruses did not significantly affect expression of a cotransfected, full-length provirus.

Cell Line↗
PubMed1987

An aberrant avian leukosis virus provirus inserted downstream from the chicken c-myc coding sequence in a bursal lymphoma results from intrachromosomal recombination between two proviruses and deletion of cellular DNA.

A chicken bursal lymphoma, LL6, contains avian leukosis virus DNA integrated 3' of the c-myc coding sequences, unlike all other examined bursal lymphomas, which have integrations 5' to c-myc. To better understand this unusual mutation, we examined a molecular clone containing the LL6 c-myc gene and determined the structure of the proviral insertion by DNA sequencing. Viral DNA begins 575 base pairs downstream of the c-myc coding sequences within the untranslated region, disrupting the use of the normal polyadenylation signal. An internal deletion of the provirus extends from within U3 in the 5' long terminal repeat to within the gp37-coding region of the env gene, disabling virus replication and protein synthesis. Both host-virus boundaries appear normal with respect to the site in viral DNA which is joined to host DNA; both long terminal repeats lack the terminal dinucleotide found in unintegrated DNA. However, in contrast to normal integrations, the six bases of cellular sequence at the 5' junction are not repeated at the 3' junction. The DNA sequences immediately downstream of the LL6 recombinant provirus are not part of the c-myc gene; they originate from the same chromosome as c-myc, but at least 15 kilobases (kb) away. In addition, DNA sequences normally residing 3' of c-myc are deleted in LL6. In summary, these results imply that the LL6 provirus is the result of recombination between two proviruses; that both proviruses were originally downstream of c-myc in the same orientation and separated by at least 15 kb; and that the recombination event was preceded, accompanied, or followed by an internal proviral deletion. No transcript could be detected within a 20-kb region downstream of the LL6 provirus, leaving unresolved the question of whether the additional chromosomal alterations make a specific contribution to LL6 tumorigenesis.

Animals↗
PubMed1981

Retroviruses as mutagens: insertion and excision of a nontransforming provirus alter expression of a resident transforming provirus.

Integration of retroviral DNA appears to occur randomly in host genomes, suggesting that retroviruses can act as insertion mutagens. We have confirmed this prediction by showing that the nontransforming retrovirus, Moloney murine leukemia virus (M-MuLV), can insert its provirus within the selectable target provided by a single provirus in a clonal rat cell line (B31) transformed by Rous sarcoma virus (RSV). Analysis of over 60 morphological revertants of M-MuLV-superinfected B31 cells revealed two lines with inserts of M-MuLV proviruses within the RSV provirus but outside the transforming gene of RSV (src), at sites 0.6 and 4.0 kb from the 5' end. The inserts did not inactivate initiation of RSV RNA synthesis but did affect elongation or processing, or both, generating species with the 5' end of RSV RNA linked to sequences that presumably derive from the inserted M-MuLV DNA. In one mutant line, most of the insert was excised at low frequency, apparently by homologous recombination between repeated sequences at the ends of M-MuLV DNA. After excision, RSV src mRNA was present in normal amounts, and the cells resumed a transformed appearance. In at least four independent lines, large portions of the left end of the RSV provirus (from 1 to 6 kb) and variable amounts of leftward flanking cellular DNA (from 0.5 to 10-15 kb or more) were deleted, without nearby insertions of M-MuLV NA. The deletions removed the putative promoter for synthesis of RSV RNA; in the two cases examined, no RSV RNA was detected. These deletions may represent a second mutational effect of the superinfection by M-MuLV.

Animals↗
PubMed1984

Variations of endogenous chicken proviruses: characterization of new loci of endogenous proviruses in the genome of Italian partridge chickens.

The composition and structure of endogenous proviruses present in the genome of Italian Partridge chickens were studied by the method of blot hybridization using RAV-2 [32P]DNA or LTR of RSV as hybridization probes. The genomes of 5 out of 39 chickens analyzed did not contain endogenous proviruses related to RAV-2. Different sets of five so far undescribed endogenous proviruses, differing in the structure and location, were detected in the DNA of other IP chickens. None of them is identical in its structure to the DNA of the endogenous chicken virus RAV-0, all five loci of endogenous proviruses of IP chickens were defective. The origin, the patterns of genetic variation and the function of endogenous proviruses are discussed.

Animals↗
PubMed2003

Quantification of Human T-lymphotropic virus type I (HTLV-I) provirus load in a rural West African population: no enhancement of human immunodeficiency virus type 2 pathogenesis, but HTLV-I provirus load relates to mortality.

Human T-lymphotropic virus type I (HTLV-I) provirus load was examined in a cohort of a population in Guinea-Bissau among whom human immunodeficiency virus (HIV) type 2 is endemic. Geometric mean of HIV-2 RNA load among HTLV-I-coinfected subjects was significantly lower than that in subjects infected with HIV-2 alone (212 vs. 724 copies/mL; P=.02). Adjusted for age, sex, and HIV status, the risk of death increased with HTLV-I provirus load; mortality hazard ratio was 1.59 for each log10 increase in HTLV-I provirus copies (P=.038). There is no enhancing effect of HTLV-I coinfection on HIV-2 disease, but high HTLV-I provirus loads may contribute to mortality.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

[Molecular cloning of MuLV proviruses integrated into the genome of mouse erythroleukemia cells. I. Characteristics of endogenous proviruses].

The library of genes was obtained from erythroleukemic AKR cells (C-1), that were maintained as suspension culture. Thirty four clones that had homology with 60-70S RNA of Rauscher Leukemia virus (RLV) were separated from this library. The restriction mapping was carried out with 14 clones, that contained most extensive proviral sequences. One clone (107) contains proviral sequences that are derived from one of the components of the RLV complex. The other 13 clones contain sequences of endogenous xenotropic viruses. The endogenous retroviral sequences obtained differ in restrictive maps from proviruses of ecotropic and xenotropic infectious endogenous MuLV and, apparently, might be attributed as non-inducible infectious xenotropic MuLV of class III. Some of the cloned retroviral sequences had symmetrical structure, that is typical for integrated proviruses, i. e. these sequences were separated from flanking cellular ones by long terminal repeats. All investigated retroviral sequences are deletion mutants of MuLV proviruses. It was shown that the inner regions of proviruses diverged more than the long terminal repeats. The expression of the main inner MuLV polypeptide (p30) was detected in NIH 3T3 cells, transfected with DNA of some clones.

Animals↗
PubMed1979

Structural studies on oncornavirus-related sequences in chicken genomic DNA: two-step analyses of EcoRI and Bgl I restriction digests and tentative mapping of a ubiquitous endogenous provirus digests and tentative mapping of a ubiquitous endogenous provirus.

DNA from a variety of uninfected chicken cell types has been analyzed by using restriction endonuclease digestion and RPC-5 ion-exchange chromatography followed by agarose gel electrophoresis. Endogenous retrovirus sequences were detected by using a 32P-labeled avian leukosis viral RNA probe. One simple pattern was identified in an individual containing unexpressed endogenous proviral genes (gs-chf-phenotype for group-specific antigens and chicken helper factor) that was common to all individuals studied. A tentative restriction has been derived for this and one other gs-chf-endogenous provirus. Other gs-chf-individuals and individuals with other phenotypes (e.g., gs+ chf+ and gsl chlfhE) showed more complicated patterns that often included additional bands and thus probably additional proviruses. RNA from an avian sarcoma virus was used to detect cellular sequences (sarc) homologous to the viral transforming gene (src). Results have revealed that a single restriction endonuclease EcoRI fragment of 13 x 10(6) daltons contains the majority of these sequences and confirm that they are not adjacent to the endogenous provirus.

Animals↗
PubMed1990

Human immunodeficiency virus-infected individuals contain provirus in small numbers of peripheral mononuclear cells and at low copy numbers.

In human immunodeficiency virus (HIV)-infected individuals, the proportion of circulating mononuclear cells (PBMCs) which carry HIV provirus and the number of HIV proviral sequences per infected PBMC have been matters for conjecture. Using a double polymerase chain reaction which allows the detection of single molecules of provirus and a method of quantifying the provirus molecules, we have measured provirus frequencies in infected individuals down to a level of one molecule per 10(6) PBMCs. As a general rule, only a small proportion of PBMCs contain provirus (median value of samples from 12 patients, one per 8,000 cells), and most if not all of the infected cells carry a single provirus molecule. The frequency of provirus-carrying cells correlated positively both with the progression of the disease and with the success with which virus could be isolated from the same patients by cocultivation methods. Of seven asymptomatic (Centers for Disease Control stage II) patients, all but one contained one provirus molecule per 6,000 to 80,000 cells; of five Centers for Disease Control stage IV patients, all but one contained one provirus molecule per 700 to 3,300 cells. When considered in conjunction with estimates of the frequency of PBMCs that express viral RNA, our results suggest that either (i) the majority of provirus-containing cells are monocytes or (ii) most provirus-containing lymphocytes are transcriptionally inactive. We also present nucleotide sequence data derived directly from provirus present in vivo which we show is not marred by the in vitro selection of potential virus variants or by errors introduced by Taq polymerase. We argue from these data that, of the provirus present in infected individuals, the proportion which is defective is not high in the regions sequenced.

Base Sequence↗
PubMed1995

Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas.

Evi-2, a common site of viral integration in BXH-2 myeloid lymphomas, is located within a large intron of the Nf1 tumor suppressor gene. Viral integration at Evi-2 appears to induce disease by disrupting normal Nf1 expression. During our attempts to characterize the nature of the proviruses located at Evi-2, we found that approximately half of the proviruses were defective nonecotropic proviruses (A. M. Buchberg, H. G. Bedigian, N. A. Jenkins, and N. G. Copeland, Mol. Cell. Biol. 10:4658-4666, 1990). This was surprising, since most proviruses characterized at other BXH-2 common integration sites are full-length ecotropic viruses. In the studies described here, we found that this defective provirus carries two large deletions, one in pol and one in env, and is structurally related to another murine retrovirus, the murine AIDS retrovirus. By using oligonucleotide probes specific for this defective provirus, designated MRV, we showed that MRV-related proviruses are carried as endogenous germ line proviruses in most inbred strains. In addition, we identified the endogenous MRV provirus that gives rise to the defective proviruses identified at Evi-2. We present a model that accounts for the positive selection of MRV proviruses at Evi-2, which may allow selective identification of common viral integration sites harboring tumor suppressor genes.

Acquired Immunodeficiency Syndrome↗
PubMed2026

Unraveling the diversity, function, and virus-host interactions of archaeal proviruses.

Archaea, the third domain of life, play critical roles in global biogeochemical cycles. However, archaeal proviruses integrated into host genomes remain largely unexplored. To bridge this gap, we conducted a large-scale mining of genomes spanning all presently known 21 archaeal phyla for their proviruses. We identified 770 archaeal proviruses across 12 archaeal phyla and 84 families, which clustered into 655 viral operational taxonomic units (vOTUs). Among these, 86.1% of the vOTUs were novel at the species level, and 69.3% could not be classified at the family level, substantially expanding the known diversity of archaeal viruses. Additionally, phylogenomic analysis supported the proposal of 16 putative novel viral families, further extending the current taxonomy landscape of archaeal viruses. Notably, 21.8% of the identified proviruses were predicted to adopt a lytic lifestyle, suggesting that these proviruses may retain the capacity to enter the lytic cycle under appropriate conditions. Host prediction indicated only 14 out of the 655 vOTUs might have potential across-lineage infection abilities. We detected 63 anti-defense genes encoded by 61 provirus genomes, such as anti-CRISPR and anti-RM, suggesting an ongoing evolutionary arms race between hosts and proviruses. However, only 10 auxiliary metabolic genes (AMGs) were identified, suggesting a limited impact of proviruses in the modulation of host metabolism through AMGs. This study establishes a systematic global genomic atlas of archaeal proviruses, advancing our understanding of their distribution and diversity while providing a foundation for future research into how proviruses regulate archaeal metabolism and ecosystem functioning.

anti-defense system↗
PubMed2001

Feline leukaemia provirus load during the course of experimental infection and in naturally infected cats.

Feline leukaemia virus (FeLV) infection in domestic cats can vary in its outcome (persistent, transient, no infection) for reasons that are not entirely known. It was hypothesized that the initial virus and provirus load could significantly influence the course of retrovirus infection. To determine the role of provirus loads, two methods of PCR, a nested PCR and a fluorogenic probe-based (TaqMan) real-time quantitative PCR, which were specific to the U3 region of FeLV-A were established. FeLV provirus in naturally and experimentally infected cats was then measured. Only 3 weeks after experimental FeLV-A infection, persistently infected cats demonstrated higher provirus loads and lower humoral immune responses than cats that had overcome antigenaemia. Lower initial provirus loads were associated with successful humoral immune responses. Unexpectedly, provirus in the buffy-coat cells of two cats that tested negative for the p27 antigen (a marker for viraemia) was also detected. In 597 Swiss cats, comparison of p27 antigen levels with PCR results revealed broad agreement. However, similar to the experimental situation, a significant number of animals (10%) was negative for the p27 antigen and FeLV-positive by PCR. These cats had a mean provirus load 300-fold lower than that of animals testing positive for the p27 antigen. In conclusion, an association between the provirus load and the outcome of FeLV infection was found. Detection of provirus carriers should contribute to further the control of FeLV. In addition, quantification of provirus loads will lead to a better understanding of FeLV pathogenesis and anti-retrovirus protective mechanisms.

Animals↗
PubMed2005

Precise identification of endogenous proviruses of NFS/N mice participating in recombination with moloney ecotropic murine leukemia virus (MuLV) to generate polytropic MuLVs.

Polytropic murine leukemia viruses (MuLVs) are generated by recombination of ecotropic MuLVs with env genes of a family of endogenous proviruses in mice, resulting in viruses with an expanded host range and greater virulence. Inbred mouse strains contain numerous endogenous proviruses that are potential donors of the env gene sequences of polytropic MuLVs; however, the precise identification of those proviruses that participate in recombination has been elusive. Three different structural groups of proviruses in NFS/N mice have been described and different ecotropic MuLVs preferentially recombine with different groups of proviruses. In contrast to other ecotropic MuLVs such as Friend MuLV or Akv that recombine predominantly with a single group of proviruses, Moloney MuLV (M-MuLV) recombines with at least two distinct groups. In this study, we determined that only three endogenous proviruses, two of one group and one of another group, are major participants in recombination with M-MuLV. Furthermore, the distinction between the polytropic MuLVs generated by M-MuLV and other ecotropic MuLVs is the result of recombination with a single endogenous provirus. This provirus exhibits a frameshift mutation in the 3' region of the surface glycoprotein-encoding sequences that is excluded in recombinants with M-MuLV. The sites of recombination between the env genes of M-MuLV and endogenous proviruses were confined to a short region exhibiting maximum homology between the ecotropic and polytropic env sequences and maximum stability of predicted RNA secondary structure. These observations suggest a possible mechanism for the specificity of recombination observed for different ecotropic MuLVs.

Animals↗
PubMed1987

Replication-defective chimeric helper proviruses and factors affecting generation of competent virus: expression of Moloney murine leukemia virus structural genes via the metallothionein promoter.

Two chimeric helper proviruses were derived from the provirus of the ecotropic Moloney murine leukemia virus by replacing the 5'long terminal repeat and adjacent proviral sequences with the mouse metallothionein I promoter. One of these chimeric proviruses was designed to express the gag-pol genes of the virus, whereas the other was designed to express only the env gene. When transfected into NIH 3T3 cells, these helper proviruses failed to generate competent virus but did express Zn2+-inducible trans-acting viral functions needed to assemble infectious vectors. One helper cell line (clone 32) supported vector assembly at levels comparable to those supported by the Psi-2 and PA317 cell lines transfected with the same vector. Defective proviruses which carry the neomycin phosphotransferase gene and which lack overlapping sequence homology with the 5' end of the chimeric helper proviruses could be transfected into the helper cell line without generation of replication-competent virus. Mass cultures of transfected helper cells produced titers of about 10(4) G418r CFU/ml, whereas individual clones produced titers between 0 and 2.6 X 10(4) CFU/ml. In contrast, defective proviruses which share homologous overlapping viral sequences with the 5' end of the chimeric helper proviruses readily generated infectious virus when transfected into the helper cell line. The deletion of multiple cis-acting functions from the helper provirus and elimination of sequence homology overlapping at the 5' ends of helper and vector proviruses both contribute to the increased genetic stability of this system.

Animals↗
PubMed2024

Discovery and characterization of complete genomes of 38 head-tailed proviruses in four predominant phyla of archaea.

Archaea play a significant role in natural ecosystems and the human body. Archaeal viruses exert a considerable influence on the structure and composition of archaeal communities and their associated ecological environments. The present study revealed the complete genomes of 38 archaeal head-tailed proviruses through comprehensive data mining. The hosts of these proviruses were identified as belonging to the following four dominant phyla: Halobacteriota, Thermoplasmatota, Thermoproteota, and Nanoarchaeota. In addition to the 14 proviruses of halophilic archaea related to the Graaviviridae family, the remaining proviruses exhibited limited genetic similarities to known (pro)viruses, suggesting the existence of 14 potential novel families. Of the 38 archaeal proviruses, 30 have the potential to lyse host cells. Eleven proviruses contain genes linked to antiviral defense mechanisms, including those involved in restriction modification (RM), clustered regularly interspaced short palindromic repeat (CRISPR)-associated (CRISPR-Cas) nucleases, defense island system associated with restriction-modification (DISARM), and DNA degradation (Dnd). Moreover, auxiliary metabolic genes were identified in the proviruses of Bathyarchaeia and Halobacteriota archaea, including those involved in carbohydrate and amino acid metabolism. Our findings indicate the diversity of archaeal viruses, their interactions with archaeal hosts, and their roles in the adaptation of the host.IMPORTANCEThe field of archaeal virology has seen a rapid expansion through the use of metagenomics, yet the diversity of these viruses remains largely uncharted. In this study, the complete genomes of 38 novel archaeal proviruses were identified for the following four dominant phyla: Halobacteriota, Thermoplasmatota, Thermoproteota, and Nanoarchaeota. Two families and six genera of Archaea were the first to be identified as hosts for viruses. The proviruses were found to contain diverse genes that were involved in distinct adaptation strategies of viruses to hosts. Our findings contribute to the expansion of the lineages of archaeal viruses and highlight their intricate interactions and essential roles in enabling host survival and adaptation to diverse environmental conditions.

Archaea↗
PubMed1999

Rapid quantification of HTLV-I provirus load: detection of monoclonal proliferation of HTLV-I-infected cells among blood donors.

In this report, we quantified HTLV-I provirus load using the AmpliSensor system, which utilizes fluorescence to measure PCR products. With this method, provirus loads could be measured within 6 hr, and the results obtained correlated well with those obtained by other methods. Samples from 256 blood donors, who were positive for antibodies against HTLV-I, were analyzed, showing that provirus load ranged from less than 0.1% to 56% among carriers. We analyzed the association between provirus load and the biomarkers age and sex and found that it was not influenced by either. Provirus load was better correlated with soluble interleukin-2 receptor (sIL-2R) levels than with antibody titer against the virus. Among 18 blood donors with high provirus load (more than 10%), Southern blotting detected monoclonal integration of HTLV-I in infected cells in 2 cases, both of them showing high sIL-2R levels (more than 900 U/ml). Sequential analyses of provirus load showed stable levels of provirus in the same carriers, suggesting that some factors other than age or sex determined provirus load in infected individuals. Thus, this rapid method is a useful tool for the early detection of adult T-cell leukemia and other HTLV-I-associated diseases.

Adolescent↗
PubMed1988

Mouse mammary tumor proviruses from a T-cell lymphoma are associated with the retroposon L1Md.

Four Charon 4A clones containing mouse mammary tumor virus (MMTV) proviruses and their cellular flanking sequences were obtained from partial EcoRI libraries of a C57BL/6 T-cell lymphoma with both endogenous and newly acquired MMTV proviruses. The cellular flanking sequences of three of four MMTV proviruses contained DNA homologous to the 3' end of the long interspersed retroposon L1Md. Two of the three proviruses were newly acquired in the lymphoma DNA, and these MMTV proviruses appeared to be 5 kilobases downstream and in the same transcriptional orientation as the L1 sequence. The third provirus was endogenous Mtv-9 and was located less than 500 base pairs from the 3' end of L1. Seven additional clones containing MMTV proviruses were isolated from partial MboI libraries of a B6 T-cell lymphoma. Five of the seven clones contained L1 elements in the cellular DNA flanking MMTV DNA. At least two clones (including one with the Mtv-8 provirus) had multiple L1 copies flanking the MMTV provirus, and one clone contained a single MMTV long terminal repeat directly integrated into a truncated L1 sequence. Although the frequencies of B1 and L1 in random library clones were similar, only one MMTV-containing clone hybridized to the abundant repetitive element B1. These data suggest a nonrandom association between MMTV and L1Md.

Animals↗
PubMed1980

Proviruses of mouse mammary tumor virus in normal and neoplastic tissues from GR and C3Hf mouse strains.

We analyzed two experimental situations to assess the role of endogenous mouse mammary tumor virus (MMTV) DNA in the genesis of mammary carcinomas. (i) GR mice carry in their germ line one or more proviruses indistinguishable by limited restriction mapping from the proviruses introduced into cells by experimental infection with the highly tumorigenic virus isolated from GR mouse milk, MMTV(GR). Most tumors arising in GR mice contain one or more proviruses at various sites in tumor DNA in addition to those present endogenously. Detection of these new proviruses is possible as a consequence of the clonal or quasiclonal character of the tumors. (ii) C3H/He mice carry three units of endogenous viral DNA, none of which resembles the DNA of the commonly encountered strains of milk-borne MMTV. Nevertheless, MMTV-associated tumors arise late in life when these animals are removed from the influence of milk-borne virus; the responsible agent, MMTV(C3Hf), can also produce tumors in BALB/c mice. We found that tumors arising in both C3Hf/He mice and BALB/c mice infected with MMTV(C3Hf) were clonal or quasiclonal and contained one or more new copies of proviral DNA at various sites in the host genome. These new proviruses were readily distinguished from the proviruses of the common milk-borne virus strains and closely resembled unit II of endogenous MMTV DNA (Cohen et al., J. Virol., 32:483-496). Thus, in both experimental systems, we found evidence for new proviruses in mammary tumors, despite the preexistence of similar or identical proviruses in the germ line. The results suggest that the repositioning of MMTV proviruses may be required for the full expression of the oncogenic potential of endogenous MMTV DNA.

Animals↗