A portion of the feline leukaemia virus genome is not endogenous in cat cells

Okabe, Hiromi; duBuy, Jeannine; Gilden, Raymond V.; Gardner, Murray B.

doi:10.1002/ijc.2910220114

Cited by 17 publications

(11 citation statements)

References 30 publications

(36 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FISH also detected one copy among four X chromosomes and three copies per normal Y chromosome; thus, the total number of enFeLV copies per diploid genome averaged 19.75 in females and 22.5 in males. Half of this diploid average yields 9.87 and 11.25 copies per haploid genome in females and males, respectively, rendering the FISH-based estimate consistent with the previous hybridization studies of reassociation kinetics that had estimated 6 to 10 enFeLV copies per haploid genome (5,39,40,42).…”

Section: Discussionsupporting

confidence: 84%

See 1 more Smart Citation

Insertional Polymorphisms of Endogenous Feline Leukemia Viruses

Roca

Nash

Menninger

et al. 2005

J Virol

View full text Add to dashboard Cite

The number, chromosomal distribution, and insertional polymorphisms of endogenous feline leukemia viruses (enFeLVs) were determined in four domestic cats (Burmese, Egyptian Mau, Persian, and nonbreed) using fluorescent in situ hybridization and radiation hybrid mapping. Twenty-nine distinct enFeLV loci were detected across 12 of the 18 autosomes. Each cat carried enFeLV at only 9 to 16 of the loci, and many loci were heterozygous for presence of the provirus. Thus, an average of 19 autosomal copies of enFeLV were present per cat diploid genome. Only five of the autosomal enFeLV sites were present in all four cats, and at only one autosomal locus, B4q15, was enFeLV present in both homologues of all four cats. A single enFeLV occurred in the X chromosome of the Burmese cat, while three to five enFeLV proviruses occurred in each Y chromosome. The X chromosome and nine autosomal enFeLV loci were telomeric, suggesting that ectopic recombination between nonhomologous subtelomeres may contribute to enFeLV distribution. Since endogenous FeLVs may affect the infectiousness or pathogenicity of exogenous FeLVs, genomic variation in enFeLVs represents a candidate for genetic influences on FeLV leukemogenesis in cats.Endogenous feline leukemia virus (enFeLV) sequences are present in the genome of the domestic cat, Felis catus. They are homologous to exogenous feline leukemia viruses, which are oncogenic retroviruses capable of inducing both proliferative and degenerative diseases (15, 34). Whereas exogenous FeLVs are transmitted horizontally, endogenous feline leukemia proviruses are part of the germ line and are transmitted from parent to offspring as integral components of chromosomes (5,20). Endogenous FeLVs are found in wild species of the genus Felis closely related to the domestic cat, although they are not present in species from other lineages within the Felidae (4, 56-58). Thus, enFeLVs are believed to have entered the germ line after the initial radiation of lineages in the cat family but before the radiation of domestic cat lineage species (3,23,25), although subsequent additional integrations into the germ line may also have occurred (50).Endogenous FeLV sequences do not by themselves produce infectious virus but readily recombine with exogenous feline leukemia viruses, notably in the env region that codes for the viral coat, producing recombinant viruses with altered biological activity and pathogenicity (4,17,21,43,44,51,53,54,60). For example, the recombinant subgroup C viruses have been found to induce aplastic anemia (18). Furthermore, portions of the enFeLV env region are transcribed and translated in lymphoma and other cell lines (26), producing a truncated envelope protein that inhibits infection by exogenous subgroup B feline leukemia viruses (26). Transcription and translation of enFeLVs have also been demonstrated in tissues from healthy cats, including lymphoid tissue, suggesting a protective role for enFeLVs in vivo (7, 26). Likewise, inoculation with recombinant subgroup B exogenous FeLV attenuates ...

show abstract

Section: Discussionsupporting

confidence: 84%

“…The probe template excluded the proviral LTRs in order to preclude detection of ca. 150 copies of enFeLV LTRs without associated coding regions that are present in the genome (6,8,40). The presence of exogenous FeLV proviruses in the genomes of the four cats was ruled out by PCR screening (see Materials and Methods).…”

Section: Resultsmentioning

confidence: 99%

Insertional Polymorphisms of Endogenous Feline Leukemia Viruses

Roca

Nash

Menninger

et al. 2005

J Virol

View full text Add to dashboard Cite

show abstract

“…For example, for cat 1449 (12). Comparison of the sequence organization of the endogenous U5 segment from different cell lines and from tissues of uninfected cats shows that the major hybridizing bands are conserved but that the relative amount of U5 DNA in a given band varies significantly.…”

Section: Resultsmentioning

confidence: 99%

The U3 portion of feline leukemia virus DNA identifies horizontally acquired proviruses in leukemic cats.

Casey¹,

Roach²,

Mullins³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The presence and location of DNA sequences related to the U3 and U5 portions ofthe infectious exogenous feline leukemia virus (FeLV) long terminal repeat (LTR) in various cat DNAs have been determined by hybridization experiments. In uninfected cat DNAs, the U5 LTR segment from the GardnerArnstein strain B virus is present at approximately 150 copies per cell. This level is approximately 10-fold greater than that of endogenous internal FeLV sequences. The U5 sequences differ in copy number and, to some extent, in location from one animal to another. For any one animal, the sequence organization ofthe U5

show abstract

“…The U3 region forms the 5Ј end of each proviral LTR (in enFeLV-AGTT, the 568-bp LTR includes a 423-bp U3 region). The U3 region has been used as a straightforward means of distinguishing between exFeLV and enFeLV sequences in hybridization studies (7,29), and the U3 sequences of enFeLV-AGTT and enFeLV-GGAG readily identified them as enFeLVs and not exFeLVs. Because of the absence of homology, exFeLV LTRs were not included in the LTR phylogenetic analyses, which revealed that enFeLV LTRs cluster into two groups ( Fig.…”

mentioning

confidence: 99%

Genomically Intact Endogenous Feline Leukemia Viruses of Recent Origin

Roca

Pecon-Slattery

O’Brien

2004

J Virol

View full text Add to dashboard Cite

We isolated and sequenced two complete endogenous feline leukemia viruses (enFeLVs), designated enFeLV-AGTT and enFeLV-GGAG. In enFeLV-AGTT, the open reading frames are reminiscent of a functioning FeLV genome, and the 5 and 3 long terminal repeat sequences are identical. Neither endogenous provirus is genetically fixed in cats but polymorphic, with 8.9 and 15.2% prevalence for enFeLV-AGTT and enFeLV-GGAG, respectively, among a survey of domestic cats. Neither provirus was found in the genomes of related species of the Felis genus, previously shown to harbor enFeLVs. The absence of mutational divergence, polymorphic incidence in cats, and absence in related species suggest that these enFeLVs may have entered the germ line more recently than previously believed, perhaps coincident with domestication, and reopens the question of whether some enFeLVs might be replication competent.Endogenous feline leukemia virus (enFeLV) sequences are present in the genome of the domestic cat, Felis catus, with an estimated 6 to 12 copies per haploid genome (4,17,28,30,31). These sequences are homologous to exogenous FeLVs (exFeLVs), which are horizontally transmitted oncogenic retroviruses capable of inducing both proliferative and degenerative diseases (12,27). Endogenous feline leukemia proviruses are part of the germ line and are transmitted from parent to offspring as integral components of chromosomes (4, 17). enFeLV sequences do not produce infectious virus, and attempts to rescue or induce endogenous virus by cocultivation in cell lines have failed (3,19). Restriction enzyme mapping has revealed the presence of large deletions in some enFeLVs, which would render them incapable of producing an exogenous virus (41, 42). Molecular copies of enFeLVs without major deletions were found in DNA transfection studies also to be noninfectious, presumably owing either to alterations in sequences regulating gene expression or to coding sequence mutation (42). Both frameshift and nonsense mutations have been identified in the gag and env regions of full-length enFeLVs (5, 27).Although they do not produce infections on their own, enFeLV sequences readily recombine with exFeLVs (32, 37, 43). Transmissible exFeLVs lack recombinant enFeLV segments and are classified as subgroup A (12, 15). The two other exFeLV subgroups, B and C, result from recombination between enFeLV segments and exFeLVs (27,32,35,43). Recombinant viruses may exhibit altered biological activity and pathogenicity (13,33,37,39,47); for example, the recombinant subgroup C viruses have been found to induce aplastic anemia (14). Additionally, segments of enFeLVs are transcribed and translated in lymphoma and other cell lines: a truncated enFeLV envelope protein has been detected that inhibits infection by subgroup B exFeLVs (24). Transcription and translation of enFeLV genes have also been demonstrated in tissues from healthy cats, including lymphoid tissue, raising the prospect of a protective role for enFeLVs in vivo (6,24). In contrast, a protein derived from an enFeLV env...

show abstract

A portion of the feline leukaemia virus genome is not endogenous in cat cells

Cited by 17 publications

References 30 publications

Insertional Polymorphisms of Endogenous Feline Leukemia Viruses

Insertional Polymorphisms of Endogenous Feline Leukemia Viruses

The U3 portion of feline leukemia virus DNA identifies horizontally acquired proviruses in leukemic cats.

Genomically Intact Endogenous Feline Leukemia Viruses of Recent Origin

Contact Info

Product

Resources

About