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

Casey, James W.; Roach, Arthur; Mullins, James I.; Burck, Kathy B.; Nicolson, Margery; Gardner, Murray B.; Davidson, Norman

doi:10.1073/pnas.78.12.7778

Cited by 66 publications

(38 citation statements)

References 16 publications

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“…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%

“…The number of copies of enFeLV per haploid genome has been estimated as 6 to 12 (5,20,39,41,42), arranged in a nontandem manner (20), while the number of freestanding long terminal repeats (LTRs), believed to have lost their associated coding regions through unequal crossing over during recombination, is ϳ150 (8). Despite the biomedical impact of feline leukemia viruses and the established capacity of endogenous feline leukemia viruses to recombine with exogenous virus to influence infection and disease progression, the genomic distribution and variation of enFeLVs among domestic cats have not been well characterized.…”

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confidence: 99%

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Insertional Polymorphisms of Endogenous Feline Leukemia Viruses

Roca

Nash

Menninger

et al. 2005

J Virol

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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 ...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Insertional Polymorphisms of Endogenous Feline Leukemia Viruses

Roca

Nash

Menninger

et al. 2005

J Virol

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“…We based the RNA qPCR assay on the U3 sequence of FeLV-61E-A (the replication competent, non-acutely pathogenic component of the FeLV-FAIDS complex) (Mullins et al, 1986;Hoover et al, 1987;Donahue et al, 1988;Overbaugh et al, 1988) both to increase the probability of detecting other strains of FeLV-A, owing to the conservation of the U3 region, (Casey et al, 1981;Berry et al, 1988) and to minimize the potential for detection of RNA that may under some circumstances be transcribed from the endogenous env sequences present in the feline genome (Busch et al, 1983;McDougall et al, 1994). Our assay proved to be highly sensitive, specific, reproducible, and allowed reliable quantitation.…”

Section: Discussionmentioning

confidence: 99%

“…We designed a primer/probe set to amplify exogenous and not endogenous FeLV sequences within the U3 region of FeLV-61E-A (Casey et al, 1981;Berry et al, 1988) as previously described (Torres et al, 2005). These primers and probe were used to detect both FeLV RNA and FeLV DNA.…”

Section: Primers and Probe For Rna And Dna Qpcr Assaysmentioning

confidence: 99%

Development and application of a quantitative real-time PCR assay to detect feline leukemia virus RNA

Torres¹,

O’Halloran²,

Larson³

et al. 2008

Veterinary Immunology and Immunopathology

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We previously defined four categories of FeLV infection, designated as abortive, regressive, latent, and progressive. To determine if detectable viral DNA is transcriptionally active in the absence of antigenemia, we developed and validated a real-time viral RNA qPCR assay. This assay proved to be highly sensitive, specific, reproducible, and allowed reliable quantitation. We then applied this methodology, together with real-time DNA qPCR and p27 capsid antigen capture ELISA, to examine cats challenged with FeLV. We found that circulating viral RNA and DNA levels were highly correlated and the assays were almost in perfect agreement. This indicates that the vast majority of viral DNA is transcriptionally active, even in the absence of antigenemia. The real-time qPCR assays are more sensitive than the most commonly used FeLV diagnostic assay, the p27 capsid antigen capture ELISA. Application of qPCR assays may add greater depth in understanding of FeLV-host relationships.

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“…has no close counterpart in the germ-line DNA of cats (Casey et at., 1981), it can be concluded that the FeLV-B/GM1 U3 sequence is of exogenous FeLV origin. It is interesting that no infectious FeLV has yet been found to contain an enFeLV U3 sequence, even though some enFeLV LTRs are active in directing the transcription of reporter genes in transient expression assays (Berry et al, 1988).…”

Section: G~b-3 Ii61ementioning

confidence: 99%