Structural diversity and nuclear protein binding sites in the long terminal repeats of feline leukemia virus

Fulton, Ruth; Plumb, Mark; Shield, Lesley; Neil, James C.

doi:10.1128/jvi.64.4.1675-1682.1990

Cited by 57 publications

(53 citation statements)

References 49 publications

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“…1,2 FeLV is transmitted among domestic cats and is associated with a variety of neoplastic and nonneoplastic diseases. [18][19][20][21][22][23][24][25][26] Some peculiar FeLV strains induce specific diseases such as immunodeficiency and pure red cell aplasia. [27][28][29] Cats with naturally occurring thymic lymphoma are infected with FeLVs that have a repetition of the enhancer sequence in the long terminal repeats of the viral genome.…”

Section: Discussionmentioning

confidence: 99%

Hematologic Abnormalities and Outcome of 16 Cats with Myelodysplastic Syndromes

Hisasue¹,

Okayama²,

Okayama³

et al. 2001

J Vet Int Med

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We investigated the hematologic abnormalities and prognoses in 16 cats with myelodysplastic syndromes (MDS). Nonregenerative anemia, thrombocytopenia, and neutropenia were observed in 15, 13, and 4, respectively, of the 16 cats with MDS. Morphologic abnormalities characteristic of MDS included megaloblastoid rubricytes (9 cats), hyposegmentation of neutrophils (7 cats), nuclear abnormality of rubricytes (10 cats) and neutrophils (13 cats), and micromegakaryocytes (10 cats). Disease in these 16 cats was subclassified into refractory anemia (RA; 8 cats), RA with excess of blasts (RAEB; 5 cats), RAEB in transformation (RAEB in T; 1 cat), and chronic myelomonocytic leukemia (CMMoL; 2 cats), according to the human French-American-British (FAB) classification. In the cats in which the clinical outcome was known, 3 of 6 cats with high blast cell count MDS, including RAEB, RAEB in T, and CMMoL, developed acute myeloid leukemia, but only 1 of 8 cats with low blast cell count MDS (RA) developed acute myeloid leukemia. Based on the Dusseldorf scoring system for the prognosis of human MDS, the survival times of the cats showing high scores (> or =3 points) were significantly shorter than those of the cats with low scores (<3 points). The FAB classification and Dusseldorf scoring system were considered to be useful for predicting the prognosis of feline MDS. Furthermore, 15 of the 16 cats with MDS in this study were infected with feline leukemia virus, indicating its possible etiologic role in the pathogenesis of feline MDS.

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Section: Discussionmentioning

confidence: 99%

Hematologic Abnormalities and Outcome of 16 Cats with Myelodysplastic Syndromes

Hisasue¹,

Okayama²,

Okayama³

et al. 2001

J Vet Int Med

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“…Therefore, we could rule out false negative results in the U3-PCR due to PCR inhibitors or poor DNA quality (fragmentation by autolysis or treatment). The band represents endogenous gp70 sequences, but may also be exogenously acquired (Fulton et al, 1990;Berry et al, 1988). 16 of the immunohistologically positive cats additionally showed a band at 305 bp indicating exogenously acquired gp70 originating from the FeLV subtypes A or C (Fulton et al, 1990;Berry et al, 1988).…”

Section: Gp70-pcrmentioning

confidence: 93%

High prevalence of non-productive FeLV infection in necropsied cats and significant association with pathological findings

Suntz

Failing

Hecht

et al. 2010

Veterinary Immunology and Immunopathology

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Applying a combination of semi-nested PCR and immunohistology (IHC), the presence of exogenous feline leukemia virus infection was studied in 302 necropsied cats with various disorders. 9% showed the classical outcome of persistent productive FeLV infection which was represented by FeLV antigen expression in different organs. 152 cats (50%) harboured exogenous FeLV-specific proviral sequences in the bone marrow but did not express viral antigen. These cats were considered as horizontally but non-productively infected. Statistical evaluation showed a significant association of non-productive horizontal FeLV infection with a variety of parameters. Non-productively infected cats were statistically significantly older and more often originated from animal shelters than cats without exogenous FeLV infection. Furthermore, some pathological disorders like anemia, panleukopenia, and purulent inflammation showed significant association with non-productive FeLV infection. No significant association was found with lymphosarcoma, known for a long time to be induced by productive FeLV infection.

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“…Proviral gene expression is regulated by cis-acting promoter and enhancer sequences in the U3 region of the LTR. This region contains a cluster of consensus sequences that encode putative binding sites for nuclear proteins (Figure 1) (Fulton et al, 1990;Plumb et al, 1991). The two major transcription products of proviral DNA are a full-length RNA, which is either incorporated as infectious virion RNA or used as the template for trans- Fulton et al (1990)).…”

Section: Viral Structure Genetic Organization and Felv Gene Productsmentioning

confidence: 99%

“…This region contains a cluster of consensus sequences that encode putative binding sites for nuclear proteins (Figure 1) (Fulton et al, 1990;Plumb et al, 1991). The two major transcription products of proviral DNA are a full-length RNA, which is either incorporated as infectious virion RNA or used as the template for trans- Fulton et al (1990)). These include sequences homologous to LVB and nuclear factor l (NF1) binding sites, the SV 40 core enhancer sequence (CORE), a glucocorticoid response element (GRE) sequence, and a novel FeLV-specific binding site (FLV-1), The FeLV precursor proteins and the known and deduced mature proteins are discussed in detail in the text.…”

Section: Viral Structure Genetic Organization and Felv Gene Productsmentioning

confidence: 99%

“…Second, some thymic tumours associated with FeLV-A/61E (Rohn et al, 1994) or the Rickard strain of FeLV (FeLV-A/R) (Fulton et al, 1990;Neil et al, 1991) and some spontaneous FeLV-associated lymphoid (and myeloid) malignancies (Matsumoto et al, 1992) are linked to proviruses that contain direct repeats of enhancer motifs in the U3 region of the LTR. These LTR repeats likely augment the enhancer and promoter functions of the viral LTR; and they would increase the expression of nearby rearranged host proto-oncogenes.…”

Section: Pathogenesis Of Felv-induced Lymphomasmentioning

confidence: 99%

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4 Haematological disorders associated with feline retrovirus infections

Linenberger¹,

Abkowitz²

1995

Baillière's Clinical Haematology

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Feline oncornavirus and lentivirus infections have provided useful models to characterize the virus and host cell factors involved in a variety of marrow suppressive disorders and haematological malignancies. Exciting recent progress has been made in the characterization of the viral genotypic features involved in FeLV-associated diseases. Molecular studies have clearly defined the causal role of variant FeLV env gene determinants in two disorders: the T-lymphocyte cytopathicity and the clinical acute immunosuppression induced by the FeLV-FAIDS variant and the pure red cell aplasia induced by FeLV-C/Sarma. Variant or enFeLV env sequences also appear to play a role in FeLV-associated lymphomas. Additional studies are required to determine the host cell processes that are perturbed by these variant env gene products. In the case of the FeLV-FAIDS variant, the aberrant env gene products appear to impair superinfection interference, resulting in accumulation of unintegrated viral DNA and cell death. In other cases it is likely that the viral env proteins interact with host products that are important in cell viability and/or proliferation. Understanding of these mechanisms will therefore provide insights to factors involved in normal lymphohaematopoiesis. Similarly, studies of FeLV-induced haematological neoplasms should reveal recombination or rearrangement events involving as yet unidentified host gene sequences that encode products involved in normal cell growth regulation. These sequences may include novel protoncogenes or sequences homologous to genes implicated in human haematological malignancies. The haematological consequences of FIV are quite similar to those associated with HIV. As with HIV, FIV does not appear to directly infect myeloid or erythroid precursors, and the mechanisms of marrow suppression likely involve virus, viral antigen, and/or infected accessory cells in the marrow microenvironment. Studies using in vitro experimental models are required to define the effects of each of these microenvironmental elements on haematopoietic progenitors. As little is known about the molecular mechanisms of FIV pathogenesis, additional studies of disease-inducing FIV strains are needed to identify the genotypic features that correlate with virulent phenotypic features. Finally, experimental FIV infection in cats provides the opportunity to correlate in vivo virological and haematological changes with in vitro observations in a large animal model that closely mimics HIV infection in man.

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Structural diversity and nuclear protein binding sites in the long terminal repeats of feline leukemia virus

Cited by 57 publications

References 49 publications

Hematologic Abnormalities and Outcome of 16 Cats with Myelodysplastic Syndromes

Hematologic Abnormalities and Outcome of 16 Cats with Myelodysplastic Syndromes

High prevalence of non-productive FeLV infection in necropsied cats and significant association with pathological findings

4 Haematological disorders associated with feline retrovirus infections

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